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PubMed1989

Lymphoid infiltrates of the orbit and conjunctiva. A morphologic and immunophenotypic study of 99 cases.

Most of the earlier clinicopathologic studies of orbital and conjunctival lymphoid infiltrates were done before the development of immunohistologic methods. In this study, we have examined 99 lymphoid infiltrates of the orbit and conjunctiva immunohistologically and correlated clinical and histologic features with immunophenotype. Sixty-six infiltrates expressed monotypic immunoglobulin; one case was immunoglobulin-negative, B-lineage; and 32 infiltrates expressed polytypic immunoglobulin. Using histologic criteria, 36 cases were malignant (35 monotypic; one immunoglobulin-negative, B-lineage), 44 were indeterminate (31 monotypic, 13 polytypic), and 19 were benign (all polytypic). Combining histologic and immunophenotypic criteria, 67 cases were diagnosed as malignant lymphoma. Seventy-six percent of the lymphomas were classified as low-grade according to the Working Formulation; small lymphocytic lymphoma (45%) was the most common histologic subtype. Cytologic atypia (p less than .0001) and Dutcher bodies (p less than .05) were found only in lymphomas. Similarly, bilateral involvement (p less than .05) and dissemination at time of presentation (p less than .001) occurred only in lymphomas. No other histologic or clinical features reliably distinguished lymphomas from benign orbital and conjunctival lymphoid infiltrates. Nineteen patients had a prior history of extraorbital malignant lymphoma, and eight patients had a history of pseudolymphoma. Patients with a history of malignant lymphoma more often presented with dissemination (p less than .001) and less often had the small lymphocytic subtype (p = .07) than patients without a history of lymphoma. However, not all patients with a history of extraorbital lymphoma had monotypic orbital and conjunctival infiltrates, and the incidence of monotypic orbital and conjunctival lesions in these patients was similar to that of the patients without a history of lymphoma. Patients with a history of pseudolymphoma always presented with localized disease (p less than .01) and more often had benign lesions (p = .08) as compared with patients without a history of pseudolymphoma. We conclude that the presence of either cytologic atypia or Dutcher bodies is a reliable criterion of malignant lymphoma in the orbit and conjunctiva. However, for one-third of the cases in this study, immunohistologic studies were the only means of distinguishing malignant from benign lymphoid infiltrates.

Conjunctiva↗

PubMed2000

Infiltrative keratitis associated with extended wear of hydrogel lenses and Abiotrophia defectiva.

PURPOSE: Infiltrative keratitis is a common complication associated with extended wear of hydrogel lenses. Causative bacteria are often isolated from the lens at the time of an event. We report a case where three repeated occurrences of infiltrative keratitis were associated with contamination of the contact lenses by Abiotrophia defectiva. METHODS: A 34-year-old man participating in a clinical trial of extended wear hydrogel contact lenses experienced three episodes of infiltrative keratitis. The clinical presentation was observed using a biomicroscope. At the time of each event, the contact lenses were removed aseptically and ocular swabs were taken for bacterial identification and enumeration. The condition was monitored until full resolution. RESULTS: The condition was characterized by irritation, marked bulbar and limbal injection, and multiple focal subepithelial infiltrates. Many of the infiltrates also showed overlying staining with fluorescein. In each of the three events of infiltrative keratitis, A. defectiva was cultured from the contact lens and ocular swabs. CONCLUSION: This is the first reported occurrence of infiltrative keratitis associated with A. defectiva contamination of contact lenses.

Adult↗

PubMed1998

Prevention of adriamycin-induced full-thickness skin loss using hyaluronidase infiltration.

Full-thickness skin ulceration after extravasation of the commonly used vesicant chemotherapeutic agent doxorubicin hydrochloride (Adriamycin) is a significant source of morbidity in cancer patients. Controversy exists regarding the appropriate management of this extravasation injury. Current therapy includes local hypothermia, local clysis with hyaluronidase, and surgical excision of the involved tissue. Experimental data supporting local clysis with hyaluronidase are limited despite its current use clinically. The purpose of this study was to determine the efficacy of local infiltration with heparin sodium, hyaluronidase, and saline in the prevention of extravasation ulcers in a rat model. One hundred fifty male Sprague-Dawley rats (Upjohn, Milan, Italy) weighing 240 to 260 g, anesthetized with sodium pentobarbital, were used in this study. One hundred thirty rats received a 0.3-ml subcutaneous flank injection of doxorubicin (1.5 mg/ml) followed 15 minutes later by local infiltration with saline (n = 10), 25 to 100 units of heparin (n = 30), or 2.5 to 10.0 units of hyaluronidase (n = 90). Control animals received either subcutaneous doxorubicin (n = 10) or subcutaneous saline alone (n = 10). Volumes of the infiltration solution were less than 1 ml in all groups. All animals were sacrificed at 4 weeks; presence and size of ulcers at the injection site were quantified. Statistical analysis was performed using the two-sided Fisher's exact test and Student's t test. Control rats injected with saline alone did not develop ulceration in any case. All rats injected with doxorubicin alone developed ulcers with an average size of 33 mm2. Heparin infiltration decreased ulcer rate by 20 to 40 percent and decreased ulcer size by up to 67 percent. Local infiltration with hyaluronidase decreased ulcer rate by 50 to 60 percent (p < 0.05, two-sided Fisher's exact test) and decreased ulcer size by up to 50 percent ( p < 0.05, Student's t test). In this rat extravasation injury model, local infiltration with saline, heparin, or hyaluronidase decreased ulcer size after doxorubicin extravasation. This effect may be secondary to dilution of the extravasant. Additionally, local infiltration with hyaluronidase decreased ulcer rate by at least 50 percent. The mechanism of this phenomenon presumably relates to the ability of hyaluronidase to temporarily decrease the viscosity of the hyaluronic acid component of ground substance, thus allowing greater diffusion of doxorubicin into the surrounding tissue and therefore decreasing its local concentration.

Animals↗

PubMed1985

Renal allograft cell infiltrates associated with irreversible rejection.

All 74 renal transplant biopsies performed between 11/78 and 8/84 at Duke University and Durham VA Medical Centers having cellular infiltrates that could be phenotyped by immunoperoxidase labeling were examined to identify histologic and immunopathologic features which correlated with rejection. Monoclonal antibodies identifying hematopoietic cells, T cells, T helper cells, T cytotoxic-suppressor cells, macrophages, and B cells were used, and each phenotype population was graded separately based on pattern of infiltration: cortical-diffuse (CD), perivascular (PV), and cortical-aggregate (CA). Histologic and immunofluorescent studies were used to evaluate acute (humoral) and cellular types of vascular and interstitial inflammation. By univariate analysis, patients having irreversible rejection within 10 weeks postbiopsy (n = 23) had significantly higher grades of both acute vascular (humoral) inflammation and TC-S cell infiltrates in a CD pattern as compared with those who had good graft function. Multivariate (Cox regression) analysis was also performed considering biopsy changes, therapy before and after biopsy, and intervals between transplant, rejection onset, and biopsy--as well as other factors potentially affecting the biopsy or graft outcome. Of nine cell phenotype-pattern combinations, only TC-S infiltrates in a CD pattern were associated with a significant (P less than 0.03) relative risk (RR) of subsequent failure from rejection (RR = 8.2). When those cases with significant acute (humoral) inflammation (n = 10) were excluded, the relative risk of TC-S-CD infiltrates increased to 46.4 (P less than 0.04). These findings indicate that the location, as well as the number and type of cell infiltrates are critical in evaluating cellular forms of rejection, and that the extent of diffuse, cortical TC-S infiltration on biopsy provides the greatest predictor of subsequent irreversible graft failure.

Acute Disease↗

PubMed1999

Pulmonary infiltrates in liver transplant recipients in the intensive care unit.

BACKGROUND: A frequent dilemma is discerning the likelihood of pneumonia and the need for empiric antibiotic therapy in liver transplant recipients with pulmonary infiltrates in the intensive care unit (ICU). METHODS: We performed a prospective, observational study of consecutive liver transplant recipients developing pulmonary infiltrates in the ICU. RESULTS: Of 90 consecutive liver transplant patients in the ICU over a 3-year period, 44% (40) developed pulmonary infiltrates. The etiologies were pneumonia (38%, 15 of 40), pulmonary edema (40%, 16 of 40), atelectasis (10%, 4 of 40), adult respiratory distress syndrome (8%, 3 of 40), contusion (3%, 1 of 40), and unknown (3%, 1 of 40). Pneumonia was due to methicillin-resistant Staphylococcus aureus in 27% (4 of 15), Pseudomonas aeruginosa (27%, 4 of 15), invasive aspergillosis (20%, 3 of 15), and Enterobacter cloacae, Serratia marcescens, Pneumocystis carinii pneumonia, and unknown (7%, 1 of 15) in one each. None of the patients had cytomegalovirus or herpes simplex virus pneumonia. Seventy-five percent of methicillin-resistant Staphylococcus aureus and all Aspergillus pneumonias, but only 14% of the Gram-negative pneumonias, occurred within 30 days of transplantation. Twenty-seven percent of the pneumonias occurred >365 days after transplantation; all of these were in patients with recurrent viral hepatitis C virus or hepatitis B virus, disseminated posttransplant lymphoproliferative disorder, or late rejection. Of patients with pneumonia, 87% were ventilated and 40% had bacteremia. Clinical pulmonary infection score (Pugin score) >6 (73% vs. 6%, P = 0.0001), abnormal temperature (73% versus 28%, P = 0.005), and creatinine level >1.5 mg/dl (80% versus 50%, P = 0.05) were predictors of pneumonia versus other etiologies of pulmonary infiltrates. Overall mortality in patients with pulmonary infiltrates was 28% (11 of 40); pneumonia as etiology (P = 0.06), creatinine level >1.5 mg/dl (P = 0.028), higher blood urea nitrogen (P = 0.017), and worse APACHE neurological score (P = 0.04) were predictors of poor outcome. CONCLUSIONS: Our data have implications not only for identifying pneumonia as a potential cause of pulmonary infiltrates, but for the likely etiology of the pneumonia and thus the selection of empiric antibiotic therapy in critically ill liver transplant recipients. Pugin score >6 in patients with pulmonary infiltrates warrants antimicrobial therapy. Early onset within 30 days after transplantation raises the spectra of aspergillosis.

Adult↗

PubMed2003

Contact lens-associated corneal infiltrates.

PURPOSE This review article examines recent studies pertaining to contact lens-associated corneal infiltrates (CLACI) that occur in the absence of culture-proven microbial infection. METHODS The literature was reviewed in regard to the clinical appearance, incidence and risk, etiology, pathophysiology, differential diagnosis, and management of CLACI. Recent insights are presented in the context of future directions for prevention of CLACI. RESULTS Contact lens-associated corneal infiltrates may manifest in various forms that require careful observational skills to ensure proper diagnosis. Although the reported incidence of CLACI varies widely, even a low percentage of contact lens wearers would constitute a substantial number of affected individuals. Any one or a combination of multiple mechanical, hypoxic, or toxic stimuli associated with contact lens use can induce proinflammatory responses that lead to infiltration of inflammatory cells into the cornea. A number of candidate cytokines, chemokines, adhesion molecules, and so forth have been identified. In addition to differentiation from microbial keratitis, CLACI also should be differentiated from ocular disorders not associated with contact lenses but involving corneal infiltrates and from contact lens-associated disorders that may resemble infiltrates. Management of CLACI can range from simple monitoring of the patient to the use of pharmacologic intervention. CONCLUSIONS The small percentage of affected lens wearers translates into a notable number of individuals who, although not experiencing a vision-threatening event, are inconvenienced by the development of infiltrates. Design of preventive measures for CLACI should focus on the elimination of various mechanical, hypoxic, and toxic stimuli that can induce infiltrates and on the approaches for molecular intervention of the inflammatory cascade initiated by the stimuli.

Contact Lenses↗

PubMed2005

The size, location, and clinical severity of corneal infiltrative events associated with contact lens wear.

PURPOSE: The purpose of this study is to determine the relationship between the size, location, and clinical severity of corneal infiltrative events (CIEs) associated with contact lens wear. METHODS: We examined a series of contact lens wearers, presenting consecutively to a large hospital clinic, who had any form of CIE. The severity of the CIE was quantified using a clinical severity matrix based on scores attributed to each of 10 signs and symptoms. The infiltrate was accurately drawn on a schematic diagram of the ocular surface, and from this, we determined its size (i.e., largest dimension) and distance from the limbus. Cartograms were constructed to illustrate the size and location of the corneal infiltrates according to wearing modality and lens type. RESULTS: Useable data pertaining to 111 patients were analyzed. A significant positive correlation was found between the distance of the infiltrate from the limbus versus clinical severity (p = 0.002), but not between the distance of the infiltrate from the limbus versus infiltrate size (p = 0.97). The cartograms revealed a tendency for infiltrates to occur in the superior cornea of patients wearing extended wear silicone hydrogel lenses (p = 0.0002) in the central cornea of patients wearing daily wear hydrogel daily disposable lenses (p = 0.007) and in the peripheral cornea of patients wearing daily wear hydrogel (excluding daily disposable) lenses (p = 0.0006). CONCLUSIONS: These data statistically validate the previously held anecdotal notion that CIEs which occur in the peripheral cornea are less clinically severe than those which occur in the central cornea. Consideration of the distribution of CIEs may facilitate a better understanding of the etiology of these events and can serve to alert practitioners as to their likely clinical presentation.

Adult↗

PubMed1988

Characterization of the mononuclear infiltrate in basal cell carcinoma: a predominantly T cell-mediated immune response with minor participation of Leu-7+ (natural killer) cells and Leu-14+ (B) cells.

We investigated the peritumoral inflammatory infiltrate in 22 basal cell carcinoma (BCC) from 18 patients using a series of monoclonal antibodies. In all the 22 BCC the infiltrate consisted mainly of T cells (55 +/- 15%) and only in three cases an invasion of the tumor nests by these cells was observed. The T helper (TH) subset predominated over the T suppressor/cytotoxic (TS/C) subset (TH/TS/C ratio of 1.9 +/- 0.8). In 8 of 22 BCC mild infiltrate was observed with 48 +/- 13% T cells and a TH/TS/C ratio of 1.5 +/- 0.6. In 14 of 22 BCC moderate to heavy infiltrate with 59 +/- 15% T cells and a TH/TS/C ratio of 2.0 +/- 1.0 was observed. There was a significant difference in the percentage of T cells in BCC with moderate to heavy infiltrate and that in BCC with mild infiltration. The mean percentage of HLA-DR+ cells was 54 +/- 11%; Langerhans cells (LC) 4 +/- 5%; and Leu-M5+ (monocytes and macrophages) 16 +/- 11%. Less than 2% Leu-14+(B) cells were seen in the infiltrate. The mean percentage of Leu-7+ (natural killer) cells was 4 +/- 4%, and only 1 of 22 BCC Leu-7+ cells invaded tumor nests, contacting with tumor cells. From these results we concluded that T cells play a major role in the defence against BCC proliferation. The main role of Langerhans cells and Leu-M5+ cells may be that of antigen presentation. B cells and NK cells probably play a minor role in the local defence against BCC proliferation.

Adult↗

PubMed1979

Evidence for thyroid antigen-reactive T lymphocytes infiltrating the thyroid gland in Graves' disease.

We have investigated the relative distribution and some in vitro functions of thyroid-infiltrating immunocompetent cells obtained at fine-needle aspiration biopsy in twelve patients with Graves' disease and thirteen patients with Hashimoto's thyroiditis. In both disorders the predominant (57--59%) thyroid-infiltrating cell was a small lymphocyte. Significant numbers of plasma cells (10%) were seen only in Hashimoto's thyroiditis. Mononuclear phagocytes (monocytes plus macrophages) were present in similar numbers (12--18%) in both disorders. In both Graves' and Hashimoto's disease there was a relative reduction of (thymus-dependent) lymphocytes in the thyroid gland as compared to the blood. Blood and thyroid-infiltrating T lymphocytes were tested for in vitro cell-mediated immunity (CMI) to thyroid antigen in the leucocyte migration inhibition test (LMT). CMI was readily demonstrated in the blood of most patients with Graves' and Hashimoto's disease. When the thyroid-infiltrating lymphocytes were tested for CMI in the LMT, only the infiltrating cells from patients with Graves' disease displayed CMI, whereas the thyroid-infiltrating lymphocytes in Hashimoto's disease were negative. Fractionation of the immunocompetent cells demonstrated that the thyroid antigen-induced LMT response of blood and thyroid-infiltrating lymphocytes in Graves' disease is a T lymphocyte-dependent phenomenon.

Adolescent↗

PubMed1987

The influence of HLA-A,B and -DR matching on leucocyte infiltration in renal allografts.

The influence of donor and recipient HLA-A,B and -DR matching on the cellular infiltration in renal allografts was examined in 78 transplant recipients who received either cyclosporin (Cy) or azathioprine and low-dose prednisolone (AP) immunosuppression. Transplant biopsies (n = 161) were routinely obtained up to 40 days after transplantation, and biopsy material was therefore available from both rejecting grafts and grafts with stable function. Tissue sections were labelled with a panel of monoclonal antibodies and stained using an indirect immunoperoxidase technique. Cellular infiltration was assessed using a morphometric point counting technique. In AP-treated patients with well-functioning grafts, poor HLA-AB and HLA-DR matching was associated with increased leucocyte infiltration, while in patients receiving Cy therapy the effect of matching on cellular infiltration was seen only during rejection in grafts poorly matched for HLA-AB antigens. In addition, where an effect of HLA-AB matching on cellular infiltration was found, CD8+, but not CD4+ cells, were significantly increased in number, while when an HLA-DR matching effect was seen, a significant increase was observed in the CD4+ and not the CD8+ infiltration. Thus, HLA matching may influence the magnitude of the cellular response in renal allografts and the phenotype of the infiltrating cells.

Azathioprine↗

PubMed1996

Pre-emptive effect of pre-incisional versus post-incisional infiltration of local anaesthesia on children undergoing hernioplasty.

BACKGROUND: Although promising in experimental studies of post-traumatic pain, the concept of pre-emptive analgesia is still controversial in a clinical setting. Thus, we wanted to compare the clinical efficacy of wound infiltration with local anaesthesia before surgery with wound infiltration after hernioplasty in children. METHODS: Fifty children aged 2-10 years scheduled for hernioplasty were randomly assigned into two groups. Group 1 (n = 28) was infiltrated before surgery with bupivacaine 2.5mg/ml, 1mg/kg after induction of general anaesthesia. After surgery they were infiltrated with the same volume of 0.9% saline. Group 2 (n = 22) was infiltrated with 0.9% saline before surgery and bupivacaine 2.5 mg/ml, 1mg/kg after surgery. The study was performed double-blindly. In both groups anaesthesia was induced with thiopenthone and maintained with nitrous oxide and halothane, adjusted to keep haemodynamic measurements stable. All children were given paracetamol 15-20 mg/kg rectally when admitted to the recovery ward. Painscore (OPS) and analgesic requirements were registered postoperatively. After 48 h the parents completed a standardised questionnaire and they were interviewed by telephone after one week. RESULTS: The pre-incisional group needed significantly less halothane during the procedure compared with the post-incisional group (P < 0.05). The pre-incisional group also had a tendency towards faster awakening after the end of anaesthesia and a significantly lower OPS-pain score 30 min after the operation (P < 0.03). There were no differences between the two groups regarding need for additional analgesia: meperidine i.v. during the first 5 h postoperatively, and paracetamol thereafter. There were no differences between the groups regarding activity level, appetite and quality of sleep in the first week. In both groups the need for opioid analgesics was low: 54% in the pre-incisional group and 45% in the post-incisional group did not receive any opioid analgesic treatment. The children were virtually fully recovered after the first 24 h. CONCLUSION: Perioperative infiltration with a local anaesthetic in children undergoing hernioplasty results in a smooth recovery with little need for opioids postoperatively. Apart from a lower anaesthetic requirement and a reduced postoperative pain level after 30 min in the pre-incisional bupivacaine group, there was no difference between infiltration before (pre-emptive) or after surgery.

Analgesia↗

PubMed2004

Hepatic cytotoxic T-cell infiltrates in patients with peripheral T-cell proliferative diseases/lymphomas: clinicopathological and molecular analysis.

Seventy patients with various types of peripheral T-cell proliferative disease/lymphoma who manifested with prolonged fever, weight loss, anemia, lymphadenopathy, hepatosplenomegaly and elevated serum levels of alkaline phosphatase and/or lactate dehydrogenase were evaluated. Histopathological examination of the livers revealed T-cell infiltration into the hepatic sinusoids and portal tracts. The morphology of the infiltrated T cells varied from mature small lymphocytes to malignant lymphoid cells. The liver pathology was classified into four groups on the basis of cellular atypia. Group A and group B showed mature lymphoid cell infiltration; however, only group B had multiple large areas of hepatocellular necrosis. Group C showed atypical lymphoid cell infiltration and in group D malignant lymphoid cell infiltrates were demonstrated. The majority of the antigenic phenotypes of these T-cell infiltrates were CD3+, CD4-, CD8+, CD20-, CD45RO+, CD56-, CD57-, TIA-1+ and betaF1-. Epstein-Barr virus RNA in the nuclei of the infiltrated T cells was recorded in 38.6% of the patients and was more common in groups C and D. Patients in groups B, C and D had a very poor prognosis, median survival was only 1 month, whereas median survival in group A patients was 36 months. Chemotherapy was not effective in improving survival. Monoclonal band/s of T-cell receptors (TCR) beta and/or gamma gene rearrangements were detected in 88.6% of patients, and DNA-sequence analysis showed high identity to the human TCR germline gene.

Adult↗

PubMedDate not supplied

Cyclosporin A inhibits eosinophilic infiltration into the conjunctiva mediated by type IV allergic reactions.

BACKGROUND: Eosinophils are important effector cells in severe allergic conjunctivitis such as vernal keratoconjunctivitis. Infiltration of eosinophils into the conjunctiva is mediated by type I and type IV allergic reactions. Cyclosporin A (CsA) eye drops are administered therapeutically for severe allergic conjunctivitis, but the mechanism by which CsA acts, that is, by inhibiting type I, type IV or both types of allergic reactions, is not known. We investigated whether CsA eye drops inhibit type I, type IV or both types of allergic reactions in the conjunctiva. METHODS: Experimental immune-mediated blepharoconjunctivitis (EC) was induced in BALB/c mice by either active immunization or passive immunization by transfer of ragweed (RW)-primed splenocytes and RW-specific IgE, followed by RW challenge to the conjunctiva. These mice were treated in eye drops with vehicle, 0.1% CsA, 0.5% CsA or 0.1% betamethasone five times (1 and 2 h before RW challenge and 1, 2 and 3 h after RW challenge). Twenty-four hours after the challenge, the conjunctivas were harvested for histological analysis to evaluate eosinophilic infiltration. To evaluate effects of CsA eye drops on systemic immune responses, sera and spleens were collected from actively immunized mice at the time of sacrifice to examine serum IgE levels and cellular immune responses, respectively. RESULTS: CsA eye drops significantly inhibited eosinophilic infiltration into the conjunctiva in actively immunized EC-developing mice compared with vehicle-treated mice. The CsA-induced inhibition was similar to inhibition induced by 0.1% betamethasone. Serum IgE levels and splenocyte responses in CsA-treated mice were equivalent to those in vehicle-treated mice. Betamethasone treatment inhibited eosinophilic infiltration into the conjunctiva induced by both splenocyte transfer and IgE transfer, while CsA treatment inhibited infiltration induced by splenocyte transfer. CONCLUSIONS: CsA eye drops inhibited eosinophilic infiltration into the conjunctiva without affecting systemic immune responses. CsA predominantly inhibits eosinophilic infiltration by interfering with the type IV allergic reaction in the conjunctiva.

Animals↗

PubMed2005

Mesenchymal cells infiltrating a bladder acellular matrix gradually lose smooth muscle characteristics in intraperitoneally regenerated urothelial lining tissue in rats.

OBJECTIVE: To characterize serial long-term histological changes in mesenchymal cells infiltrating a collagen-based matrix, as in a hollow organ with differentiated urothelial lining created intraperitoneally by grafting cultured urothelial cells, mesenchymal cells with smooth-muscle immunohistochemical characteristics infiltrated into the scaffold, despite no mesenchymal cells being seeded into the scaffold before grafting. MATERIALS AND METHODS: To regenerate a urothelial lining tissue intraperitoneally, rat urothelial cells were cultured and seeded with the feeder-layer technique onto bladder acellular matrix (BAM). After 7 days of cultivation to attach urothelial cells on the BAM, the matrix was folded with the urothelial cells inside and grafted onto the mesentery of the previously partially cystectomized rat. RESULTS: The grafted urothelial cells on the BAM, which formed a monolayer before grafting, stratified into three to four layers as early as 4 days after grafting. Although the regenerated urothelium became thinner with time, there was urothelial stratification and a peculiar angular appearance on the apical surface of the regenerated urothelium even after 56 days. The mesenchymal cells infiltrating the BAM showed positive immunohistochemical staining to alpha-smooth muscle actin or desmin at 7 days. Subsequently, the number of actin- or desmin-positive cells gradually decreased with time. On transmission electron microscopy, the infiltrating mesenchymal cells were characterized as myofibroblasts at 7 days. Smooth muscle-like cells were identified at 14 and 28 days, and fibrocytes were the main population at 56 days. CONCLUSIONS: Although epithelial-mesenchymal interactions have been assumed to be one of the most critical factors in smooth-muscle development, mesenchymal cells infiltrating the scaffold in this intraperitoneal regeneration model gradually lost smooth muscle characteristics with time. These results suggest that interactions between cultured urothelial cells and infiltrating mesenchymal cells alone could not maintain the smooth muscle character of infiltrating mesenchymal cells.

Animals↗

PubMed2004

Protective effects of FTY720 on chronic allograft nephropathy by reducing late lymphocytic infiltration.

BACKGROUND: Lymphocytic infiltration is obvious throughout early and late stages of chronic allograft nephropathy. Early infiltrating lymphocytes are involved in initial insults to kidney allografts, but the contribution of late infiltration to long-term allograft attrition is still controversial. Early application of FTY720 reduced the number of graft infiltrating lymphocytes, and inhibited acute rejection. The present study investigated the potential of FTY720 to reduce the number of infiltrating lymphocytes even at a late stage, and, thus, slow the pace of chronic allograft nephropathy. METHODS: Fisher (F344) rat kidneys were orthotopically transplanted into Lewis recipients with an initial 10-day course of cyclosporine A (1.5 mg/kg/day). FTY720, at a dose of 0.5 mg/kg/day, or vehicle was administered to recipients either from weeks 12 to 24 or from 20 to 24 after transplantation. Animals were harvested 24 weeks after transplantation for histologic, immunohistologic, and molecular analysis. RESULTS: FTY720, either initiated at 12 or 20 weeks after transplantation, reduced urinary protein excretion, and significantly ameliorated glomerulosclerosis, interstitial fibrosis, tubular atrophy, and intimal proliferation of graft arteries at 24 weeks after transplantation. Furthermore FTY720 markedly suppressed lymphocyte infiltration and decreased mRNA levels of interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta), and platelet-derived growth factor-B (PDGF-B) but enhanced the number of apoptotic cells in grafts. CONCLUSIONS: FTY720 ameliorated chronic allograft nephropathy even at advanced stages. Furthermore, our data suggest that this effect was achieved by a reduction of graft infiltrating lymphocytes.

Animals↗

PubMed1995

In-Ceram failure behavior and core-veneer interface quality as influenced by residual infiltration glass.

PURPOSE: Crown and fixed partial denture fabrication using In-Ceram all-ceramic restorative material (Vita Zahnfabrik, Bad Säckingen, Germany) involves the veneering of a glass-infiltrated alumina core with porcelain. The manufacturer instructs that excess infiltration glass be removed from all core surfaces before++ porcelain application; however, meticulous removal may not be practical. This study evaluates the failure behavior of two different types of In-Ceram structures with or without thin layers of excess infiltration glass left on core surfaces. MATERIALS AND METHODS: Two groups of porcelain-veneered incisor crowns were fabricated having either (1) excess infiltration glass removed from the aluminous core (n = 10) or (2) a thin layer (0.1 to 0.3 mm) of excess glass remaining on the core (n = 10). Each crown was loaded on its incisal edge against a flat compression platen at 0.5 mm/min. Two groups of core disks (thickness, 1 mm; radius, 7.5 mm) underwent similar surface treatments; i.e., group A as recommended (n = 15) and group B having excess glass (n = 15). Disks were veneered with porcelain, polished to 1.5 mm, and loaded in biaxial flexure at 0.5 mm/min. All fracture surfaces were analyzed using light microscopy and a select sample were examined using scanning electron microscopy. A simple two-dimensional finite-element model was used to evaluate the stress state at the core-veneer interface of bend samples. RESULTS: Failure loads were significantly higher for crowns having excess glass (Student's t test, P < .004). Weibull moduli were indistinguishable (m = 6.2) between crown groups, consistent with the microscopic impression that they shared a common failure mode. Microscopic evaluation of cross-sectioned crowns showed core-veneer interfaces with less porosity in the presence of excess infiltration glass. Failure loads for the disk groups were indistinguishable (Student's t test, P > .8). Scanning electron microscopic analysis of disk samples revealed that failures originated either at core-veneer interfaces or at lower disk surfaces, consistent with the finite-element analysis. CONCLUSION: Excess infiltration glass on the core surface will not degrade the strength of In-Ceram structures. Central incisor crowns (as tested) were strengthened by excess infiltration glass, but disk samples (stressed differently) were not. Finite-element results suggest that disk failure originates from three possible sources.

Aluminum Oxide↗

PubMed1999

Angiocentric CD3(+) T-cell infiltrates in human immunodeficiency virus type 1-associated central nervous system disease in children.

A significant proportion of brain tissue specimens from children with AIDS show evidence of vascular inflammation in the form of transmural and/or perivascular mononuclear-cell infiltrates at autopsy. Previous studies have shown that in contrast to inflammatory lesions observed in human immunodeficiency virus type 1 (HIV-1) encephalitis, in which monocytes/macrophages are the prevailing mononuclear cells, these infiltrates consist mostly of lymphocytes. Perivascular mononuclear-cell infiltrates were found in brain tissue specimens collected at autopsy from five of six children with AIDS and consisted of CD3(+) T cells and equal or greater proportions of CD68(+) monocytes/macrophages. Transmural (including endothelial) mononuclear-cell infiltrates were evident in one patient and comprised predominantly CD3(+) T cells and small or, in certain vessels, approximately equal proportions of CD68(+) monocytes/macrophages. There was a clear preponderance of CD3(+) CD8(+) T cells on the endothelial side of transmural infiltrates. In active lesions of transmural vasculitis, CD3(+) T-cell infiltrates exhibited a distinctive zonal distribution. The majority of CD3(+) cells were also CD8(+) and CD45RO+. Scattered perivascular monocytes/macrophages in foci of florid vasculitis were immunoreactive for the p24 core protein. In contrast to the perivascular space, the intervening brain neuropil was dominated by monocytes/macrophages, microglia, and reactive astrocytes, containing only scant CD3(+) CD8(+) cells. Five of six patients showed evidence of calcific vasculopathy, but only two exhibited HIV-1 encephalitis. One patient had multiple subacute cerebral and brainstem infarcts associated with a widespread, fulminant mononuclear-cell vasculitis. A second patient had an old brain infarct associated with fibrointimal thickening of large leptomeningeal vessels. These infiltrating CD3(+) T cells may be responsible for HIV-1-associated CNS vasculitis and vasculopathy and for endothelial-cell injury and the opening of the blood-brain barrier in children with AIDS.

AIDS Dementia Complex↗

PubMed1982

Role for endotoxin in the leukocyte infiltration accompanying Escherichia coli inflammation.

Escherichia coli organisms induce polymorphonuclear leukocyte (PMNL) infiltration during clinical infection and also in a rabbit dermal model of inflammation. We investigated the factors which may mediate this host response to E. coli. In vitro incubation of Formalin-killed E. coli in heat-inactivated rabbit plasma or balanced salt solution generated in the supernatant factors which induced in vivo PMNL infiltration upon intradermal injection into rabbits. However, these supernatants, in the presence or absence of plasma, did not induce PMNL migration in vitro. The in vivo activity was stable at 100 degrees C and of high molecular weight (30,000). Antiserum to O antigen or to core glycolipid, but not to K or H antigen, as well as polymyxin B inhibited the release or activity of these E. coli-derived factors. The intradermal injection of 0.02 to 0.2 mug of four different endotoxin preparations or lipid A also induced marked PMNL infiltration in vivo. However, these preparations did not stimulate PMNL migration in vitro and failed to generate chemotactic activity in plasma except at very high concentrations (500 mug/ml). Anti-O serum inhibited PMNL infiltration induced by endotoxins with the corresponding O antigen and anti-core glycolipid serum inhibited all four endotoxins tested, whereas polymyxin B inhibited the activity of the endotoxins as well as that of lipid A. Base hydrolysis of endotoxin abolished PMNL infiltration. It is concluded that (i) endotoxin shed from E. coli (killed or live) may be one factor mediating the PMNL infiltration induced by this organism, (ii) endotoxin probably acts independent of in vivo complement activation, (iii) the activity is dependent on the lipid A moiety, and (iv) antibody binding to O or core glycolipid antigens can modify endotoxin so as to diminish its capacity to induce PMNL infiltration in vivo.

Animals↗