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PubMed2005

Impaired cytotoxicity in Papillon-Lefèvre syndrome.

Papillon-Lefèvre syndrome (PLS), palmoplantar hyperkeratosis with periodontitis, has been genetically characterized. However, suspected associated immune dysfunctions remain elusive. The purpose of this study was to evaluate peripheral blood lymphocyte levels and natural killer (NK) cell cytotoxicity in PLS. Twenty patients and 20 healthy controls were examined. Peripheral blood lymphocytes were analyzed by flow cytometry for surface markers. NK cell cytotoxicity against K562 cells was determined by means of a 51Cr release assay. White blood cell differential and proportions of B-, T-, T-helper, T-suppressor, and NK cells revealed only sporadic borderline variations from control values. In contrast, NK cell cytotoxicity was consistently and severely depressed (32-53% of control values) in all patients. To the best of our knowledge, this newly described impairment of NK cell cytotoxic function is the first consistent immune dysfunction reported in PLS. This suggests that the impaired NK cell cytotoxicity might contribute to the pathogenesis of PLS-associated periodontitis.

Adolescent↗
PubMed1996

Endophthalmitis associated with microbial keratitis.

PURPOSE: The purpose of the study is to investigate possible risk factors, organisms cultured, and visual acuity outcomes of endophthalmitis associated with microbial keratitis. METHODS: Records were reviewed of all patients with both positive corneal and positive intraocular cultures at the Bascom Palmer Eye Institute between January 1, 1990, and March 31, 1995. RESULTS: Thirteen (92.9%) of 14 patients identified had documented keratitis before the diagnosis of endophthalmitis was made. Thirteen (92.9%) patients recently had used 1% prednisolone acetate eye drops, 2 (14.3%) received oral prednisone, and 5 (35.7%) were being treated for systemic conditions associated with relative immune dysfunction. Eight (57.1%) patients had a history of ocular surgery, and seven (50.0%) had wound abnormalities. Eight (57.1%) patients lacked an intact posterior capsule, four (28.6%) had a corneal perforation, and three (21.4%) had a history of dry eye. Gram-negative organisms (7), Staphylococcus aureus (3), streptococcal species (2), and fungi (4) were the most frequently isolated organisms. Coagulase-negative staphylococci were not isolated. Six (42.9%) patients achieved a post-treatment visual acuity of 20/200 or better. Three (21.4%) patients underwent enucleation or evisceration. Although not statistically significant, there was an association between appropriate initial antibiotic therapy and improved visual outcomes. CONCLUSION: Patients in whom endophthalmitis associated with microbial keratitis develops have a frequent history of corticosteroid use, systemic conditions associated with relative immune dysfunction, lack of an intact posterior capsule, dry eye, wound abnormalities, and/or corneal perforation. In general, agents cultured consisted of organisms less frequently reported to be the causative agents in series of postoperative and post-traumatic endophthalmitis. Post-treatment visual outcomes generally were poor.

Anti-Inflammatory Agents↗
PubMed2004

Surgical trauma: hyperinflammation versus immunosuppression?

BACKGROUND: Experimental and clinical studies have brought evidence that surgical trauma markedly affects the immune system, including both the specific and the non-specific immune response. MATERIALS AND METHODS: This report reviews the present knowledge on the mechanisms of surgical trauma-induced immune dysfunction and outlines experimental and clinical approaches to find effective treatment strategies. RESULTS: Major surgical trauma induces an early hyperinflammatory response, which is characterized by (1) pro-inflammatory tumour necrosis factor alpha (TNF), interleukin (IL)-1, and IL-6 cytokine release and (2) neutrophil activation and microvascular adherence, as well as (3) uncontrolled polymorphonuclear (PMN) and macrophage oxidative burst. The massive and continuous IL-6 release induces an acute phase response, but, more importantly, also accounts for the up-regulation of major anti-inflammatory mediators, such as prostaglandin (PG) E2, IL-10 and transforming growth factor (TGF)-ss. This results in surgical, trauma-induced, immunosuppression, as indicated by (1) monocyte deactivation, reflected by the lack of monocytic TNF- production upon lipopolysaccharide (LPS) stimulation, and (2) a shift of the Th1/Th2 ratio towards a Th2-dominated cytokine pattern. The imbalance between pro-inflammatory and anti-inflammatory cytokines and immuno-competent cells determines the phenotype of disease and should help the physician to compose the therapeutic strategy. In fact, recent clinical studies have shown that both the initial uncontrolled hyperinflammation and the continued cell-mediated immunosuppression represent primary targets to counteract post-surgery immune dysfunction. The balance between inflammatory and anti-inflammatory forces may be restored by interferon gamma (IFN-gamma) to counteract monocyte deactivation; the anti-inflammatory PGE2 may be inhibited by indomethacin to attenuate immunosuppression; or the initial hyperinflammation may be targeted by administration of anti-inflammatory substances, such as granulocyte colony-stimulating factor (G-CSF), hydoxyethyl starch, or pentoxifylline. CONCLUSIONS: When drawing up the therapeutic regimen the physician should not consider hyperinflammation versus immunosuppression, but hyperinflammation and immunosuppression, aiming at restoring an appropriate mediator- and immune cell-associated balance.

Cytokines↗
PubMed1999

Viral and immunologic examination of human immunodeficiency virus type 1-infected, persistently seronegative persons.

Persons who were human immunodeficiency virus type 1 (HIV-1)-infected but who remained persistently seronegative (HIPS) on HIV-1 antibody tests were examined through AIDS case surveillance. Six such individuals (HIPS-1 to -4, -7, and -9) were examined to determine whether their persistent seronegativity was attributable to immune dysfunction or infection with atypical HIV. Of the 6, 4 had antibody titers to at least 1 other common pathogen. In vitro stimulation of peripheral blood mononuclear cells from HIPS-4 and HIPS-7 with pokeweed mitogen or phosphorothioate oligodeoxynucleotide (direct B cell mitogen) did not produce HIV-1-specific antibody. Reconstitution experiments with recombinant interleukin (rIL)-4 and rIL-12 also had no impact on antibody production. Virus isolates from HIPS-4 and -9 were R5X4-tropic, whereas HIPS-7 was CCR5-tropic only. Sequence analysis of long terminal repeat, p24, and env gp41 did not reveal any specific mutation, and phylogenetic analysis confirmed that all 6 virus specimens were HIV-1 subtype B. These data suggest that the lack of a detectable antibody response in these patients may be the result of immune dysfunction.

Amino Acid Sequence↗
PubMed1998

Acute ethanol exposure prior to thermal injury results in decreased T-cell responses mediated in part by increased production of IL-6.

Previous studies by our laboratory have demonstrated that acute ethanol exposure prior to thermal injury results in suppression of cellular immune responses when compared with thermal injury alone. Ethanol exposure and burn injury are independently known to result in elevated IL-6, a cytokine with potent immunosuppressive properties. Therefore, we examined the role of IL-6 in the immune dysfunction in mice following a 15% body surface area scald (or sham) injury combined with acute ethanol (or vehicle) treatment. At 24 h post-injury, we observed slightly suppressed splenocyte proliferative responses and elevated circulating IL-6 (149+/-15 pg/mL) in mice receiving burn alone compared with those receiving sham injury (31+/-7 pg/mL). In contrast, burn + ethanol treated mice showed a profound suppression of splenocyte proliferation (20% of control) and significantly elevated circulating IL-6 levels (738+/-218 pg/mL). The suppressed splenocyte proliferative response was found to be macrophage dependent. Furthermore, IL-6 production was significantly elevated (p < .05) in splenic macrophage cultures from burn + ethanol mice (159+/-6 pg/mL) when compared with burn alone (109+/-10 pg/mL). Treatment of the splenocyte cultures from burn + ethanol mice with an anti-IL6 monoclonal antibody resulted in partial restoration of splenocyte proliferation. Taken together, these data strongly suggest that the immune dysfunction observed in ethanol-exposed, thermally injured mice is mediated in part by elevated levels of IL-6.

Alcohol Drinking↗
PubMedDate not supplied

Developmental phases of inflammation-induced massive lymphoid hyperplasia and extensive changes in epithelium in an experimental model of allergy: implications for a direct link between inflammation and carcinogenesis.

Direct evidence that inflammation is linked to carcinogenesis has yet to be established. Very few data are available on the developmental phases of inflammation-induced immune dysfunction that may lead to tumorigenesis. In a series of studies conducted in the 1980s and 1990s, an experimental model of acute and chronic inflammation was established in guinea pig conjunctiva by topical application of fluoresceinyl ovalbumin (FLOA) for up to 30 months. In this updated report, some of the findings are reanalyzed and expanded to identify that at lease 3 developmental phases were involved during the entire course of inflammatory responses including (1) an acute response (phase A) involving IgE-mast cell sensitization and degranulation; (2) an intermediate phase (phase B), a desensitization phenomenon and loss of mast cell function and neovascularization; (3) a chronic response (phase C) and induction of massive lymphoid hyperplasia, follicular formation with germinal centers, increased swollen goblet cells, extensive epithelial thickening and thinning, and angiogenesis. The results suggest evidence of a direct association between inflammation and the development of tumor-like lesions in lymphoid tissues and extensive changes in adjacent epithelia. Confirmation that inflammation induces irreversible changes in lymphoid and epithelial tissues leading to lymphoid tumorigenesis and/or carcinogenesis requires further studies. Understanding the developmental phases of immune dysfunction may provide unique opportunities for diagnosis and treatment of inflammatory diseases, autoimmune disorders, and cancers including lymphomas associated with Sjogren syndrome, squamous cell carcinoma of the conjunctiva, and other lymphomas or epithelial cancers. It is suggested that inflammatory mediators are ideal targets (biomarkers) for diagnosis, chemoprevention, and therapy for several cancers.

Acute Disease↗
PubMed2004

Altered cyclooxygenase-2 expression and nitric oxide metabolism following major elective surgery.

BACKGROUND AND AIMS: Postoperative variation in immune function leads to increased susceptibility to infections. Cyclooxygenase-2 (COX-2)-generated Prostaglandin-E(2) (PGE(2)), which signals through the PGE(2) receptor (EP receptor), as well as nitric oxide metabolites (NOx), appear to be important in postoperative immune dysfunction. It is unclear, however, how these substrates and receptors change over time. This study was conducted to evaluate postoperative changes in inflammatory mediator production and monocyte COX-2 and EP receptor expression. MATERIALS AND METHODS: Nineteen patients had blood drawn preoperatively and up to 1 week postoperatively. Plasma NOx levels were measured. Peripheral blood mononuclear cell (PBMC) COX-2 and EP receptor mRNA expression were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). PBMC PGE(2), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and IL-10 productions were evaluated by enzyme-linked immunosorbent assay (ELISA) kits. Statistical analyses were by ANOVA and Student's t tests. RESULTS: Postoperatively, PBMC mean PGE(2) and IL-6 productions were significantly increased at all time points. Mean TNF-alpha production was maximal on postoperative day 2, while mean IL-10 production was unchanged. Mean circulating NOx levels demonstrated a biphasic response decreasing early postoperatively and normalizing at postoperative day (POD) 7. PBMC COX-2 enzyme and EP receptor mRNA expression were unchanged. CONCLUSIONS: Altered PBMC PGE(2) production and plasma NOx levels support a role for altered macrophage activity, which may contribute to immune dysfunction in the postoperative period.

Adult↗
PubMed1991

Lymphoid organs function as major reservoirs for human immunodeficiency virus.

The total number of human immunodeficiency virus type 1 (HIV-1)-infected circulating CD4+ T lymphocytes is considered to be a reflection of the HIV burden at any given time during the course of HIV infection. However, the low frequency of HIV-infected circulating CD4+ T lymphocytes and the low level or absence of plasma viremia in the early stages of infection do not correlate with the progressive immune dysfunction characteristic of HIV infection. In this study, we have determined whether HIV-infected circulating CD4+ T lymphocytes are a correct reflection of the total pool of HIV-infected CD4+ T cells (i.e., HIV burden). To this end, HIV burden has been comparatively analyzed in peripheral blood and lymphoid tissues (lymph nodes, adenoids, and tonsils) from the same patients. The presence of HIV-1 DNA in mononuclear cells isolated simultaneously from peripheral blood and lymphoid tissues of the same patients was determined by polymerase chain reaction amplification. We found that the frequency of HIV-1-infected cells in unfractionated or sorted CD4+ cell populations isolated from lymphoid tissues was significantly higher (0.5-1 log10 unit) than the frequency in peripheral blood. Comparable results were obtained in five HIV seropositive patients in the early stages of disease and in one patient with AIDS. These results demonstrate that a heavy viral load does reside in the lymphoid organs, indicating that they may function as major reservoirs for HIV. In addition, the finding of a heavy viral load in the lymphoid organs of patients in the early stages of disease may explain the progressive depletion of CD4+ T lymphocytes and the immune dysfunction associated with the early stages of HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed2006

A mutant signal transducer and activator of transcription 5b, associated with growth hormone insensitivity and insulin-like growth factor-I deficiency, cannot function as a signal transducer or transcription factor.

CONTEXT: A natural missense mutation in the signal transducer and activator of transcription (STAT) 5b gene was recently identified in association with a female patient presenting with severe growth failure and immune dysfunction. The mutation results in an alanine to proline substitution at residue 630 (A630P) in the src-homology-2 domain, a region essential for docking of STATs to phospho-tyrosines on activated receptors, STAT dimerization, and stabilization of phospho-STAT-DNA interactions. OBJECTIVE: The purpose of this study was to explore the molecular mechanisms underlying the GH insensitivity and IGF-I deficiency caused by the A630P-mutated STAT5b. RESULTS: In reconstitution experiments using HEK293 cells, both GH and interferon-gamma were unable to activate mutant STAT5b (A630P), as demonstrated by lack of immunodetectable phospho-tyrosyl-STAT5b (A630P) and inability to drive luciferase reporter activity. However, the Src family of nonreceptor kinases [constitutively active v-src and epithelial growth factor-induced c-src] tyrosine-phosphorylated STAT5b(A630P). The v-src-induced phospho-STAT5b(A630P) translocated to the nucleus but, unlike wild-type Stat5b, was unable to bind DNA. CONCLUSIONS: The A630P mutation disrupts the src-homology-2 architecture such that: 1) mutant STAT5b most likely cannot dock to phospho-tyrosines on ligand-activated receptors; and 2) stable interactions with DNA are prevented. Because STAT5b (A630P) is an inefficient signal transducer and transcription factor, the detrimental impact on signaling pathways important for normal growth and immunity explains, in part, the complex clinical phenotype of GH insensitivity and immune dysfunction.

Adenoviridae↗
PubMed1997

Zinc deficiency: changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects.

Cell-mediated immune dysfunctions and susceptibility to infections have been observed in zinc-deficient human subjects. In this study, we investigated the production of cytokines and characterized the T-cell subpopulations in three groups of mildly zinc-deficient subjects. These included head and neck cancer patients, healthy volunteers who were found to have a dietary deficiency of zinc, and healthy volunteers in whom we induced zinc deficiency experimentally by dietary means. We used cellular zinc criteria for the diagnosis of zinc deficiency. We assayed enzyme-linked immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated peripheral blood mononuclear cells and assessed by flow cytometry the differences in T-cell subpopulations. Our studies showed that the cytokines produced by TH1 cells were particularly sensitive to zinc status, inasmuch as the production of interleukin-2 (IL-2) and interferon-gamma were decreased even though the deficiency of zinc was mild in our subjects. TH2 cytokines (IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer cell lytic activity also was decreased in zinc-deficient subjects. Recruitment of naive T cells (CD4+CD45 RA+) and CD8+ CD73+ CD11b-, precursors of cytolytic T cells, were decreased in mildly zinc-deficient subjects. An imbalance between the functions of TH1 and TH2 cells and changes in T-cell subpopulations are most probably responsible for cell-mediated immune dysfunctions in zinc deficiency.

Adult↗
PubMed2006

[Heterogeneity changes in secretion ability of monocyte/macrophage and its significance after trauma hemorrhage in rat].

OBJECTIVE: To investigate the relationship between the heterogeneity in secretion ability of monocyte (Mo)/macrophage and the immune dysfunction after severe trauma. METHODS: Twenty-four healthy Wistar rats were randomly divided into normal control group and trauma hemorrhage 1, 4 and 7 days groups. The contents of interleukin-6 (IL-6) and IL-10 secretion of Mo/macrophage from different anatomical regions were determined by radioimmunoassay. RESULTS: (1)In normal rats, the ability to secrete IL-6 and IL-10 was different among alveolar macrophages (AM), peritoneal macrophages (PM) and Mo. PM showed the highest ability to secrete IL-10 while Mo had the highest ability to secrete IL-6. (2)After trauma hemorrhage, the secretion of IL-6 and IL-10 by AM were increased dramatically. On the contrary, the secretion of IL-6 by PM was declined from the 1st day to the 4th day, then increased even over that of the normal control group on the 7th day. However, the secretion of IL-10 by PM was significantly elevated on the 1st day after trauma hemorrhage, peaking on the 4th day, and only slight lowering was found on the 7th day. The secretion of IL-6 by Mo was declined gradually all the time, reaching the lowest point on the 7th day. On the contrary, the secretion of IL-10 by Mo was increasing, reaching its peak on the 7th day. CONCLUSION: The heterogeneity of secretion ability of Mo/macrophage obtained from different anatomical regions is present under normal condition, and is more obvious following a severe injury. This change may play an important role in the immune dysfunction and the development of complications after trauma.

Animals↗
PubMed2001

Tumor-induced sensitivity to apoptosis in T cells from patients with renal cell carcinoma: role of nuclear factor-kappaB suppression.

Antitumor immunity fails to adequately develop in many cancer patients, including those with renal cell carcinoma (RCC). A number of different mechanisms have been proposed to explain the immune dysfunction observed in cancer patient T cells. Here we show that T cells from RCC patients display increased sensitivity to apoptosis. Tumor-infiltrating lymphocytes (TILs) display the most profound sensitivity, because 10-15% of those cells are apoptotic when assessed by terminal deoxynucleotidyltransferase-mediated nick end labeling in situ, and the number of apoptotic TILs further increases after 24 h of culture. Peripheral blood T cells from RCC patients are not directly apoptotic, although T lymphocytes derived from 40% of those individuals undergo activation-induced cell death (AICD) upon in vitro stimulation with phorbol myristate acetate and ionomycin. This is in contrast to T cells from normal individuals, which are resistant to AICD. TILs and peripheral blood T cells from RCC patients also exhibit impaired activation of the transcription factor, nuclear factor (NF)-kappaB. Additional findings presented here indicate that the heightened sensitivity of patient T cells to apoptosis may be tumor induced, because supernatants from RCC explants sensitize, and in some instances directly induce, normal T cells to apoptosis. These same supernatants also inhibit NF-kappaB activation. RCC-derived gangliosides may represent one soluble tumor product capable of sensitizing T cells to apoptosis. Pretreatment with neuraminidase, but not proteinase K, abrogated the suppressive effects of tumor supernatants on both NF-kappaB activation and apoptosis. Additionally, gangliosides isolated from tumor supernatants not only inhibited NF-kappaB activation but also sensitized T cells to AICD. These findings demonstrate that tumor-derived soluble products, including gangliosides, may contribute to the immune dysfunction of T cells by altering their sensitivity to apoptosis.

Apoptosis↗
PubMed1994

Factors associated with initiation of primary medical care for HIV-infected persons.

PURPOSE: To examine the degree of immune dysfunction of human immunodeficiency virus (HIV)-infected patients at the time of presentation and to identify factors associated with early and late initial primary medical care for HIV infection as measured by CD4+ lymphocyte count. PATIENTS AND METHODS: Two hundred fifty-one consecutive outpatients without prior primary care for HIV infection were assessed at a municipal hospital HIV intake clinic (derivation group). Sociodemographic and clinical variables were examined for their association with CD4+ cell count on presentation in bivariate and stepwise linear regression analyses. Variables of interest were examined in 123 similar patients at a second site to assess the generalizability of our findings (validation group). RESULTS: In the derivation group, 30% of patients presented for initial primary care with CD4+ cell counts less than 200/mm3, 51% had counts from 201/mm3 to 500/mm3, and only 19% had counts greater than 500/mm3. Twenty-seven percent of patients had delayed seeking medical care for longer than 1 year and 12%, for more than 2 years after an initial positive HIV serologic evaluation. Three variables were significant and independent predictors of CD4+ cell count on presentation: Haitian ethnicity (P = 0.05) and HIV-related symptoms (P = 0.005) were associated with lower CD4+ cell counts; and female sex (P = 0.009) was associated with higher CD4+ cell counts. With HIV-related symptoms excluded from the model, a history of cocaine use was also a significant predictor for higher CD4+ cell count (P = 0.02). In the validation group, which included few Haitians, results for female sex and HIV-related symptoms showed a similar association. CONCLUSIONS: Most HIV-infected patients presented for primary care with advanced immune dysfunction. A substantial percentage of patients waited over a year to initiate medical care after testing positive for HIV. Haitian patients presented later for primary HIV care as measured by CD4+ cell count. Women presented with significantly higher CD4+ cell counts than did men. Since few characteristics examined could clearly identify the majority of late-presenting HIV-infected patients, improved general and targeted efforts are needed to link all HIV-infected people with primary medical care before the development of advanced disease.

Adult↗
PubMedDate not supplied

Basal and lipopolysaccharide-inducible membrane alkaline phosphatase of lymphoid cells from mice with immune system dysfunctions.

The expression of membrane alkaline phosphatase (mAlPase) activity is an enzymatic marker of activated but not resting B cells which can be used on unseparated lymphoid cell suspensions. It is higher in lymphoid cell suspensions from mice with higher proportions of B cells (athymic mice) or with more activated B cells (autoimmune mice) than in those of control mice.

Alkaline Phosphatase↗
PubMed2005

Infections in patients with Shwachman-Diamond syndrome.

Shwachman-Diamond syndrome (OMIM 260400) is a multisystemic disorder characterized by pancreatic insufficiency, bone marrow dysfunction, skeletal abnormalities and immune dysfunction. Prompted by the case of a 13-year-old girl with Shwachman-Diamond syndrome who presented with pneumonia attributable to Pseudomonas aeruginosa, we review infectious complications of this disease. Pneumonia, recurrent otitis media and skin infections/abscesses constitute the majority of infections among these children.

Adolescent↗
PubMed2003

Dysfunctional immune-privilege in morbid obesity: implications and effect of gastric bypass surgery.

BACKGROUND: Despite the epidemiological evidence linking obesity and cancer, there has never been a causal link. We believe the chronic inflammation present in obesity may predispose the obese to cancer through Fas-receptor over-expression and L-selectin under-expression in leukocytes, and elevated Fas ligand secretion in tumors affecting the morbidly obese. METHODS: Leukocytes from 25 patients having gastric bypass surgery were compared to 15 normal controls preoperatively and at 1, 3, 6, and 12 months postoperatively using flow cytometry to measure CD3, CD4, CD8, CD56, CD62 (L-selectin), CD69, and CD95 (Fas antigen) expression on T lymphocytes, B lymphocytes, natural killer cells, and neutrophils. RESULTS: The percentage of CD95 + T cells was significantly elevated from controls (69.4% vs 56%, P = 0.005). This difference persisted through 1 month postoperatively. Furthermore, expression of CD95 per cell, was significantly greater in these patients than that of the controls (80.2 vs 62.6 gmf, P = 0.018) preoperatively, and this continued to 1 month. Polymorphonuclear cells also displayed a similar elevation in CD95 gmf expression preoperatively (54.1 vs 40.7 gmf, P = 0.023) which normalized by 3 months. Natural killer cells did not display elevated numbers of CD95 gmf preoperatively, but they did experience a significant decline by 12 months. Additionally, there was significant reduction in the number of naiveT cells [(T cells without L-selectin (CD62L)], when compared to normals preoperatively (41.8% vs 51.3%, P = 0.001). There was no statistical difference between the postoperative patients and the controls by 3 months. CD69 was not different at baseline from controls in T or B cells, but there was a significant decrease by 12 months. CONCLUSION: The reduced expression of L-selectin combined with the elevated levels of CD95 suggests that morbid obesity predisposes patients to sites of immune privilege. This could be the mechanism for increased rates of cancer and wound infections seen in obesity. Surgically-induced weight loss eliminates these risk factors.

Adolescent↗