SEARCH · PubMed Health

Results for “Inflammatory”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

PubMed1995

Inflammatory sarcomatoid carcinoma of the lung: report of three cases and clinicopathologic comparison with inflammatory pseudotumors in adult patients.

Although the capacity for some pulmonary carcinomas to mimic sarcomas is well recognized, their potential resemblance to selected benign lesions of the lung is currently underappreciated. The authors herein report three examples of sarcomatoid bronchogenic carcinoma with a deceptively bland appearance and an investment of reactive inflammation, such that they resembled pseudotumors histologically. These lesions occurred in two men and one woman who were 44, 61, and 63 years old, respectively, at diagnosis. All patients presented with a productive cough, hemoptysis, or chest pain. Their pulmonary masses were irregularly marginated radiographically, and ranged in size from 2.5 to 5.5 cm. Two were treated with lobectomy, and one underwent a wedge excision, followed by radiotherapy to the thorax. Despite these measures, each patient with inflammatory sarcomatoid carcinoma (ISC) died of disease or is likely to do so. Microscopically, ISCs were composed of uniform spindle cell proliferations with only modest nuclear pleomorphism, limited mitotic activity, and an arrangement in fascicles, storiform configurations, or haphazard arrays. Lymphocytes and plasma cells were interspersed throughout each of them, and keloidal stromal collagen was apparent internally in two examples. Two of the neoplasms also invaded pulmonary blood vessels or bronchi. A comparison group of 10 adults with pulmonary inflammatory pseudotumors (IPs) of the fibrous histiocytoma type shared several clinical attributes with ISC and showed closely similar histological features, except that the IPs lacked mitoses and invasiveness, and contained xanthoma cells or multinucleated elements in some cases in this series. Immunohistochemical analyses showed consistent dissimilarities between ISC and IP; keratin and epithelial membrane antigen were present in ISC but not IP, whereas actin was observed only in the proliferating spindle cells of IP. In summary, the potential clinicopathologic overlap between ISC and IP suggests that caution should be exercised in the separation of these two lesions. In particular, it is unwise to attempt to make this distinction in an intraoperative frozen section setting.

Adult↗

PubMed1992

Markers of inflammatory activation: upregulation of complement receptors CR1 and CR3 on synovial fluid neutrophils from patients with inflammatory joint disease.

Expression of the C3 receptors CR1 and CR3 was investigated on neutrophils from paired peripheral blood and synovial fluid samples from 34 patients with inflammatory joint disease (21 patients with rheumatoid arthritis (RA) and 13 patients with other articular diseases (OAD)). Using monoclonal antibodies (anti-CD35, anti-CD11b) and immunofluorescence flow cytometric analyses the percentages of positively labeled cells and the relative fluorescence intensities (as a measure of receptor number) were determined. CR1 and CR3 were found to be present on the majority (> 85%) of circulating neutrophils from normal subjects, RA and OAD patients, and on synovial fluid neutrophils from both patient groups. A strong correlation between neutrophil CR1 and CR3 expression was observed in peripheral blood samples from normal subjects (r = 0.81; P = 0.001), RA (r = 0.79; P = 0.001), and OAD patients (r = 0.83; P = 0.001); in each case the levels of CR3 expression were approximately twice those recorded for CR1. Both CR1 and CR3 expression was upregulated on synovial fluid neutrophils compared with that observed on the corresponding peripheral blood cells. Mean percentage increases observed were: RA patients: CR1, 16.5% (P < 0.001) and CR3, 28.7% (P < 0.001); and OAD patients: CR1, 4.1% and CR3, 26.9% (P = 0.001). Correlation of serum and synovial fluid IL-6, IL-8, and immune complex levels with neutrophil CR1 and CR3 expression failed to demonstrate any significant relationship between the concentrations of these soluble factors and receptor expression. Upregulation of CR1 and CR3 receptors, reflecting neutrophil activation within the inflamed joint, is a consistent finding in patients with inflammatory arthropathies.

Adult↗

PubMed2005

Are risk factors for breast cancer similar in women with inflammatory breast cancer and in those with non-inflammatory breast cancer?

PURPOSE: The aim of the study was to compare reproductive factors in patients with inflammatory breast cancer (IBC), and with non-inflammatory breast cancer (non-IBC). The study was performed in two centers: one French including 49 IBC patients and 140 non-IBC and another Tunisian including 97 IBC and 139 non-IBC. Unconditional logistic regression was used for the analyses. PATIENTS AND METHODS: The French IBC patients had a lower educational level, a higher body mass index and a longer cumulative duration of breast-feeding, and they included a greater proportion of non-European women, than the non-IBC patients. In the multivariate analysis, only breast-feeding duration remained associated with the IBC status (P=10(-3)). These results could not be verified in the Tunisian series, because the duration of breast-feeding was unavailable in this center. RESULTS: This study suggests that the etiology of IBC might be different of that of non-IBC.

Body Mass Index↗

PubMed2004

Inflammatory myofibroblastic tumor (inflammatory pseudotumor) of the neck infiltrating the trachea.

Inflammatory myofibroblastic tumor (IMT), popularly known as inflammatory pseudotumor, is a slow growing quasi-neoplastic lesion with a distinct histologic appearance and benign clinical course. A case of a neck IMT with infiltration into the trachea causing asthmalike symptoms in a 12-year-old girl is described. Both tracheal and neck IMT have been described, but no other case has displayed this infiltration. A review of the pertinent literature and the etiology, diagnosis, treatment, and outcomes of this tumor are discussed. It is important to consider IMT in a differential diagnosis because it can be easily misdiagnosed as a malignancy. A surgeon must not perform radical surgery, radiation, or chemotherapy until a final pathologic diagnosis is made because of the nature of this lesion.

Asthma↗

PubMed2006

Effects of hormone replacement therapy on plasma pro-inflammatory and anti-inflammatory cytokines and some bone turnover markers in postmenopausal women.

OBJECTIVE: The present study was undertaken to evaluate plasma TNFalpha, IL-1beta, IL-10; and urinary hydroxyproline (Hyp) and calcium (Ca) as bone resorption markers in postmenopausal women compared with premenopausal ones; and to assess the effects of HRT upon these cytokines and bone turnover markers. PATIENTS AND METHODS: The study involved 50 healthy postmenopausal women, and 25 healthy premenopausal women (control group). Postmenopausal women were randomly divided into two subgroups: women receiving cycle HRT schedule (0.625 mg conjugated estrogen from days 1 to 28+5 mg medroxyprogesterone acetate from days 18 to 28) for 2 months (n=25); and second subgroup consisted of women receiving continue HRT schedule (0.625 mg conjugated estrogen+2.5 mg medroxyprogesterone acetate from days 1 to 28) for 2 months (n=25). Plasma TNFalpha, IL-1beta and IL-10 concentrations were measured with ELISA kits. Fasting urinary Hyp was measured by Ehrlich's spectrophotometric reaction. Ca was determined by oxalate precipitation and the redox titration procedure. Statistical significance was analysed by Kruskal-Wallis plus post hoc Mann-Whitney U-tests for multiple comparisons, Wilcoxon signed ranks test for paired data, and Pearson correlation test. RESULTS: Compared with premenopausal individuals, postmenopausal women have increased plasma TNFalpha, IL-1beta, IL-10 (p<0.0001, p<0.0001, and p<0.001, respectively); and increased urinary Hyp and Ca concentrations (p<0.05). HRT (both cycle and continue schedules) lead to a significant decrease in TNFalpha, IL-1beta and urinary Hyp concentrations, and has no effect uppon IL-10 levels. HRT reverses increased urinary Hyp and Ca excretion to the premenopausal level. There is a significant positive correlation between pre- and post-HRT IL-1beta levels in both cycle and continue subgroups (r=0.437, p<0.05; and r=0.656, p<0.01, respectively), and between pre-HRT IL-1beta and urinary Ca (r=0.509, p<0.01; and r=0.415, p<0.05). There is a significant negative correlation between post-HRT IL-10 and TNFalpha levels in continue HRT receiving group (r=-0.446, p<0.05). Urinary Hyp in cycle and continue HRT received subgroups are correlated with post-treatment values (r=0.455, p<0.05; and r=0.776, p<0.01). CONCLUSIONS: Plasma TNFalpha, IL-1beta, IL-10; and urinary Hyp and Ca increase with menopause. We suggest that the increase of IL-10 is secondary to the elevation of TNFalpha and IL-1beta and that the increase of IL-10 is a compensatory mechanism, by which this anti-inflammatory cytokine counteracts to pro-inflammatory TNFalpha and IL-1beta, and thus balances their osteoclast activating and oxidative stress-related effects. Two months duration HRT (cycle and continue schedule) lead to the significant decrease in plasma TNFalpha, IL-1beta and urinary Hyp concentrations. HRT reverses increased Hyp and Ca excretion to the premenopausal level. So, HRT, decreasing Th1 cytokines (TNFalpha, IL-1beta) probably improve the aberation of Th1/Th2 balance that is implicated in various pathological conditions. However, because of the relatively small number of participants and short duration of the therapy, further studies are necessary to establish a risk/benefit ratio for HRT to view effects on cytokine pattern and bone metabolism.

Aged↗

PubMed1999

Downregulation of T helper type 1 immune response and altered pro-inflammatory and anti-inflammatory T cell cytokine balance following conventional but not laparoscopic surgery.

BACKGROUND: The clinical advantages of laparoscopic procedures result from a minimized surgical trauma. The present study was performed to investigate immunosupression following laparoscopic operations as compared with open surgery. Our analysis focused on the T cell secretion of cytokines that regulate the critical balance of either T helper type-1 (Th1)- and Th2-mediated immune responses on pro- and antiinflammatory activities. METHODS: In a prospective study, immunological data of 26 patients submitted to laparoscopic cholecystectomy (LCE) and 17 patients undergoing conventional cholecystectomy (CCE) for symptomatic cholecystolithiasis were compared. Patients with acute cholecystitis and patients developing postoperative complications or receiving immunosuppressive medication were excluded. Production of interferon (IFN)-gamma, interleukin (IL)-2, IL-4, tumor necrosis factor (TNF)-alpha, and IL-10 by isolated T cells stimulated by cross-linking of CD3 and CD28 was evaluated preoperatively as well as on postoperative days 1 and 6 or 7. Cytokines were measured by immunoenzymometric assay. RESULTS: IFN-gamma, TNF-alpha, and IL-2 production by T cells decreased significantly by 48.3%, 36.6%, and 36.8%, respectively, on postoperative day 1 after CCE, but not after LCE. These results indicate severe suppression of Th1-type and proinflammatory cytokines after the open operation. In contrast, IL-4 and IL-10 did not show significant changes in either group suggesting that Th2 cell response and anti-inflammatory activity remained normal. CONCLUSIONS: The present study shows that open, but not laparoscopic cholecystectomy is associated with a marked suppression of T lymphocytes functions as indicated by deregulation of both the Th1/Th2 and the pro-/anti-inflammatory cytokine balance. The results therefore suggest that downregulation of Th1 cell-mediated immune response and pro-inflammatory activity of T cells is a hallmark of open, but not laparoscopic surgery.

Adult↗

PubMed1999

The dynamic responses of pro-inflammatory and anti-inflammatory cytokines of human mononuclear cells induced by uromodulin.

This study was undertaken to examine the dynamic response of human peripheral blood mononuclear cells (PBMC) in the secretion of proinflammatory and anti-inflammatory cytokines induced by uromodulin (URO). Levels of tumor necrosis factor-alpha (TNFalpha), TNF soluble receptor (sTNFRI and II), interleukin 1-beta (IL-1beta), and IL-1 receptor antagonist (IL-1Ra) in the supernatants of URO-stimulated PBMC were measured by ELISA. URO stimulated the secretion of all these cytokines in a dose dependent manner except sTNFRI. Peak levels of TNFalpha and IL-1beta were reached at 6-12 h, while 5-10 fold higher in sTNFR II and IL-1Ra levels were observed at 24-48 h after URO stimulation. URO-induced secretion of TNFalpha, IL-1beta, sTNFRII and IL-1Ra could be enhanced by human plasma. Specifically, serum proteins including C3, sCD14 and IgG not only bound to URO but also enhanced URO-induced TNFalpha secretion of PBMC. Collectively, our data suggest that URO might have dual immunomodulating effect through regulating the secretion of proinflammatory and anti-inflammatory cytokines, and that serum binding proteins might enhance this activity.

Adjuvants, Immunologic↗

PubMed1997

Cellular inflammatory responses and mediator release during early developing late-phase allergic cutaneous inflammatory responses: effects of cetirizine.

BACKGROUND: Events in developing cutaneous late-phase allergic reactions can be characterized by a combination of skin chamber and biopsy approaches. In some previous studies, cetirizine reportedly inhibited mediator release and/or inflammatory cell responses in late-phase reactions. OBJECTIVE: This study was carried out to determine the effects of cetirizine on early late-phase reactions by using skin chamber and skin biopsy specimens. METHODS: Skin chamber responses during a 6-hour challenge with pollen antigens were assessed in 15 sensitive subjects during randomized, crossover treatment with cetirizine (20 mg/day) or placebo for 7-day periods with measurements of humoral and cellular components. Biopsy specimens of the underlying dermis were obtained. RESULTS: During cetirizine treatment, there was significant (p < 0.01) inhibition of immediate wheal and flare reactions to pollen antigens (34, 46%), codeine (41, 65%), and histamine (38, 68%). However, gross late-phase reactions at 6 hours were unaffected. During both cetirizine and placebo treatment, there was significantly greater accumulation at antigen sites in: (1) skin chamber levels of histamine, total cells, lactoferrin, and eosinophil cationic protein; (2) eosinophils (total and activated) on appended cover glasses; (3) deposition of lactoferrin and eosinophil cationic protein in the underlying dermis. However, these responses were not significantly different during cetirizine treatment compared with placebo treatment periods. CONCLUSION: A persistent pattern of inflammatory cell accumulation with release of granule proteins during early late-phase reactions was unaffected by cetirizine treatment.

Antigens↗

PubMed2001

Pro-inflammatory and anti-inflammatory cytokine mRNA induction in the periphery and brain following intraperitoneal administration of bacterial lipopolysaccharide.

Gram-negative bacteria-derived lipopolysaccharide (LPS or endotoxin) is known to play an important role in immune and neurological manifestations during bacterial infections. LPS exerts its effects through cytokines, and peripheral or brain administration of LPS activates cytokine production in the brain. In this study, we investigated cytokine and neuropeptide mRNA profiles in specific brain regions and peripheral organs, as well as serum tumor necrosis factor (TNF)-alpha protein levels, in response to the intraperitoneal administration of LPS. For the first time, the simultaneous analysis of interleukin (IL)-1beta system components (ligand, signaling receptor, receptor accessory proteins, receptor antagonist), TNF-alpha, transforming growth factor (TGF)-beta1, glycoprotein 130 (IL-6 receptor signal transducer), OB protein (leptin) receptor, neuropeptide Y, and pro-opiomelanocortin (opioid peptide precursor) mRNAs was done in samples from specific brain regions in response to peripherally administered LPS. The same brain region/organ sample was assayed for all cytokine mRNA components. Peripherally administered LPS up-regulated pro-inflammatory cytokine (IL-1beta and/or TNF-alpha) mRNAs within the cerebral cortex, cerebellum, hippocampus, spleen, liver, and adipose tissue. LPS also increased plasma levels of TNF-alpha protein. LPS did not up-regulate inhibitory (anti-inflammatory) cytokine (IL-1 receptor antagonist and TGF-beta1) mRNAs in most brain regions (except for IL-1 receptor antagonist in the cerebral cortex and for TGF-beta1 in the hippocampus), while they were increased in the liver, and IL-1 receptor antagonist was up-regulated in the spleen and adipose tissue. Overall, peripherally administered LPS modulated the levels of IL-1beta system components within the brain and periphery, but did not affect the neuropeptide-related components studied. The data suggest specificity of transcriptional changes induced by LPS and that cytokine component up-regulation in specific brain regions is relevant to the neurological and neuropsychiatric manifestations associated with peripheral LPS challenge.

Activin Receptors, Type I↗

PubMed1992

Metabolic activity in inflammatory and non-inflammatory aneurysms of the abdominal aorta.

Inflammatory aneurysms of the abdominal aorta (IAA) comprise 10-15% of all aortic aneurysms (AA) but their aetiology and pathogenesis are obscure. Destruction of mural elastin is a prominent feature of IAA, and both increased elastolysis and decreased inhibition of elastolysis have been implicated. In order to study these factors, we have examined the peripheral blood of three groups of patients; 15 with inflammatory aortic aneurysms (IAA), 61 with simple aortic aneurysms (SAA) and 35 with aorto-iliac occlusive disease (OD). In all cases, alpha-1-anti-trypsin (A-1-AT), alpha-2-macroglobulin (A-2-MG), elastase inhibitory activity (E.I.A.), elastase-anti-trypsin complex, C-reactive protein (CRP), caeruloplasmin (CP) and plasma viscosity were measured. Patients with IAA had a significantly higher plasma viscosity (Mann-Whitney, p less than 0.05), E.I.A. (Mann-Whitney, p less than 0.01) and levels of A-1-AT, CRP, CP and elastase/anti-trypsin complex (Mann-Whitney, all p less than 0.05) than patients in the other two groups. There was no difference in the levels of A-2-MG between any of the groups. This study refutes the theory that reduced inhibition of elastase activity predisposes to the formation of SAA. In patients with IAA, raised marker levels indicate ongoing destruction of elastin, and suggest a difference in pathogenesis between IAA and SAA. The study also suggests that IAA are highly active metabolically, as opposed to the more degenerative SAA.

Acute-Phase Proteins↗

PubMed1999

CD40 signaling of monocyte inflammatory cytokine synthesis through an ERK1/2-dependent pathway. A target of interleukin (il)-4 and il-10 anti-inflammatory action.

Ligation of CD40 on monocytes through its interaction with CD40 ligand (CD154) present on activated T helper cells, results in activation of monocyte inflammatory cytokine synthesis and rescue of monocytes from apoptosis induced through serum deprivation. Both of these consequences of CD40 stimulation have been shown to be dependent on the induction of protein tyrosine kinase activity. CD40-mediated activation of protein tyrosine kinase activity and subsequent inflammatory cytokine production are abrogated by treatment of monocytes with the T helper type 2 cytokines interleukin 4 (IL-4) and interleukin 10 (IL-10). In the current study we demonstrate that stimulation of monocytes through CD40 resulted in the phosphorylation and activation of the extracellular signal-regulated kinases 1 and 2 (ERK1/2) mitogen-activated protein kinases, whereas phosphorylation of mitogen-activated protein kinases family members p38 and c-Jun N-terminal kinase was not observed in response to this stimuli over the time course examined. PD98059, an inhibitor of the upstream activator of ERK1/2, the MAP/ERK kinase MEK1/2, suppressed IL-1beta and tumor necrosis factor-alpha production in a dose-dependent fashion. Pretreatment of monocytes with IL-4 and IL-10 inhibited CD40-mediated activation of ERK1/2 kinase activity when used individually, and are enhanced in effectiveness when used in combination. Together, the data demonstrate that CD40-mediated induction of IL-1beta and tumor necrosis factor-alpha synthesis is dependent on a MEK/ERK pathway which is obstructed by signals generated through the action of IL-4 and IL-10.

CD40 Antigens↗

PubMed2004

Methicillin-resistant Staphylococcus aureus colonization in inflammatory versus non-inflammatory skin diseases: who should be screened?

The prevalence of methicillin-resistant Staphylococcus aureus (MRSA) was prospectively investigated in a dermatology outpatient setting. Swabs were taken from anterior nares, perineum and lesional skin in 229 patients with erosive inflammatory skin diseases (n=88), venous leg ulcers (n=58) or basal cell carcinoma (n=83) and processed by standard methods. The isolated MRSA strains were characterized by pulsed-field gel electrophoresis after digestion with the restriction enzyme SmaI. MRSA carriage was detected in 10/88 patients with inflammatory skin diseases, 5/58 with venous leg ulcers and 0/83 with basal cell carcinoma. Most of the MRSA isolates could be identified as either the Rhine-Hessen epidemic strain or local epidemic strains. None of the isolated strains was resistant to vancomycin, gentamicin or mupirocin. MRSA is uncommon in outpatients in our dermatology clinic; however, the presence of chronic ulcers and erosions was significantly associated with MRSA positivity. Therefore, patients with chronic ulcers and erosions should be screened for MRSA colonization to implement infection control measures.

Adult↗

PubMed2006

Measurement of nitric oxide may differentiate between inflammatory and non-inflammatory prostatitis.

OBJECTIVE: The majority of patients with prostatitis have chronic non-bacterial prostatitis/chronic pelvic pain syndrome of inflammatory type (Category IIIA) or non-inflammatory type (Category IIIB), based on the National Institutes of Health classification. The aim of this study was to investigate whether measurement of nitric oxide (NO) formation in the prostatic urethra can be used as a marker for inflammation in the evaluation of patients with chronic prostatitis/pelvic pain syndrome. MATERIAL AND METHODS: A total of 25 men with prostatitis were examined. In 8 patients >10 white blood cells/high-power field (WBC/hpf) were found in expressed prostatic secretion (EPS) (Category IIIA), whereas the other 17 had no signs of inflammation (Category IIIB). NO production was measured using a silicon catheter, with the catheter balloon being placed in the prostatic urethra. Room air (5 ml) was incubated for 5 min and analyzed. NO formation in the urinary bladder was also measured. RESULTS: The NO concentration in the prostatic urethra was significantly higher in the 8 patients with >10 WBC/hpf than in those with <10 WBC/hpf. The NO concentration in the urinary bladder was low in both groups. CONCLUSIONS: We found an elevated NO concentration in the prostatic urethra in patients with >10 WBC/hpf in the EPS but not in those with <10 WBC/hpf, which supports the theory of different pathogeneses for Categories IIIA and IIIB. Measurement of NO production in the prostatic urethra can be used to discriminate between the two categories and as the method is easy and fast it may represent an attractive alternative to the four-glass test.

Adult↗

PubMed2005

Inflammatory and anti-inflammatory cytokines in chronic heart failure: potential therapeutic implications.

Persistent inflammation, involving increased levels of inflammatory cytokines, seems to play a pathogenic role in chronic heart failure (HF) by influencing heart contractility, inducing hypertrophy and promoting apoptosis, contributing to myocardial remodeling. While several stimuli may be operating such as heat shock proteins, microbial antigens and oxidative stress, it seems that the inflammatory response to these stimuli may represent a common final pathogenic pathway in HF regardless of the initial event. Traditional cardiovascular drugs appear to have little influence on the cytokine network, and immunomodulatory therapy has emerged as a possible new treatment modality in HF. Several animal studies and also some clinical studies have suggested that downregulation of inflammation may improve cardiac performance. However, the results from the placebo-controlled anti-tumor necrosis factor studies suggest no improvement or even adverse effects of such therapy. Although somewhat disappointing, these negative results do not necessarily argue against the 'cytokine hypothesis'. These studies just underscore the challenges in developing treatment modalities that can modulate the cytokine network in HF patients resulting in beneficial net effects. Further research will have to identify more precisely the most important actors in the immunopathogenesis of chronic HF in order to develop more specific immunomodulating agents for this disorder.

Animals↗

PubMed1988

Cloning and characterization of a cDNA for murine macrophage inflammatory protein (MIP), a novel monokine with inflammatory and chemokinetic properties.

In the course of studies on cachectin/TNF being conducted in our laboratory, a novel macrophage product has been detected and characterized. Termed macrophage inflammatory protein or MIP, this protein appears to be an endogenous mediator of the inflammatory events induced by endotoxin. A cDNA cloned probe for this protein has been isolated from a lambda gt10 phage library prepared from poly(A)+ RNA obtained of endotoxin-induced RAW264.7 cells. The sequence codes for a 92 amino acid-long polypeptide, of which 69 amino acids correspond to the mature product. The sequence predicts a molecular weight of 7,889 and structural analysis of the protein indicates a characteristic signal sequence alpha-helix and a hydrophobic core. Sequence data also confirm no sequence similarity to any other protein listed in the Dayhoff data base.

Amino Acid Sequence↗

PubMed2006

Immune reconstitution inflammatory syndrome presenting as sinusitis with inflammatory pseudotumor in an HIV-infected patient: a case report and review of the literature.

Immune reconstitution inflammatory syndrome (IRIS) encompasses a variety of conditions that occur among HIV-infected patients in a temporal relationship with increases in CD4 cell count as a result of highly active antiretroviral therapy (HAART). Most conditions associated with IRIS are infectious. Malignancies, such as Kaposi's sarcoma, have also been reported. We report a case of sinusitis with presumptive inflammatory pseudotumor as a manifestation of IRIS that occurred 20 weeks after the initiation of HAART.

AIDS-Related Opportunistic Infections↗

PubMed1997

Midkine, a retinoic acid-inducible heparin-binding cytokine in inflammatory responses: chemotactic activity to neutrophils and association with inflammatory synovitis.

Midkine (MK) is a retinoic acid-inducible heparin-binding cytokine. In the inflammatory synovitis of rheumatoid arthritis and osteoarthritis, MK was detected in synovial fluid, synoviocytes, and endothelial cells of new blood vessels. Normal synovial fluid and noninflammatory synovial tissue did not contain detectable MK. Therefore, MK showed inflammation-associated expression in these cases. Furthermore, MK was found to promote chemotaxis of neutrophils in the range of 10 ng/ml. The mode of action of MK was found to be haptotactic; the substrate-bound form of MK was the active one. MK is also known to promote fibrinolysis. These activities of MK are in agreement with the modes of MK expression in various pathological statuses, and thus MK is proposed to be an important molecule regulating inflammatory responses.

Adult↗

PubMed1997

Reproductive condition and the low-dose endotoxin-induced inflammatory response in rats. Glomerular influx of inflammatory cells and expression of adhesion molecules.

These experiments were designed to study the increased sensitivity of pregnant rats to endotoxin. Pregnant (Pr), cyclic (C), and progesterone (P)-treated pseudopregnant rats with or without a decidualized uterus (PSP and DEC rats, respectively) received infusions of an ultra-low dose of endotoxin (1.0 microg/kg BW) and were killed 3 days later. Pr, PSP, and DEC rats were infused on Day 14, C rats on diestrus. Endotoxin-infused rats were compared with saline-infused rats in the same reproductive conditions. The inflammatory reaction of the glomeruli of the kidneys was studied by immunohistochemical methods using 4-microm cryostat sections stained with specific monoclonal antibodies against neutrophils (polymorphonuclear cells, PMNs) and monocytes (MOs), and against the adhesion molecules ICAM-1 and VCAM-1 on the endothelium, and LFA-1, MAC-1, and VLA-4 on the leukocytes. Endotoxin infusion increased glomerular PMN and MO number in Pr, PSP, and DEC rats, all of which have elevated P levels, but not in C rats, which do not. The endotoxin-induced expression of adhesion molecules, associated with this influx of inflammatory cells, varied with the reproductive condition. In C rats there was no increased adhesion molecule expression after endotoxin treatment, in Pr rats there was increased expression of both the combinations ICAM-1/LFA-1 and VCAM-1/VLA-4. DEC rats did not express either of these combinations (although there was expression of ICAM-1); PSP rats expressed the combination ICAM-1/MAC-1. Adhesion molecule expression thus seems to be regulated by ovarian (e.g., P) and placental factors (e.g., of trophoblastic and decidual origin). Because the different combinations of adhesion molecules in the various reproductive conditions after exposure to endotoxin led to more or less the same leukocyte influx under these conditions, the increased sensitivity to endotoxin of pregnant individuals cannot be reduced to differences in leukocyte influx into the glomeruli.

Animals↗