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Local Inflammatory Response (local + inflammatory_response)
Selected AbstractsLocal inflammatory response in choriodecidua induced by Ureaplasma urealyticumBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 11 2007R Aaltonen Ureaplasma urealyticum is the bacterial species most often connected with preterm birth, although it often colonises the amniotic fluid without any adverse effects. The induction of preterm labour seems to depend on whether the bacteria produce an inflammatory reaction. In vitro stimulation of choriodecidual tissue with high amounts of U.urealyticum or with lipopolysaccharide induced a qualitatively similar inflammatory response detected by the production of tumour necrosis factor alpha, followed by secretion of anti-inflammatory cytokine interleukin-10 and of prostaglandin E2. Lower quantities of bacteria failed to induce any response. [source] Post-ictal fever: a rare symptom of partial seizuresEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007A. O. Rossetti Although fever may induce seizures, especially in children, its occurrence following epileptic spells has been rarely described, except from generalized convulsive status epilepticus. We present two patients suffering from focal seizures accompanied by episodes of post-ictal fever, and review similar reports in the literature of the last 40 years. Temperature changes following non-convulsive seizures might be induced by gene upregulation occurring in the hypothalamus, the nucleus tractus solitarius, or in other brain regions, producing a local inflammatory response. Direct propagation of electrical discharges seems less consistent with the timing of development of this symptom. Heterogeneity of reported clinical features argues against the assumption of a definite localizing or lateralizing value for post-ictal fever. [source] The Effect of Ascorbic Acid on Helicobacter pylori Induced Cyclooxygenase 2 Expression and Prostaglandin E2 Production by Gastric Epithelial Cells in vitroHELICOBACTER, Issue 1 2005Geoff V. Smith ABSTRACT Background., Cyclooxygenase 2 (COX-2) is induced by the presence of Helicobacter pylori (H. pylori) on the gastric mucosa as part of the inflammatory response; this results in the synthesis of prostaglandins that amplify the local inflammatory response. The presence of H. pylori inhibits the secretion of ascorbate into the gastric lumen. Interestingly, ascorbate inhibits the growth of H. pylori and low dietary levels are associated with an increased risk of gastric adenocarcinoma. We therefore investigated the effect of ascorbate on H. pylori mediated COX-2 induction and prostaglandin production in vitro. Methods.,H. pylori was cocultured with gastric epithelial cells in the presence of ascorbate at physiological concentrations. The expression of COX-2 was assessed by Western blotting and prostaglandin E2 (PGE2) was assessed by ELISA. Results., Ascorbate inhibited gastric cell PGE2 synthesis but not in COX-2 expression in response to H. pylori. In the absence of the organism, ascorbate also reduced PGE2 expression in cells that constitutively express COX-2, again with no reduction of COX-2 protein expression. Conclusions., Physiological concentrations of ascorbate inhibit PGE2 but not COX-2 expression in response to H. pylori in gastric epithelial cells. [source] Effect of pro-inflammatory and immunoregulatory cytokines on human tenocytesJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 8 2010Thilo John Abstract Tendon injury induces a local inflammatory response, characterized by the induction of pro-inflammatory cytokines. The aim of the present study was to analyze the effects of TNF,, IL-6 and IL-10 on key parameters of tendon homeostasis. Cultured primary human tenocytes were treated with the recombinant cytokines IL-6, IL-10, TNF,, or combinations of TNF, with IL-6 and IL-10 (10 ng/mL, 6, 24 h). Expression of type I collagen, elastin, MMP-1, TNF,, IL-1,, IL-6, IL-10, and suppressors of cytokine signaling (SOCS1, 3) was analyzed with the use of RTD-PCR, immunocytochemistry, and Western blot analysis. In response to TNF,, tenocytes reduced their type I collagen deposition but increased their elastin gene expression and highly upregulated their expression for MMP-1, pro-inflammatory (TNF,, IL-1,) and immunoregulatory (IL-6, IL-10) cytokines. TNF, stimulation augmented SOCS1, whereas SOCS3 expression in tenocytes was also induced by IL-6. The treatment of tenocytes with IL-6 and IL-10 had no effect on cytokine expression. Neither IL-6 nor IL-10 modulated the observed effects of TNF, significantly. These results indicate that TNF, strongly activates the tenocytes to amplify their own TNF, expression and, subsequently, that of other regulatory cytokines and matrix degrading enzymes. However, the impact of IL-6 and IL-10 on tenocytes remains unclear. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1071,1077, 2010 [source] Interleukin-1 modulates periprosthetic tissue formation in an intramedullary model of particle-induced inflammationJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 3 2005Noah J. Epstein Abstract Interleukin-1 (IL-1) is a proinflammatory cytokine that has been implicated in wear-debris associated total joint replacement failure. We hypothesized that the absence of the IL-1 type-1 receptor would mitigate the inflammatory response to titanium particles and decrease periprosthetic inflammatory tissue in a murine intramedullary rod model. Methods: An intramedullary rod with and without commercially pure titanium particles was placed in the femora of 24 wild type mice (WT) and 24 mice lacking a functional type-1 receptor to IL-1. Femora were analyzed histologically and by ELISA of organ culture explant supernatants. Results: The presence of titanium particles in WT mice stimulated increased expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1) relative to rod only controls. In contrast, IL-6 and MCP-1 expression were diminished in IL-lrl-KO mice exposed to titanium particles. Additionally, the formation of a periprosthetic fibro-inflammatory membrane in IL-lrl-KO mice was blunted at 2 weeks when compared to that in wild-type mice. Inflammatory changes and the quality of periprosthetic bone of IL-lrl-KO mice was similar to WT mice in response to titanium particles. Conclusions: These results implicate IL-1 as an important modulator in the local inflammatory response to intramedullary titanium particles. MCP-1 appears to be significantly modulated in IL-lrl-KO mice in response to titanium particles. This may be responsible, in part, for the diminished periprosthetic membrane observed in IL-lrl-KO mice at 2 weeks. Expansion of this murine model of intramedullary particle-induced inflammation to other gene targets may contribute to a more mechanistic understanding of wear-debris associated prosthesis failure. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Cellular inflammatory response to porcine collagen membranesJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2003Maria G. Patino Objectives:, The purpose of this study was to assess local inflammatory changes associated with the implantation of three different porcine collagen membranes having potential use in periodontal regeneration. Methods:, Materials were implanted subcutaneously into prepared sites along the dorsal skin surface of 60 female Wistar rats. Saline and turpentine were used as negative and positive controls, respectively. Animals were killed and biopsies obtained after 3 d, and at 1, 2, 4, 6, and 8 weeks after membrane implantation. A panel of six monoclonal antibodies was used to identify circulating monocytes (ED1), resident tissue macrophages (ED2), lymphoid macrophages (ED3), Ia-antigen expression (OX6), T-lymphocytes (OX19), and B-lymphocytes (OX33). Cells identified by each antibody were subjected to quantitative immunocytochemistry to compare any differences present among groups. Sera obtained 8 weeks after grafting were used in immunoblotting assays to detect the presence of systemic antiporcine antibodies. Results:, We found that the mononuclear cell subsets associated with implantation of porcine collagen membranes were similar to those obtained with saline administration. On the other hand, the use of turpentine resulted in an inflammatory infiltrate characterized by significantly higher numbers of all six monoclonal cell subsets at all time periods evaluated, compared to either saline or any of the membranes (P < 0.001). Conclusions:, The collagen membranes do not appear to be associated with a significant local inflammatory response, nor a systemic immune response, and thus appear to be well tolerated, rendering them useful in periodontal regeneration. [source] Nasal CpG oligodeoxynucleotide administration induces a local inflammatory response in nonallergic individualsALLERGY, Issue 9 2009A. Månsson Background:, We have previously demonstrated the presence of toll-like receptor 9 in the nasal mucosa of both healthy and allergic individuals. CpG motifs, found in bacterial and viral DNA, elicit strong immunostimulatory effects via this receptor. CpG is known to skew the immune system towards a T helper 1 (Th1) profile, thereby suppressing Th2-driven allergic responses. This study was designed to examine the effects of CpG administration in the human nose. Methods:, Twenty subjects, of whom 10 suffered from seasonal allergic rhinitis (AR), were challenged intranasally with CpG outside pollen season. Symptom scores, nasal airway resistance (NAR), and nasal and pulmonary nitric oxide (NO) levels were assayed prior to challenge and 30 min, 6, 24 and 48 h post challenge. The presence of leukocytes and various cytokines were analyzed in nasal lavage (NAL) fluids before and after CpG exposure. Results:, Increased NAR, nasal NO production and secretion of interleukin (IL)-1,, IL-6, and IL-8 were seen after CpG exposure. Further analysis revealed that this inflammatory response was more marked in healthy subjects than among patients with AR, although a higher basal inflammatory response was recorded in the allergic group. In vitro experiments suggest that the effects induced by CpG are mediated by epithelial cells and neutrophils. Conclusion:, Nasal administration of CpG induces a local airway inflammation, more distinct among healthy than allergic individuals. The reduced responsiveness to CpG in allergic patients might be related to the ongoing minimal persistent inflammation. Results from cytokine analyses reflect the ability of CpG to induce a pro-inflammatory Th1-like immune response. [source] Gestational Hypoxia Induces White Matter Damage in Neonatal Rats: A New Model of Periventricular LeukomalaciaBRAIN PATHOLOGY, Issue 1 2004Olivier Baud In the premature infant, periventricular leukomalacia, usually related to hypoxic-ischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sparague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2 -90% N2) from embryonic day 5(E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from p0 to P14 than in controls. Specific white matter cysts wear detected between p0 and p7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period. [source] Structure and biology of complement protein C3, a connecting link between innate and acquired immunityIMMUNOLOGICAL REVIEWS, Issue 1 2001Arvind Sahu Summary: Complement protein C3 is a central molecule in the complement system whose activation is essential for all the important functions performed by this system. After four decades of research it is now well established that C3 functions like a double-edged sword: on the one hand it promotes phagocytosis, supports local inflammatory responses against pathogens, and instructs the adaptive immune response to select the appropriate antigens for a humoral response; on the other hand its unregulated activation leads to host cell damage. In addition, its interactions with the proteins of foreign pathogens may provide a mechanism by which these microorganisms evade complement attack. Therefore, a clear knowledge of the molecule and its interactions at the molecular level not only may allow the rational design of molecular adjuvants but may also lead to the development of complement inhibitors and new therapeutic agents against infectious diseases. A.S. is a Wellcome Trust Overseas Senior Research Fellow in Biomedical Science in India. This research was supported by National Institutes of Health grants AI 30040, GM 56698, HL28220, and AI 48487. [source] PPAR, and PPAR, effectively protect against HIV-induced inflammatory responses in brain endothelial cellsJOURNAL OF NEUROCHEMISTRY, Issue 2 2008Wen Huang Abstract Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors which down-regulate inflammatory signaling pathways. Therefore, we hypothesized that alterations of PPAR functions can contribute to human immunodeficiency virus-1 (HIV-1)-induced dysfunction of brain endothelial cells. Indeed, treatment with HIV-1 transactivator of transcription (Tat) protein decreased PPAR transactivation in brain endothelial cells. We next stably over-expressed PPAR, and PPAR, in a newly developed cell line of human brain endothelial cells (hCMEC/D3 cells). Tat-induced up-regulation of inflammatory mediators, such as interleukin (IL)-1,, tumor necrosis factor-,, CCL2, and E-selectin were markedly attenuated in hCMEC/D3 over-expressing PPAR, or PPAR,. These results were confirmed in CCL2 and E-selectin promoter activity studies. Similar protective effects were observed in hCMEC/D3 after activation of PPAR, by exogenous PPAR agonists (dPGJ2 and rosiglitazone). PPAR over-expression also prevented Tat-induced binding activity and transactivation of nuclear factor-,B. Importantly, increased PPAR activity attenuated induction of IL-1,, tumor necrosis factor-,, CCL2, and E-selectin in hCMEC/D3 cells co-cultured with HIV-1-infected Jurkat cells. The protective effects of PPAR over-expression were reversed by the antagonists of PPAR, (MK886) or PPAR, (GW9662). The present data suggest that targeting PPAR signaling may provide a novel therapeutic approach to attenuate HIV-1-induced local inflammatory responses in brain endothelial cells. [source] Contribution of C5-mediated mechanisms to host defence against Echinococcus granulosus hydatid infectionPARASITE IMMUNOLOGY, Issue 9 2000Ana Marķa Ferreira The aim of this work was to investigate the contribution of complement C5-mediated mechanisms, with an emphasis on inflammation, to host defences against Echinococcus granulosus hydatid disease. Thus, we compared the systemic and local inflammatory responses induced by the parasite, and the outcome of infection, between congenic C5-sufficient (B10.D2 n/SnJ) and C5-deficient (B10.D2 o/SnJ) mice challenged with protoscoleces. Indirect evidence of in-vivo complement activation during the establishment phase was obtained; infection induced serum amyloid P and eosinophil responses which were dependent on C5. Early recruitment of polymorphonuclear cells was not dependent on the presence of C5. The higher capacity of C5-sufficient mice to recruit eosinophils was also observed during the cystic phase of infection, and mice recruiting more eosinophils developed lower parasite masses. Analysis of the outcome of infection after 8 months showed that C5-sufficient mice were more resistant to infection than C5-deficient mice in terms of individuals with no cysts; this trend was not statistically significant. In addition, C5-deficient mice developed higher numbers of large (> 5 mm in diameter) cysts and higher cyst weights than C5-sufficient mice indicating that C5-mediated mechanisms are detrimental for parasite growth. Taken together, our results suggest that complement, through C5-mediated effectors, contributes to host defences by both restricting the establishment of infection and controlling the growth of established cysts. This contribution may, at least partially, be associated with the ability of C5a to promote eosinophil infiltration. [source] Bacterial vaginosis , a microbiological and immunological enigma,APMIS, Issue 2 2005Review article The development of bacterial vaginosis (BV) among women of childbearing age and the resulting quantitative and qualitative shift from normally occurring lactobacilli in the vagina to a mixture of mainly anaerobic bacteria is a microbiological and immunological enigma that so far has precluded the formulation of a unifying generally accepted theory on the aetiology and clinical course of BV. This critical review highlights some of the more important aspects of BV research that could help in formulating new basic ideas respecting the biology of BV, not least the importance of the interleukin mediators of local inflammatory responses and the bacterial shift from the normally occurring lactobacilli species: L. crispatus, L. gasseri, L. jensenii, and L. iners to a mixed flora dominated by anaerobic bacteria. [source] | |||||||||||||