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Host Defence Response (host + defence_response)
Selected AbstractsRoles of Toll-like receptors in innate immune responsesGENES TO CELLS, Issue 9 2001Kiyoshi Takeda Innate immunity recognizes invading micro-organisms and triggers a host defence response. However, the molecular mechanism for innate immune recognition was unclear. Recently, a family of Toll-like receptors (TLRs) was identified, and crucial roles for these receptors in the recognition of microbial components have been elucidated. The TLR family consists of 10 members and will be expanding. Each TLR distinguishes between specific patterns of microbial components to provoke innate immune responses. The activation of innate immunity then leads to the development of antigen-specific adaptive immunity. Thus, TLRs control both innate and adaptive immune responses. [source] DOES THE CYTOSKELETON OF INTESTINAL EPITHHELIAL CELLS FUNCTION AS A CELLULAR ALARM TO IDENTIFY THE E. COLI INFECTIONJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2001Zhe Li Intestinal epithelial cells play an important role in regulating host immunity in response to intestinal infection. Pathogenic bacteria (EPEC and EHEC) cause profound cytoskeletal rearrangement in intestinal epithelial cells during attachment or invasion. Rearrangement of cytoskeletal proteins could be a signal to up-regulate host defence response. Aims, To determine the role of actin cytoskeleton and microtubles in IL-8 mRNA response to E. coli infection. Methods, T84 cell monolayers in 6-well plates were infected with HB101, EPEC and EHEC (105 CFU/well) and compared with uninfected control at 3, 6 and 12 h post infection. Control and infected monolayers were treated with nocodazole (Noc, microtubule disrupter, 30 mm), taxol (Tax, microtubule stabiliser, 10 mm), cytochalasin D (CytoD, actin depolymeriser, 100 nm) and Jasplakinolide (Jasp, actin polymeriser, stabilise actin filaments, 1 mm) and studied 6 h post infection. IL-8 gene expression was measured by semiquantitative RT,PCR in control and uninfected monolayers with and without drug treatment and IL8 protein secretion by ELISA. The morphology of F-actin and ,-tubulin was examined by FITC-phaloidin staining (FAS), immunohistochemistry and confocal microscopy. Results, IL-8 mRNA and IL-8 were increased by infection with all bacterial strains at 3 and 6 h but both IL-8 mRNA and IL-8 in EHEC and EPEC infection were decreased compared with control and HB101 at 12 h. Disruption of microfilaments by Noc increased IL-8 (2.7 fold) while preservation of microfilaments by Tax inhibited IL8 response (0.5 fold) to HB101 infection only. CytoD decreased (0.1,0.5 fold) IL8 expression at all time points in all infections while stabilising actin by Jasp markedly increased the IL8 response (2,6 fold) in control, HB101, EHEC and EPEC at 3 and 6 h. CytoD inhibited Noc-induced IL8 gene expression. Confocal microscopy demonstrated that CytoD and Noc caused major morphological damage to the actin and ,-tubulin by 6 h. Similar changes were also observed in EPEC and EHEC infection at 12 h but not HB101. Jasp preserved actin stress filaments in both EPEC and EHEC. Conclusions, Disruption of microtubules and exogenous rearrangement of actin by pathogenic organism may be primary stimuli to up-regulate proinflammatory cytokine gene expression. Preservation of actin filaments is required for this response and may be necessary for signal transduction to the nucleus. [source] Suppression of the Febrile Response in Late Gestation: Evidence, Mechanisms and OutcomesJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2008A. Mouihate Fever is a beneficial host defence response. However, fever caused by the immune stimulant, lipopolysaccharide (LPS), are attenuated in many species during pregnancy, particularly near term. A number of parallel mechanisms may be responsible, and these vary in magnitude according to the time of gestation, type of inflammatory stimulus and species of animal. Some studies report a reduction in the plasma levels of circulating pro-inflammatory cytokines such as tumour necrosis factor-,, interleukin-1, and interleukin-6 along with increased levels of anti-inflammatory cytokines such as interleukin-1 receptor antagonist. Associated with the attenuated febrile response to LPS is a reduction in the activation of the prostaglandin synthesising enzyme, cyclo-oxygenase 2, resulting in reduced levels of the obligatory prostaglandin mediators of the febrile response in the brain. There is also a reduction in the sensitivity of the brain to the pyrogenic action of prostaglandins, which does not appear to be due to a change in the levels of hypothalamic EP3 prostaglandin receptors. The suppression of fever at term may be important for the health of the neonate because fever in pregnant mothers may be harmful to the late-term foetus and neonate. [source] Blockade of Kupffer cells by gadolinium chloride or dichloromethylene diphosphonate influences hepatic microcirculation after sepsis and haemorrhagic shockBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2000C. Herzog Background The liver plays a key role in the host defence response after haemorrhagic shock,resuscitation (H/R) and sepsis. Kupffer cells (KCs) have been shown to be a trigger and motor of the subsequent inflammatory response syndrome. This may lead to hepatocellular dysfunction, microcirculatory alterations and liver injury involving, for example, tumour necrosis factor ,, interleukin (IL) 1 and IL-6. In a double-blind study the effect of KC blockade with either gadolinium chloride or liposome-entrapped dichloromethylene diphosphonate (DMD) on hepatic microvascular flow after H/R and sepsis was investigated. Methods After pretreatment with intravenous gadolinium chloride 10 mg kg,1, DMD 1 mg kg,1 or saline 24 h before induction of shock, male Sprague-Dawley rats (n = 6,10 per group and time) were subjected to either haemorrhagic shock (mean arterial pressure 40 mmHg) for 60 min followed by resuscitation or lipopolysaccharide (LPS) 1 mg kg,1 intravenously. Microvascular flow was assessed by intravital microscopy of fluorescence-marked leucocytes in liver sinusoids at baseline, and 1, 6 and 12 h after shock induction. Results In saline groups, the mean(s.d.) leucocyte flow was significantly (P < 0·05) higher at 1 h (20 759(2901) ,m3 s,1) and 6 h (16 278(2916) ,m3 s,1) after H/R as well as at 6 h after LPS (17 661(3949) ,m3 s,1) compared with the baseline value (13 509(1580) ,m3 s,1). Animals pretreated with gadolinium chloride showed a significant flow increase compared with baseline (11 797(1124) ,m3 s,1) at l h following H/R (26 269(5909) ,m3 s,1). In DMD-pretreated animals leucocyte flow showed no significant change over time, following either H/R or LPS treatment. However, flow was significantly higher at baseline (18 054(998) ,m3 s,1) versus gadolinium chloride and saline groups. In addition, DMD-treated animals showed higher flow values 1 h after LPS challenge (20 665(2337) ,m3 s,1) compared with gadolinium chloride (13 110(1224) ,m3 s,1) and saline (15 311(800) ,m3 s,1) groups. Similarly, at 12 h after H/R the DMD group (21 782(1887) ,m3 s,1) had higher flow values than the gadolinium chloride (14 026(1616) ,m3 s,1) and saline (15 999(3175) ,m3 s,1) groups. Conclusion These results imply a significant influence of KCs on regulation of microvascular perfusion in liver sinusoids under normal conditions as well as after H/R and sepsis. The data indicate differential pathways and effects of blocking KCs by gadolinium chloride and DMD. © 2000 British Journal of Surgery Society Ltd [source] CD4+ CD25+ transforming growth factor-,-producing T cells are present in the lung in murine tuberculosis and may regulate the host inflammatory response,CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007C. M. Mason Summary CD4+ CD25+ regulatory T cells produce the anti-inflammatory cytokines transforming growth factor (TGF)-, or interleukin (IL)-10. Regulatory T cells have been recognized to suppress autoimmunity and promote self-tolerance. These cells may also facilitate pathogen persistence by down-regulating the host defence response during infection with Mycobacterium tuberculosis. We evaluated TGF-,+ and IL-10+ lung CD4+ CD25+ T cells in a murine model of M. tuberculosis. BALB/c mice were infected with ,50 colony-forming units of M. tuberculosis H37Rv intratracheally. At serial times post-infection, lung cells were analysed for surface marker expression (CD3, CD4, CD25) and intracellular IL-10, TGF-,, and interferon (IFN)-, production (following stimulation in vitro with anti-CD3 and anti-CD28 antibodies). CD4+ lung lymphocytes were also selected positively after lung digestion, and stimulated in vitro for 48 h with anti-CD3 and anti-CD28 antibodies in the absence and presence of anti-TGF-, antibody, anti-IL-10 antibody or rmTGF-, soluble receptor II/human Fc chimera (TGF,srII). Supernatants were assayed for elicited IFN-, and IL-2. Fluorescence activated cell sorter analyses showed that TGF-,- and IL-10-producing CD4+ CD25+ T cells are present in the lungs of infected mice. Neutralization of TGF-, and IL-10 each resulted in increases in elicited IFN-,, with the greatest effect seen when TGF,srII was used. Elicited IL-2 was not affected significantly by TGF-, neutralization. These results confirm the presence of CD4+ CD25+ TGF-,+ T cells in murine pulmonary tuberculosis, and support the possibility that TGF-, may contribute to down-regulation of the host response. [source] The expression, function and regulation of mitochondrial alternative oxidase under biotic stressesMOLECULAR PLANT PATHOLOGY, Issue 3 2010FENG HANQING SUMMARY To survive, plants possess elaborate defence mechanisms to protect themselves against virus or pathogen invasion. Recent studies have suggested that plant mitochondria may play an important role in host defence responses to biotic stresses. In contrast with animal mitochondria, plant mitochondria possess a unique respiratory pathway, the cyanide-insensitive alternative pathway, which is catalysed by the alternative oxidase (AOX). Much work has revealed that the genes encoding AOX, AOX protein and the alternative respiratory pathway are frequently induced during plant,pathogen (or virus) interaction. This raises the possibility that AOX is involved in host defence responses to biotic stresses. Thus, a key to the understanding of the role of mitochondrial respiration under biotic stresses is to learn the function and regulation of AOX. In this article, we focus on the theoretical and experimental progress made in the current understanding of the function and regulation of AOX under biotic stresses. We also address some speculative aspects to aid further research in this area. [source] | |||||||||||||