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Innate Immune Function (innate + immune_function)
Selected AbstractsEffects of possible endocrine disruptors on MyD88-independent TLR4 signalingFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2008Takahiro Ohnishi Abstract Endocrine disrupting chemicals (EDCs) may potentially worsen infectious diseases because EDCs disturb human immune function by interfering with endocrine balance. To evaluate the influence of EDCs on the innate immune function of macrophages, we investigated the effects of 37 possible EDCs on lipopolysaccharide-induced activation of the IFN-, promoter. Alachlor, atrazine, benomyl, bisphenol A, carbaryl, diethyl phthalate, dipropyl phthalate, kelthane, kepone, malathion, methoxychlor, octachlorostyrene, pentachlorophenol, nonyl phenol, p -octylphenol, simazine and ziram all inhibited the activation. Kepone and ziram showed strong inhibitory effects. Aldicarb, amitrole, benzophenone, butyl benzyl phthalate, 2,4-dichlorophenoxy acetic acid, dibutyl phthalate, 2,4-dichlorophenol, dicyclohexyl phthalate, diethylhexyl adipate, diethylhexyl phthalate, dihexyl phthalate, di- n -pentyl phthalate, methomyl, metribuzin, nitrofen, 4-nitrotoluene, permethrin, trifluralin, 2,4,5-trichlorophenoxyacetic acid and vinclozolin had no significant effects at 100 ,M. These results indicate that some agrochemicals and resin-related chemicals may potentially inhibit macrophage function, which suggests that endocrine disruptors may influence the development of infectious diseases. [source] Testosterone and innate immune function inversely covary in a wild population of breeding Dark-Eyed Juncos (Junco hyemalis)FUNCTIONAL ECOLOGY, Issue 5 2006T. J. GREIVES Summary 1Innate immunity refers to the non-specific components of the primary immune response, which act broadly to destroy pathogens. Effective innate immune responses may save an individual the energetic costs associated with activating subsequent specific immune responses. 2Testosterone can suppress immune function in vitro and in vivo. Most studies examining testosterone's effects on immunity have focused on experimentally elevated testosterone and acquired immune responses (e.g. humoral and cell-mediated responses to foreign antigens). Few studies have investigated the relationship between endogenous levels of testosterone and innate immunity. 3In a wild breeding population of Dark-Eyed Juncos (Junco hyemalis Linnaeus), we asked whether endogenous levels of testosterone measured at several points during the breeding season covaried with two components of innate immunity: total levels of non-specific immunoglobulin-G (IgG), and complement levels. 4Testosterone levels were significantly negatively correlated with both total IgG and complement activity. Both immune measures were also positively correlated with body mass. Taken together with experimental results from the same species, these results suggest that elevated testosterone levels may compromise innate as well as acquired immune function. [source] Bacteria and PAMPs activate nuclear factor ,B and Gro production in a subset of olfactory ensheathing cells and astrocytes but not in Schwann cellsGLIA, Issue 9 2007Adele J. Vincent Abstract The primary olfactory nerves provide uninterrupted conduits for neurotropic pathogens to access the brain from the nasal cavity, yet infection via this route is uncommon. It is conceivable that olfactory ensheathing cells (OECs), which envelope the olfactory nerves along their entire length, provide a degree of immunological protection against such infections. We hypothesized that cultured OECs would be able to mount a biologically significant response to bacteria and pathogen-associated molecular patterns (PAMPs). The response of OECs to Escherichia coli (E. coli) and various PAMPs was compared to that of Schwann cells (SCs), astrocytes (ACs), and microglia (MG). A subset of OECs displayed nuclear localization of nuclear factor ,B), an inflammatory transcription factor, after treatment with E. coli (20% ± 5%), lipopolysacchride (33% ± 9%), and Poly I:C (25% ± 5%), but not with peptidoglycan or CpG oligonucleotides. ACs displayed a similar level of activation to these treatments, and in addition responded to peptidoglycan. The activation of OECs and ACs was enhanced by coculture with MG (56% ± 16% and 85% ± 13%, respectively). In contrast, SCs did not respond to any treatment or to costimulation by MG. Immunostaining for the chemokine Gro demonstrated a functional response that was consistent with NF,B activation. OECs expressed mRNA for Toll-like receptors (TLRs) 2 and 4, but only TLR4 protein was detected by Western blotting and immunohistochemistry. The results demonstrate that OECs possess the cellular machinery that permits them to respond to certain bacterial ligands, and may have an innate immune function in protecting the CNS against infection. © 2007 Wiley-Liss, Inc. [source] Ethanol Exposure Impairs LPS-Induced Pulmonary LIX Expression: Alveolar Epithelial Cell Dysfunction as a Consequence of Acute IntoxicationALCOHOLISM, Issue 2 2009James E. Walker Jr Background:, Alcohol intoxication impairs innate immune responses to bacterial pneumonia, including neutrophil influx. Lipopolysaccharide (LPS)-induced chemokine (LIX or CXCL5) is a recently described chemokine produced by type-II alveolar epithelial (AE2) cells which facilitates neutrophil recruitment. The effect of acute alcohol intoxication on AE2 cell expression of LIX is unknown. Methods:, C57BL/6 mice were given an intraperitoneal (i.p.) injection of ethanol (4 g/kg) or saline 30 minutes prior to intratracheal (i.t.) injection with 10 ,g Escherichia coli LPS. In vitro stimulation of primary AE2 cells or murine AE2 cell line MLE-12 was performed with LPS and tumor necrosis factor-alpha (TNF-,). Results:, LIX protein is readily detectable in the lung but not in plasma following LPS administration, demonstrating "compartmentalization" of this chemokine during pulmonary challenge. In contrast to the CXC chemokines keratinocyte-derived chemokine and macrophage inflammatory protein-2, which are abundantly expressed in both lung tissue and alveolar macrophages, LIX expression is largely confined to the lung parenchyma. Compared to controls, intoxicated animals show a decrease in LIX and neutrophil number in bronchoalveolar lavage fluid following LPS challenge. Ethanol inhibits LIX at the transcriptional level. In vitro studies show that LPS and TNF-, are synergistic in inducing LIX by either primary AE2 or MLE-12 cells. Acute ethanol exposure potently and dose-dependently inhibits LIX expression by AE2 cells. Activation of nuclear factor-,B is critical to LIX expression in MLE-12 cells, and acute ethanol treatment interferes with early activation of this pathway as evidenced by impairing phosphorylation of p65 (RelA). Inhibition of p38 mitogen-activated protein kinase signaling, but not ERK1/2 activity, in MLE-12 cells by acute alcohol is likely an important cause of decreased LIX expression during challenge. Conclusions:, These data demonstrate direct suppression of AE2 cell innate immune function by ethanol and add to our understanding of the mechanisms by which acute intoxication impairs the lung's response to microbial challenge. [source] Effects of substitution of dietary fish oil with a blend of vegetable oils on liver and peripheral blood leucocyte fatty acid composition, plasma prostaglandin E2 and immune parameters in three strains of Atlantic salmon (Salmo salar)AQUACULTURE NUTRITION, Issue 6 2009I.K. PETROPOULOS Abstract Duplicate groups of three genetic strains of Atlantic salmon smolts were cultured on diets containing either fish oil (FO) or a blend of vegetable oils (VO). Fatty acid compositions of liver and peripheral blood leucocytes were compared. The effect of different strains and diets on innate immune parameters and plasma prostaglandin E2 were also measured. Two strains were selected as being either ,fat' or ,lean' in terms of muscle adiposity. The third strain was a commercial stock (MH). Total replacement of dietary FO with VO resulted in reduced docosahexaenoic (DHA; 22:6n -3) and eicosapentaenoic acids (EPA; 20:5n -3) in liver, while oleic (18:1n -9), linoleic (18:2n -6) and ,-linolenic (18:3n -3) acids were all increased in VO-fed fish. Fatty acid compositions of blood leucocytes showed similar changes. Evaluation of innate immune function showed that in the fat strain, circulating leucocytes were significantly lower in VO fish. The lean strain also had significantly higher serum lysozyme activity than MH fish. Reduced haematocrit was seen in VO lean fish compared with FO lean fish. This study provides evidence of strain-induced differences in liver and leucocyte fatty acid compositions and innate immunity in Atlantic salmon fed either FO- or VO-based diets. [source] The expression of the novel cytotoxic protein granzyme M by large granular lymphocytic leukaemias of both T-cell and NK-cell lineage: an unexpected finding with implications regarding the pathobiology of these disordersBRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2007William G. Morice Summary Granzyme M (GrM) is a novel cytotoxic protein normally exclusively expressed by natural killer (NK)-cells and cytotoxic T-cells with innate immune function. As most T-cell granular lymphocytic leukaemias (T-LGL) are thought to be derived from the adaptive immune system it was predicted that T-LGL would be GrM negative. Contrary to this hypothesis, bone marrow biopsy immunohistochemistry revealed that GrM was frequently expressed in both T-LGL (16 / 18) and NK-LGL (6 / 9). These unexpected results suggest commonality between T- and NK-LGL, providing further support to the notion that T-LGL is a disorder of dysregulated, chronically stimulated, adaptive cytotoxic T-cells. [source] Distinct roles of protein kinase R and toll-like receptor 3 in the activation of astrocytes by viral stimuliGLIA, Issue 3 2007Pamela A. Carpentier Abstract Impaired immune surveillance and constitutive immunosuppressive properties make the central nervous system (CNS) a particular challenge to immune defense, and require that CNS-resident cells be capable of rapidly recognizing and responding to infection. We have previously shown that astrocytes respond to treatment with a TLR3 ligand, poly I:C, with the upregulation of innate immune functions. In the current study, we examine the activation of innate immune functions of astrocytes by Theiler's murine encephalomyelitis virus (TMEV), a picornavirus, which establishes a persistent infection in the CNS of susceptible strains of mice and leads to the development of an autoimmune demyelinating disease that resembles human multiple sclerosis. Astrocytes infected with TMEV are activated to produce type I interferons, the cytokine IL-6, and chemokines CCL2 and CXCL10. We further examined the mechanisms that are responsible for the activation of astrocytes in response to direct viral infection and treatment with poly I:C. We found that the cytoplasmic dsRNA-activated kinase PKR is important for innate immune responses to TMEV infection, but has no role in their induction by poly I:C delivered extracellularly. In contrast, we found that TLR3 has only a minor role in responses to TMEV infection, but is important for responses to poly I:C. These results highlight the differences between responses induced by direct, nonlytic virus infection and extracellular poly I:C. The activation of astrocytes through these different pathways has implications for the initiation and progression of viral encephalitis and demyelinating diseases such as multiple sclerosis. © 2006 Wiley-Liss, Inc. [source] | |||||||||||||