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10.1128/IAI.00993-15 http://scihub22266oqcxt.onion/10.1128/IAI.00993-15 C4645409!4645409 !26371131     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26371131 &cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-10 modulates antigen presentation by dendritic cells through regulation of NLRP3 inflammasome assembly during Chlamydia infection |pdf=|usr=}}{{26371131 }} gab.com Text Interleukin-10 modulates antigen presentation by dendritic cells through regulation of NLRP3 inflammasome assembly during Chlamydia infection JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26371131 #FOAvip Interleukin-10 (IL-10) has been implicated in susceptibility to genital chlamydial infection and the development of tubal pathologies. IL-10 limitation also resulted in the rapid elicitation of immune responses against Chlamydia, and decreased levels of IL-10 correlated with protective anti-Chlamydia immunity. To investigate the molecular basis for these effects, we compared the reproductive pathologies and fertility rates in Chlamydia-infected wild-type (WT) and IL-10-knockout (IL-10(-/-)) mice; we also analyzed the expression of the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1? production, NLRP3 inflammasome assembly and activation, and the immunostimulatory capacity and apoptotic predilection of Chlamydia-exposed dendritic cells (DCs) from WT and IL-10(-/-) mice. Our results revealed that, in addition to the rapid clearance of infection, genitally infected IL-10(-/-) mice were protected from tubal pathologies and infertility, whereas WT (IL-10(+/+)) mice were not. Chlamydia-pulsed IL-10(-/-) DCs expressed larger numbers of TLR4/IL-1R molecules and had enhanced IL-1? production. In addition, NLRP3 inflammasome assembly was suppressed in IL-10(-/-) DCs through the inhibition of the P2X purinoceptor 7 (P2X7) receptor (P2X7R), an ATP-gated ion channel, and a decrease in intracellular Ca(2+) levels, which inhibited DC apoptosis. Thus, the potent immunostimulatory capacity of IL-10-deficient DCs is due, at least in part, to the suppression of the intracellular inflammasome assembly, which prevents DC apoptosis, allowing efficient antigen presentation. The results indicate that IL-10 deficiency enables efficient antigen presentation by DCs for rapid and enhanced immune activation against Chlamydia, which results in rapid microbial clearance, which prevents tubal pathologies during infection. Our finding has important implications for the induction of protective immunity against Chlamydia and other infectious and noninfectious diseases by vaccines. Twit Text FOAVip Interleukin-10 modulates antigen presentation by dendritic cells through regulation of NLRP3 inflammasome assembly during Chlamydia infection ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26371131 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26371131 #FOAvip English Wikipedia <ref>{{Cite pmid|26371131 }}</ref> Interleukin-10 modulates antigen presentation by dendritic cells through regulation of NLRP3 inflammasome assembly during Chlamydia infection #MMPMID26371131 Omosun Y ; McKeithen D ; Ryans K ; Kibakaya C ; Blas-Machado U ; Li D ; Singh R ; Inoue K ; Xiong ZG ; Eko F ; Black C ; Igietseme J ; He Q Infect Immun 2015[Dec]; 83 (12 ): 4662-72 PMID26371131 show ga Interleukin-10 (IL-10) has been implicated in susceptibility to genital chlamydial infection and the development of tubal pathologies. IL-10 limitation also resulted in the rapid elicitation of immune responses against Chlamydia, and decreased levels of IL-10 correlated with protective anti-Chlamydia immunity. To investigate the molecular basis for these effects, we compared the reproductive pathologies and fertility rates in Chlamydia-infected wild-type (WT) and IL-10-knockout (IL-10(-/-)) mice; we also analyzed the expression of the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1? production, NLRP3 inflammasome assembly and activation, and the immunostimulatory capacity and apoptotic predilection of Chlamydia-exposed dendritic cells (DCs) from WT and IL-10(-/-) mice. Our results revealed that, in addition to the rapid clearance of infection, genitally infected IL-10(-/-) mice were protected from tubal pathologies and infertility, whereas WT (IL-10(+/+)) mice were not. Chlamydia-pulsed IL-10(-/-) DCs expressed larger numbers of TLR4/IL-1R molecules and had enhanced IL-1? production. In addition, NLRP3 inflammasome assembly was suppressed in IL-10(-/-) DCs through the inhibition of the P2X purinoceptor 7 (P2X7) receptor (P2X7R), an ATP-gated ion channel, and a decrease in intracellular Ca(2+) levels, which inhibited DC apoptosis. Thus, the potent immunostimulatory capacity of IL-10-deficient DCs is due, at least in part, to the suppression of the intracellular inflammasome assembly, which prevents DC apoptosis, allowing efficient antigen presentation. The results indicate that IL-10 deficiency enables efficient antigen presentation by DCs for rapid and enhanced immune activation against Chlamydia, which results in rapid microbial clearance, which prevents tubal pathologies during infection. Our finding has important implications for the induction of protective immunity against Chlamydia and other infectious and noninfectious diseases by vaccines. |Adoptive Transfer [MESH] |Animals [MESH] |Antigen Presentation [MESH] |Apoptosis/immunology [MESH] |Calcium/immunology/metabolism [MESH] |Carrier Proteins/genetics/*immunology [MESH] |Chlamydia Infections/genetics/*immunology/microbiology/pathology [MESH] |Chlamydia muridarum/*immunology/pathogenicity [MESH] |Dendritic Cells/*immunology/microbiology/transplantation [MESH] |Female [MESH] |Fertility/*immunology [MESH] |Gene Expression Regulation [MESH] |Host-Pathogen Interactions [MESH] |Inflammasomes/genetics/immunology [MESH] |Interleukin-10/deficiency/genetics/*immunology [MESH] |Interleukin-1beta/genetics/immunology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein [MESH] |Receptors, Interleukin-1 Type I/genetics/immunology [MESH] |Receptors, Purinergic P2X7/genetics/immunology [MESH] |Signal Transduction [MESH]Interleukin-10 modulates antigen presentation by dendritic cells throu(epmc).pdf DeepDyve Pubget Overpricing