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10.4049/jimmunol.1601293 http://scihub22266oqcxt.onion/10.4049/jimmunol.1601293 C5322190!5322190!28130498     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2017 ; 198 (5): 2133-46 Nephropedia Template TP {{tp|p=28130498|t=2017. Myeloid ATG16L1 facilitates host-bacteria interactions in maintaining intestinal homeostasis |pdf=|usr=}}{{28130498}} gab.com Text Myeloid ATG16L1 facilitates host-bacteria interactions in maintaining intestinal homeostasis JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28130498 #FOAvip Intact ATG16L1 plays an essential role in Paneth cell function and intestinal homeostasis. However, the functional consequences of ATG16L1 deficiency in myeloid cells, particularly macrophages, are not fully characterized. We generated mice with Atg16l1 deficiency in myeloid and dendritic cells and showed mice with myeloid Atg16l1 deficiency had exacerbated colitis in two acute and one chronic model of colitis with increased proinflammatory to anti-inflammatory macrophage ratios, production of proinflammatory cytokines, and numbers of IgA-coated intestinal microbes. Mechanistic analyses using primary murine macrophages showed that Atg16l1 deficiency led to increased reactive oxygen species production, impaired mitophagy, reduced microbial killing, impaired processing of MHCII antigens, and altered intracellular trafficking to the lysosomal compartments. Increased production of reactive oxygen species and reduced microbial killing may be general features of the myeloid compartment as they were also observed in Atg16l1 deficient primary murine neutrophils. A missense polymorphism (Thr300Ala) in the essential autophagy gene ATG16L1 is associated with Crohn?s disease (CD). Previous studies showed that this polymorphism leads to enhanced cleavage of ATG16L1 T300A protein and thus reduced autophagy. Similar findings were shown in primary human macrophages from controls and a population of CD patients carrying the Atg16l1 T300A risk variant and who were controlled for NOD2 CD-associated variants. This study revealed that ATG16L1 deficiency led to alterations in macrophage function that contribute to the severity of CD. Twit Text FOAVip Myeloid ATG16L1 facilitates host-bacteria interactions in maintaining intestinal homeostasis ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28130498 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28130498 #FOAvip English Wikipedia <ref>{{Cite pmid|28130498}}</ref> Myeloid ATG16L1 facilitates host-bacteria interactions in maintaining intestinal homeostasis #MMPMID28130498 Zhang H; Zheng L; McGovern DPB; Hamill AM; Ichikawa R; Kanazawa Y; Luu J; Kumagai K; Cilluffo M; Fukata M; Targan SR; Underhill DM; Zhang X; Shih DQ J Immunol 2017[Mar]; 198 (5): 2133-46 PMID28130498show ga Intact ATG16L1 plays an essential role in Paneth cell function and intestinal homeostasis. However, the functional consequences of ATG16L1 deficiency in myeloid cells, particularly macrophages, are not fully characterized. We generated mice with Atg16l1 deficiency in myeloid and dendritic cells and showed mice with myeloid Atg16l1 deficiency had exacerbated colitis in two acute and one chronic model of colitis with increased proinflammatory to anti-inflammatory macrophage ratios, production of proinflammatory cytokines, and numbers of IgA-coated intestinal microbes. Mechanistic analyses using primary murine macrophages showed that Atg16l1 deficiency led to increased reactive oxygen species production, impaired mitophagy, reduced microbial killing, impaired processing of MHCII antigens, and altered intracellular trafficking to the lysosomal compartments. Increased production of reactive oxygen species and reduced microbial killing may be general features of the myeloid compartment as they were also observed in Atg16l1 deficient primary murine neutrophils. A missense polymorphism (Thr300Ala) in the essential autophagy gene ATG16L1 is associated with Crohn?s disease (CD). Previous studies showed that this polymorphism leads to enhanced cleavage of ATG16L1 T300A protein and thus reduced autophagy. Similar findings were shown in primary human macrophages from controls and a population of CD patients carrying the Atg16l1 T300A risk variant and who were controlled for NOD2 CD-associated variants. This study revealed that ATG16L1 deficiency led to alterations in macrophage function that contribute to the severity of CD. äMyeloid ATG16L1 facilitates host-bacteria interactions in maintaining (epmc).pdf DeepDyve Pubget Overpricing