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10.3389/fmicb.2018.01488 http://scihub22266oqcxt.onion/10.3389/fmicb.2018.01488 C6043646!6043646 !30034379     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30034379 &cmd=llinks): Failed to open stream: HTTP request failed! 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Helicobacter pylori Infection Increased Anti-dsDNA and Enhanced Lupus Severity in Symptomatic Fc?RIIb-Deficient Lupus Mice |pdf=|usr=}}{{30034379 }} gab.com Text Helicobacter pylori Infection Increased Anti-dsDNA and Enhanced Lupus Severity in Symptomatic Fc RIIb-Deficient Lupus Mice JO: Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=30034379 #FOAvip The defect on Fc gamma receptor IIb (Fc?RIIb), the only inhibitory Fc?R, has been identified as one of the genetic factors increasing susceptibility to lupus. The prevalence of Helicobacter pylori (HP) and Fc?RIIb dysfunction-polymorphisms are high among Asians, and their co-existence is possible. Unfortunately, the influence of HP against lupus progression in patients with lupus is still controversial. In this study, the interactions between these conditions were tested with HP infection in 24-week-old Fc?RIIb-/- mice (symptomatic lupus). HP induced failure to thrive, increased stomach bacterial burdens and stomach injury (histology and cytokines) in both wild-type and Fc?RIIb-/- mice. While the severity of HP infection, as determined by these parameters, was not different between both strains, antibodies production (anti-HP, anti-dsDNA and serum gammaglobulin) were higher in Fc?RIIb-/- mice compared to wild-type. Accordingly, HP infection also accelerated the severity of lupus as determined by proteinuria, serum creatinine, serum cytokines, renal histology, and renal immune complex deposition. Although HP increased serum cytokines in both wild-type and Fc?RIIb-/- mice, the levels were higher in Fc?RIIb-/- mice. As such, HP also increased spleen weight and induced several splenic immune cells responsible for antibody productions (activated B cell, plasma cell and follicular helper T cell) in Fc?RIIb-/- mice, but not in wild-type. These data describe the different systemic responses against localized HP infection from diverse host genetic background. In conclusion, the mutual interactions between HP and lupus manifestations of Fc?RIIb-/-mice were demonstrated in this study. With the prominent immune responses from the loss of inhibitory signaling in Fc?RIIb-/- mice, HP infection in these mice induced intense chronic inflammation, increased antibody production, and enhanced lupus severity. Thus, the increased systemic inflammatory responses due to localized HP inducing gastritis in some patients with lupus may enhance lupus progression. More studies are needed. Twit Text FOAVip Helicobacter pylori Infection Increased Anti-dsDNA and Enhanced Lupus Severity in Symptomatic Fc RIIb-Deficient Lupus Mice ????Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=30034379 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30034379 #FOAvip English Wikipedia <ref>{{Cite pmid|30034379 }}</ref> Helicobacter pylori Infection Increased Anti-dsDNA and Enhanced Lupus Severity in Symptomatic Fc?RIIb-Deficient Lupus Mice #MMPMID30034379 Surawut S ; Panpetch W ; Makjaroen J ; Tangtanatakul P ; Thim-Uam A ; Wongphoom J ; Tumwasorn S ; Leelahavanichkul A Front Microbiol 2018[]; 9 (ä): 1488 PMID30034379 show ga The defect on Fc gamma receptor IIb (Fc?RIIb), the only inhibitory Fc?R, has been identified as one of the genetic factors increasing susceptibility to lupus. The prevalence of Helicobacter pylori (HP) and Fc?RIIb dysfunction-polymorphisms are high among Asians, and their co-existence is possible. Unfortunately, the influence of HP against lupus progression in patients with lupus is still controversial. In this study, the interactions between these conditions were tested with HP infection in 24-week-old Fc?RIIb-/- mice (symptomatic lupus). HP induced failure to thrive, increased stomach bacterial burdens and stomach injury (histology and cytokines) in both wild-type and Fc?RIIb-/- mice. While the severity of HP infection, as determined by these parameters, was not different between both strains, antibodies production (anti-HP, anti-dsDNA and serum gammaglobulin) were higher in Fc?RIIb-/- mice compared to wild-type. Accordingly, HP infection also accelerated the severity of lupus as determined by proteinuria, serum creatinine, serum cytokines, renal histology, and renal immune complex deposition. Although HP increased serum cytokines in both wild-type and Fc?RIIb-/- mice, the levels were higher in Fc?RIIb-/- mice. As such, HP also increased spleen weight and induced several splenic immune cells responsible for antibody productions (activated B cell, plasma cell and follicular helper T cell) in Fc?RIIb-/- mice, but not in wild-type. These data describe the different systemic responses against localized HP infection from diverse host genetic background. In conclusion, the mutual interactions between HP and lupus manifestations of Fc?RIIb-/-mice were demonstrated in this study. With the prominent immune responses from the loss of inhibitory signaling in Fc?RIIb-/- mice, HP infection in these mice induced intense chronic inflammation, increased antibody production, and enhanced lupus severity. Thus, the increased systemic inflammatory responses due to localized HP inducing gastritis in some patients with lupus may enhance lupus progression. More studies are needed. äHelicobacter pylori Infection Increased Anti-dsDNA and Enhanced Lupus (epmc).pdf DeepDyve Pubget Overpricing