The scoring system was determined by leukocyte mucosal infiltration with the following criteria; Score 0, normal; Score 1, mild; Score 2, moderate; Score 3 marked histopathological changes. infection in 24-week-old FcRIIb-/- mice (symptomatic lupus). HP induced failure to thrive, increased stomach bacterial burdens and stomach injury (histology and cytokines) in both wild-type and FcRIIb-/- 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 FcRIIb-/- mice compared to wild-type. Accordingly, HP infection also accelerated the Stiripentol 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 FcRIIb-/- mice, the levels were TCL1B higher in FcRIIb-/- 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 FcRIIb-/- 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 FcRIIb-/-mice were demonstrated in this study. With the prominent immune responses from the loss of inhibitory signaling in FcRIIb-/- 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. (HP), microaerophilic, spiral-shaped gram-negative bacteria, are organisms that can survive in the highly acidic stomach environment, and are known to cause chronic gastric inflammation and cancer (Mahachai et al., 2016). The infection is very common among Asians, with a prevalence rate of up to 50C80% in some countries (Thirumurthi and Graham, 2012; Xie and Lu, 2015). Interestingly, eradication of HP in some patients with associated autoimmune diseases leads to long-term remission of the autoimmune disease (Fujimura et al., 2005; Kuwana, 2014). Moreover, HP infection down-regulates the expression of Fc gamma receptor IIb (FcRIIb), the only inhibitory FcR (Bolland and Ravetch, 2000) on circulating monocyte of patients with autoimmune diseases (Asahi et al., 2008; Wu et al., 2012). As Fc receptors (FcR) is the immunoglobulin superfamily that contributes to the protective functions, in part, by inducing phagocytosis of opsonized microbes, loss of the inhibitory FcR results in effective organism control but enhances the risk of autoimmune diseases (Ravetch and Bolland, 2001). Although HP infection has shown a protective effect on the development of lupus in a case control study, especially among African-American patients, the relationship of lupus-HP is still intriguing (Sawalha et al., 2004; Hasni et al., 2011). Inadvertently, FcRIIb dysfunction polymorphisms are common in Asia (Chu et al., 2004), partially due to the genetic pressure from malarial infection (Clatworthy et al., 2007). Although FcRIIb dysfunction protects against malaria, the insufficient inhibitory signaling increases the risk of autoimmune activation. Indeed, the association between FcRIIb polymorphisms and systemic lupus erythematosus (lupus) in patients has been reported (Tsuchiya and Kyogoku, 2005). Both FcRIIb dysfunction polymorphisms and HP infection are common in the Asian population (Smith and Clatworthy, 2010; Hooi et al., 2017). While FcRIIb loss-of-function is associated with lupus (Siriboonrit et al., 2003; Tsuchiya and Kyogoku, 2005; Jakes et al., 2012), HP infection has been associated with other autoimmune diseases such as immune thrombocytopenic purpura and membranous nephropathy (Hasni et Stiripentol al., 2011). As Stiripentol chronic inflammation accelerates lupus (Hasni et al., 2011) and the co-existence of FcRIIb dysfunction polymorphisms with HP infection are possible, information on the responses of FcRIIb-/- mice to of HP infection in patients with lupus. Thus this study tested HP infection in FcRIIb-/- condition, and Administration Model HP ATCC 43504 (ATCC, Manassas, VA, United States) was cultured on supplemented Columbia agar (Oxoid, Hampshire, United Kingdom) under microaerophilic conditions (6C12% O2, 5C8% CO2) at 37C for 48 h before use. The mouse model for.
Whether or not the CYP1A1-modulating effects of isoflavones are beneficial will depend not only about concerted action with additional enzymes of the xenobiotic pathway but also about cell type or content material
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