Impaired IgA production and function exert a vital role in initiation of the imbalance between OBP and commensal microbiota

Impaired IgA production and function exert a vital role in initiation of the imbalance between OBP and commensal microbiota. functions of retinoic acid and carotenoids, including pro-vitamin A carotenoids and xanthophylls in the maturation of the gut immune system and IgA production. This is the first review article concerning the carotenoid supplements and the metabolites in the regulation of the gut microbiome. We hope this review would provide a new direction for the management of the gut microbiota dysbiosis by application of bioactive carotenoids and the metabolites. and are most abundant bacterial species in the adult human gut, accounting for more than 90% of the bacterial populations.1 Recently, gut microbiota dysbiosis has been shown to be associated with weaknesses in gut barrier function, dysregulated innate, and adaptive immune responses and also with the increased incidence of the inflammatory bowel disease (IBD) and other metabolic disorders.2,3 Studies show that antibiotics play vital roles in the progression of dysbiosis especially in the overgrowth of the resistant opportunistic bacterial pathogen (OBP).4 Another major factor is a diet which can be directly utilized by microbiota, and in turn causes changes in the composition of microbiota. Dysbiosis is usually accompanied by increased FK866 OBP and decreased commensal microbiota like and and the relationship between the OBP and production of IgA in dysbiosis are yet exclusive. Recently, experts found some bioactive molecules that would be beneficial to improve microbiota composition, and in turn reduce the risk of diseases caused by microbiota dysbiosis. Carotenoid supplementation shows encouraging improvements in the immune system maturation and IgA production.9 Here, we discuss the roles of OBP and commensal microbiota in the FK866 pathogenesis of dysbiosis via regulation of the IgA function and immune maturation, and discuss the potential of carotenoid supplementation in dysbiosis prevention and treatment. Gut microbiota dysbiosis causes diseases Dysbiosis can be comprehended with the loss of beneficial microbiota, growth of pathogenic or potentially harmful microbiota, and a decrease of overall microbiota diversity.10 There are multiple ways to influence the composition of the microbiota, including the genetics of the host, diet, infection and medical interventions, like antibiotics.11 Dysbiosis is associated with several pathological processes, including obesity, non-alcoholic fatty liver disease (NAFLD), and IBD (Table 1).12 The FK866 overgrowth of OBP can cause pathoprogression of some diseases. For example, increased large quantity of (alcohol-producing bacteria) was correlated with the elevated blood FK866 alcohol concentration in patients with non-alcoholic steatohepatitis (NASH), suggestive of involvement of imbalanced gut microbiome in the pathogenesis of NASH.13 The bacterial microbiota in IBD has also been investigated. An increase in bacteria in the phylum, such as was observed in the IBD patients.14 Also, fungal microbiota dysbiosis was also found in patients with IBD. 15 FK866 Another study exhibited that the gut microbiota dysbiosis decided the development of NAFLD.16 Dysbiosis causes the decrease in commensal microbiota, like treatment reduced the intestinal lipopolysaccharide levels, and suppressed expression of inflammatory and oxidative stress markers in the liver of ob/ob mice fed a high fat diet. 20C24 DiabetesRatio of and compared to BioBreeding diabetes prone rats (a type 1 diabetic model) 25C27 Inflammatory bowel diseaseand were similarly represented between microbiomes in healthy and obese mice, but were significantly elevated in nonalcoholic steatohepatitis.rhamnosus PL60 improved liver steatosis in diet-induced obesity mice. 13,30C32 Open in a Plxna1 separate windows Gut microbiota dysbiosis leads to IgA dysfunction There are at least two points of view of the mechanisms in the maintenance of the balance between the host and microbiota via manipulation of the gut immune.