Dysbiosis Disrupts Gut Immune Homeostasis and Promotes Gastric Diseases
AbstractPerturbation in the microbial population/colony index has harmful consequences on human health. Both biological and social factors influence the composition of the gut microbiota and also promote gastric diseases. Changes in the gut microbiota manifest in disease progression owing to epigenetic modification in the host, which in turn influences differentiation and function of immune cells adversely. Uncontrolled use of antibiotics, chemotherapeutic drugs, and any change in the diet pattern usually contribute to the changes in the colony index of sensitive strains known to release microbial content in the tissue micromilieu. Ligands released from dying microbes induce Toll-like receptor (TLR) mimicry, skew hypoxia, and cause sterile inflammation, which further contributes to the severity of inflammatory, autoimmune, and tumorous diseases. The major aim and scope of this review is both to discuss various modalities/interventions across the globe and to utilize microbiota-based therapeutic approaches for mitigating the disease burden. View Full-Text
Externally hosted supplementary file 1
Description: Authors, Response letter
Share & Cite This Article
Toor, D.; Wsson, M.K.; Kumar, P.; Karthikeyan, G.; Kaushik, N.K.; Goel, C.; Singh, S.; Kumar, A.; Prakash, H. Dysbiosis Disrupts Gut Immune Homeostasis and Promotes Gastric Diseases. Int. J. Mol. Sci. 2019, 20, 2432.
Toor D, Wsson MK, Kumar P, Karthikeyan G, Kaushik NK, Goel C, Singh S, Kumar A, Prakash H. Dysbiosis Disrupts Gut Immune Homeostasis and Promotes Gastric Diseases. International Journal of Molecular Sciences. 2019; 20(10):2432.Chicago/Turabian Style
Toor, Devinder; Wsson, Mishi K.; Kumar, Prashant; Karthikeyan, G.; Kaushik, Naveen K.; Goel, Chhavi; Singh, Sandhya; Kumar, Anil; Prakash, Hridayesh. 2019. "Dysbiosis Disrupts Gut Immune Homeostasis and Promotes Gastric Diseases." Int. J. Mol. Sci. 20, no. 10: 2432.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.