Preprint Review Version 1 This version is not peer-reviewed

Dysbiosis Promotes Gastric Diseases and Impede Therapies by Hijacking Gut Immune Homeostasis

Version 1 : Received: 16 January 2019 / Approved: 17 January 2019 / Online: 17 January 2019 (03:05:26 CET)

How to cite: Toor, D.; Wsson, M.; Goel, C.; Kaushik, N.K.; Kumar, P.; Sandhya, S.; Karthikeyan, G.; Kumar, A.; Prakash, H. Dysbiosis Promotes Gastric Diseases and Impede Therapies by Hijacking Gut Immune Homeostasis. Preprints 2019, 2019010170 (doi: 10.20944/preprints201901.0170.v1). Toor, D.; Wsson, M.; Goel, C.; Kaushik, N.K.; Kumar, P.; Sandhya, S.; Karthikeyan, G.; Kumar, A.; Prakash, H. Dysbiosis Promotes Gastric Diseases and Impede Therapies by Hijacking Gut Immune Homeostasis. Preprints 2019, 2019010170 (doi: 10.20944/preprints201901.0170.v1).

Abstract

Perturbation 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 promote gastric diseases. Changes in the gut microbiota manifest in disease progression owing to epigenetic modification in host which influences differentiation and function of immune cells adversely. Uncontrolled use of antibiotics; chemotherapeutic drugs and 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 micromillieu. Ligands released from dying microbes induce TLR mimicry on interaction with TLR abnormally which skew hypoxia and sterile inflammation contributing to severity of disease like IBD autoimmunity and cancer. Various modalities/interventions practiced across the globe and future strategies for microbiota based therapeutic approaches with special emphasis on tumor and inflammatory diseases are reviewed here. Therefore the major aim and scope of this manuscript is to both discuss various modalities/interventions across the globe and to design future microbiota based therapeutic approaches for mitigating the burden with special emphasis on tumor and Inflammatory diseases.

Subject Areas

gut microbiota; macrophages; TLR mimicry; immunoepigenetics; metabolism; sterile inflammation

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