Title : Changing microbiota in hospitalized patients increase the COVID-19 severity, a possible cause of developing the dysregulated immune response- A literature Study
Human physiological homeostasis and onset of the disease, is largely depend on the interactions among resident microbiome of skin, oral cavity, respiratory tract, gastrointestinal system, genital area, and host’s protective immunity. Gut probiotics like Faecalibacterium prausnitzii, Eubacterium rectale and bifidobacteria, influence the immunomodulatory signaling, were noted to be depleted in hospitalized patients even after the disease resolution than healthy individuals. IBD is induced by SARSCoV-2, could stimulate the severity events via alteration of the gut microbiota during/ after the respiratory infection. The viral RNA signature in the faecal samples of recovered patients and its presence for longer period, even after the clearance of the virus from respiratory tract, is suggestive of dysbiosis leading to the poor prognosis of COVID-19 in ICU patients. GM plays a significant role to stimulate the modulated antiviral immune response against invading pathogens regulating the physiological homeostasis. GM profile of COVID-19 patients has revealed the drastic depletion of dominant families of commensals viz., Bacteroidaceae, Lachnospiraceae and Ruminococcaceae, were reported to be substituted with Enterococcus, Staphylococcus, Streptococcus, Serratia etc.; consequently, developing the dysfunctional activities of Th1-Th2 cells along the lung-gut axis exchanging microbes & other toxic metabolites and translocating them to the other body organs too. It is also speculated that the gut virome and bacteriophages could also interfere in maintaining / or disrupting the homeostasis. Excessive secretion of chemokines and cytokines cause ARDS, interstitial pneumonia and organ failure. Virome/ and microbiome also interact with immune cells to regulate the immune signaling mechanisms. Therefore, it is imperative to build strategies to develop novel therapeutics in controlling these hyperinflammatory severity events.