Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), an RNA virus of the family Coronaviridae, causes coronavirus disease 2019 (COVID-19), an influenza-like disease that chiefly infects the lungs through respiratory transmission. The spike protein of SARS-CoV-2, a transmembrane protein in its outer portion, targets angiotensin-converting enzyme 2 (ACE2) as the binding receptor for the cell entry. As ACE2 is highly expressed in the gut and pulmonary tissues, SARS-CoV-2 infections frequently result in gastrointestinal inflammation, with presentations ordinarily ranging from intestinal cramps to complications with intestinal perforations. However, the evidence detailing successful therapy for gastrointestinal involvement in COVID-19 patients is currently limited. A significant change in fecal microbiomes, namely dysbiosis, was characterized by the enrichment of opportunistic pathogens and the depletion of beneficial commensals and their crucial association to COVID-19 severity has been evidenced. Oral probiotics had been evidenced to improve gut health in achieving homeostasis by exhibiting their antiviral effects via the gut–lung axis. Although numerous commercial probiotics have been effective against coronavirus, their efficacies in treating COVID-19 patients remain debated. In ClinicalTrials.gov, 19 clinical trials regarding the dietary supplement of probiotics, in terms of Lactobacillus and mixtures of Bifidobacteria and Lactobacillus, for treating COVID-19 cases are ongoing. Accordingly, the preventive or therapeutic role of probiotics for COVID-19 patients can be elucidated in the near future.
Highlights
Microorganisms 2021, 9, 1605 pulmonary tissue, angiotensin-converting enzyme 2 (ACE2) is highly expressed in the gut [3,4]; in the human small intestinal organoids model, enterocytes are infected by SARS-CoV-2, as demonstrated by confocal and electron microscopy [1,5]
Effect of Lactobacillus on the microbiome of household contacts exposed to COVID-19
Patients with COVID-19 had significant changes in fecal microbiomes, characterized by the enrichment of opportunistic pathogens and the depletion of beneficial commensals, which is vastly associated with disease severity
Summary
Microorganisms 2021, 9, 1605 pulmonary tissue, ACE2 is highly expressed in the gut [3,4]; in the human small intestinal organoids model, enterocytes are infected by SARS-CoV-2, as demonstrated by confocal and electron microscopy [1,5]. ACE2 is highly expressed in the gut [3,4]; the human small dence detailing successful therapy for gastrointestinal involvement in COVID-19 patients intestinal organoids model, enterocytes are infected by SARS-CoV-2, as demonstrated is currently limited. Increased autophagy, further leading to dysbiosis [7] Another theory is that the SARS-CoV-2 infections frequently result in gastrointestinal inflammation, with blockage of ACE2 induces the increased levels of angiotensinogen by the hyperactivation clinical presentations ranging from intestinal cramps and diarrhea to intestinal perforations of the renin–angiotensin system, resulting in the shutdown the frequent amino acid transporter.
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