Gut microbiota and COVID-19: An intriguing pediatric perspective

Abstract

Gastrointestinal (GI) involvement has been reported in approximately 50% of patients with coronavirus disease 2019 (COVID-19), which is due to the pathogenic role of inflammation and the intestinal function of the angiotensin-converting enzyme 2 and its receptor. Accumulating adult data has pointed out that gut dysbiosis might occur in these patients with a potential impact on the severity of the disease, however the role of gut microbiota in susceptibility and severity of COVID-19 disease in children is still poorly known. During the last decades, the crosstalk between gut and lung has been largely recognized resulting in the concept of “gut-lung axis” as a central player in modulating the development of several diseases. Both organs are involved in the common mucosal immune system (including bronchus-associated and gut-associated lymphoid tissues) and their homeostasis is crucial for human health. In this framework, it has been found that the role of GI dysbiosis is affecting the homeostasis of the gut-liver axis. Of note, a gut microbiome imbalance has been linked to COVID-19 severity in adult subjects, but it remains to be clarified. Based on the increased risk of inflammatory diseases in children with COVID-19, the potential correlation between gut microbiota dysfunction and COVID-19 needs to be studied in this population. We aimed to summarize the most recent evidence on this striking aspect of COVID-19 in childhood.

Impact of COVID-19 on Pediatric Inflammatory Bowel Diseases—From Expectations to Reality

“…COVID-19 infection has been associated with alterations in the gut microbiota composition [72]. Dysbiosis, characterized by an imbalance in the microbial community, may disrupt the delicate balance between the immune system and gut microbiota, potentially leading to the development of IBD [73].…”

“…Even when just the respiratory mucosa is affected, SARS-CoV-2 may change the gut microbial communities' composition [73,74]. As a result of increased inflammatory mediators, the lung becomes more permeable, allowing the virus and inflammatory mediators to move from the bloodstream into the gut [62].…”

“…The greatest amount of ACE2 receptors is found in the brush border of the intestinal epithelial cells, opening the path for SARS-CoV-2 at the digestive tract level. New virions are created in the cytoplasm of GI cells upon viral entrance, and these virions are subsequently discharged into the GI tract, where they directly impair enterocyte function and cause viral shedding in the stool [73,74]. SARS-CoV-2 causes the destruction of absorptive enterocytes, which disrupts the integrity of the intestinal barrier, increasing intestinal permeability and allowing the translocation of bacteria and other antigens from the gut into the bloodstream, promoting systemic inflammation [75].…”