Can our gut microbiome help to overcome Covid-19?
Probiotics found to assist in restoring normal immune function...
COVID-19 disrupts normal bowel flora
SARS-CoV-2 infection induces an aggressive inflammatory response which is strongly implicated in the cause of multi-organ dysfunction in some patients.(3) As a result, disease severity is likely caused not only by viral infection, but also an extreme host immune reaction. Patients with severe disease have been observed to have high levels of inflammatory markers and cytokines that reflect a strong immune response.(1)
The GI tract is the largest immunological organ and the gut microbiota is known to modulate host immune responses.(3) Gut microbial metabolic processes have been observed to strongly impact the production of cytokines. Cytokines are small proteins that act as signaling molecules that coordinate the host’s response against infection and inflammation.(4) In response to infection, excessive levels of cytokines are released leading to hyper inflammation that is observed in some patients infected with SARS-CoV-2.(4)
There is increasing evidence that the GI tract, and therefore the gut microbiome, is involved in the COVID-19 immune response observed in patients. SARS-CoV-2 has the ability to infect and replicate in the human small intestine enterocytes and viral RNA has been consistently detected in stool samples, suggesting involvement of the GI tract.(2)
In a study conducted in Hong Kong by Yeoh et al., records from 100 patients with laboratory-confirmed SARS-CoV-2 infections and 78 adults without infection were obtained. These patients’ blood and serial stool specimens were further analyzed. Shotgun sequencing of total DNA extracted from the stool samples characterized the gut microbiome composition and the concentration of inflammatory cytokines were determined from blood plasma.(2) The study found that the composition of the gut microbiome was significantly different in the patients with COVID-19 compared to the patients without COVID-19.(1)
Several commensal gut bacteria with known immunomodulatory potential, including Faecalibacterium prausnitzii, Eubacterium rectale and several bifidobacterial species were underrepresented in COVID-19 patients and remained low in samples collected up to one month after disease resolution.(2) The microbial imbalance found in the COVID-19 patients correlated with elevated concentrations of inflammatory cytokines and plasma concentrations of several cytokines, chemokines and inflammation markers.(2) These findings suggest that the gut microbiota could play a role in modulating host immune response and potentially influence disease severity and outcomes.(1)
“Our results suggest that dysbiosis weakens our immune defense, thereby predisposing to more severe SARS-CoV-2 infection and contributing to ‘long COVID,'” claimed Dr. Siew Ng of the Chinese University of Hong Kong. “Probiotics, if using the right combination of missing bacteria to boost immunity, may be potentially useful as an adjuvant therapy.” She went on to say, “The abnormal gut microbiota (dysbiosis) in COVID patients persists after clearance of the virus. These alterations could play a role in ‘long COVID.’ Clinical management not only should aim at clearing the virus but also restoring the abnormal gut microbiota,”
As a result, Dr. Ng and her colleagues developed a probiotic capsule that they used to treat patients recovering from Covid infections that helped to achieve complete symptom resolution, showed significantly reduced proinflammatory markers in their blood, had increased favorable bacteria in their stool, and developed neutralizing antibody.
These results suggest that dysbiosis, an unhealthy and unbalanced microbiome due to a loss of diversity and a decrease in beneficial microbes, weakens our immune system defenses and therefore prompts a more severe infection from SARS-CoV-2.(1) Therefore, increasing beneficial gut species could serve as a novel avenue to mitigate severe disease from SARS-CoV-2.
By Makena BrandTechnical Services Microbiologist I Works Cited: 1, 2, 3, 4