Infectious disease
Is a disrupted gut linked to how sick COVID-19 patients get?
Open access · cc by · source: Europe PMC
COVID-19 patients had a different mix of gut bacteria from healthy controls, and certain bacteria and signs of a leaky gut tracked with more severe illness and stronger inflammation.
Study at a glance
- Design
- Case-control — Hospital-based case-control comparison of COVID-19 patients (mild vs severe) and uninfected staff controls, with serial stool shotgun metagenomics, stool metaproteomics and blood biomarker, proteomic and transcriptomic data analysed by mixed linear regression.
- N
- N=71 · 63 COVID-19 patients (39 mild, 24 severe) and 8 uninfected controls provided 106 stool samples; metaproteomics used samples from 16 people; plasma LBP was measured in 148 patients from the wider cohort.
- Population
- Adults and adolescents hospitalised with COVID-19 at the Shanghai Public Health Clinical Center, January-April 2020, plus uninfected hospital-staff volunteers.
- Outcome
- Gut microbial composition, pathways and virulence genes by COVID-19 status and severity, and their associations with blood immune and inflammation markers and gut-barrier markers.
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Key findings
Overall bacterial diversity did not differ, but community composition did: patients lost 19 species, including beneficial ones such as Faecalibacterium prausnitzii, and gained 8, including opportunistic pathogens. Four species were more abundant in severe than mild disease; two of them, Burkholderia contaminans and Bacteroides nordii, were linked to lower lymphocyte and T-cell counts or higher white-cell counts and inflammation markers such as IL-6. Severe patients' stool had more bacterial virulence genes and more human proteins and DNA, suggesting damage to the gut lining, and blood LBP was higher in severe disease and correlated with inflammation.
Methodology
The researchers studied 63 patients hospitalised with COVID-19 in Shanghai early in 2020 (39 mild, 24 severe) and 8 uninfected hospital staff. They sequenced all the microbial DNA in 106 stool samples, including weekly samples from severe patients, and related bacterial species, metabolic pathways and virulence genes to blood markers of immunity and inflammation. In smaller subsets they measured human and bacterial proteins in stool and blood and a blood marker of gut leakiness, lipopolysaccharide-binding protein (LBP).
Limitations
The design compares groups at one time and cannot show whether gut changes cause severe COVID-19 or result from it, its treatments or hospital stay. There were only 8 controls, the metaproteomic subset was very small, and many microbe-biomarker associations were tested with a lenient false-discovery threshold, so some findings may be chance. Diet, physical activity, BMI and comorbidities were not fully controlled, and bacterial proteins in blood were too rarely detected for statistical testing, so the leaky-gut pathway remains a plausible hypothesis rather than a demonstrated mechanism.
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