The study is published today in Frontiers in Immunology by researchers from King’s with funding by the Medical Research Council via the UK Coronavirus Immunology Consortium, and support from the NIHR Guy’s and St Thomas’ BRC. It looked at samples of gastrointestinal tract from patients who died after being diagnosed with COVID-19 during the first wave of the pandemic.
Lymphoid tissue in the gut normally maintains healthy intestinal microbial populations which are essential for good health. Researchers observed that the system that would normally regulate the composition of the microbial communities – otherwise known as Peyer’s Patches – were severely disrupted in severe COVID-19. This was irrespective of whether there was evidence of virus present in the gut or not.
While severe COVID-19 can lead to breathing problems and high fever, some patients can experience diarrhoea, nausea and vomiting, which suggests involvement of the gastrointestinal tract.
“This study shows that in severe COVID-19, this key component of the immune system is disrupted, whether the intestine itself is infected with SARS-CoV-2 or not. This would likely contribute to the disturbances in intestinal microbial populations in COVID-19 reported by others.”
– Professor Jo Spencer from the School of Immunology & Microbial Sciences
Observations of the samples found the structure and cellularity in Peyer’s Patches – a grouping of lymphoid follicles that lines the small intestines – had been altered independent of the local levels of the virus. This included depletion of the germinal centres, which normally propagate antibody producing cells, in patients who died with COVID-19.
This resulting poor local immunity could lead to a reduction in microbial diversity, known as dysbiosis. Researchers also noted that the findings suggest that oral vaccination may not be effective if the patient is already ill, as the gut immune system is already compromised.
Professor Spencer added: “In the future it will be important to understand factors driving such lymphoid tissue dysregulation in severe inflammatory responses.”
