Persistent Systemic Microbial Translocation and Intestinal Damage During Coronavirus Disease-19

Abstract

Microbial translocation (MT) and intestinal damage (ID) are poorly explored in COVID-19. Aims were to assess whether alteration of gut permeability and cell integrity characterize COVID-19 patients, whether it is more pronounced in severe infections and whether it influences the development of subsequent bloodstream infection (BSI). Furthermore, we looked at the potential predictive role of TM and ID markers on Intensive Care Unit (ICU) admission and in-hospital mortality. Over March–July 2020, 45 COVID-19 patients were enrolled. Markers of MT [LPB (Lipopolysacharide Binding Protein) and EndoCab IgM] and ID [I-FABP (Intestinal Fatty Acid Binding Protein)] were evaluated at COVID-19 diagnosis and after 7 days. As a control group, age- and gender-matched healthy donors (HDs) enrolled during the same study period were included. Median age was 66 (56-71) years. Twenty-one (46.6%) were admitted to ICU and mortality was 22% (10/45). Compared to HD, a high degree of MT and ID was observed. ICU patients had higher levels of MT, but not of ID, than non-ICU ones. Likewise, patients with BSI had lower EndoCab IgM than non-BSI. Interestingly, patients with high degree of MT and low ID were likely to be admitted to ICU (AUC 0.822). Patients with COVID-19 exhibited high level of MT, especially subjects admitted to ICU. COVID-19 is associated with gut permeability.

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

“…It is, therefore, possible that gastro-intestinal symptoms may contribute to decreased foraging and the sickness symptom complex by protecting against the entry of other pathogens, which may cause co-infections. This is relevant because increased levels of IL-1 and T cell activation may induce intestinal permeability, resulting in increased bacterial translocation thereby aggravating the consequences of the primary infection [ 55 , 56 ], including in COVID-19 [ 57 , 58 ]. As such, gastro-intestinal symptoms may be part of the SSC complex.…”

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

“…It is, therefore, possible that gastro-intestinal symptoms may contribute to decreased foraging and the sickness symptom complex by protecting against the entry of other pathogens, which may cause co-infections. This is relevant because increased levels of IL-1 and T cell activation may induce intestinal permeability, resulting in increased bacterial translocation thereby aggravating the consequences of the primary infection [52, 53], including in COVID-19 [54, 55]. As such, gastro-intestinal symptoms may be part of the SSC complex.…”

“…The copyright holder for this this version posted September 28, 2021. ; https://doi.org/10.1101/2021.09.26.21264127 doi: medRxiv preprint consequences of the primary infection [52,53], including in COVID-19 [54,55]. As such, gastro-intestinal symptoms may be part of the SSC complex.…”

Is the Gut Microbiome a Target for Adjuvant Treatment of COVID-19?

“…The influence of COVID-19 on microbial translocation and intestinal damage was investigated [59]. Microbial translocation is the ability of microbes or their products to translocate across the normally very tight epithelial layer into the extraintestinal space and systemic circulation.…”

“…It occurs when the gut mucosal integrity is weakened. Oliva et al used three different blood markers to measure microbial translocation and intestinal damage (lipopolysaccharide binding protein, EndoCab IgM, and intestinal fatty acid binding protein) [59]. The cohort was comprised of 45 COVID-19 patients, where 46.6% were admitted to ICU.…”