LBP and iFABP mismatch in the evaluation of intestinal barrier dysfunction due to SARS-CoV-2 infection

TL;DR

This study explores how SARS-CoV-2 affects the intestinal barrier, finding that damage is mainly at tight junctions rather than enterocytes, with differences in older patients.

Contribution

The study reveals that SARS-CoV-2 causes intestinal barrier dysfunction primarily through tight junction damage, not enterocyte damage.

Findings

Intestinal damage in SARS-CoV-2 is mainly due to tight junction alteration, not enterocyte damage.

Older patients show increased intestinal epithelial damage compared to younger patients.

LBP and iFABP levels help distinguish bacterial co-infections and age-related differences in SARS-CoV-2 patients.

Abstract

•Inflammation in SARS-CoV-2 has an extrapulmonary alteration in 20 % of cases.•Intestinal damage is a direct action of the virus.•Enterocyte damage is lower to tight junction alteration.

Inflammation in SARS-CoV-2 has an extrapulmonary alteration in 20 % of cases.

Intestinal damage is a direct action of the virus.

Enterocyte damage is lower to tight junction alteration.

SARS-CoV-2 presents a hyperinflammatory scenario due to systemic inflammatory response syndrome with intense cytokine release, with consequent extrapulmonary involvement in 20 % of patients. The authors studied whether COVID-19 intestinal damage is a direct action of the virus on intestinal epithelial cells, with damage mainly at the tight junction. This is a retrospective observational study in a tertiary hospital emergency department. The authors studied 87 patients (46 patients over 61 years and 41 patients under 60 years old) with severe SARS-CoV-2 infection. The authors measured two plasma markers, LPS-Binding Protein (LBP) and ileal Fatty Acid-Binding Protein (iFABP). Furthermore, the authors evaluated the interaction between the two markers. TNF-α and IL-1 β were higher in bacterial co-infected patients and TNF-α was also higher in the older patients. Plasma iFABP levels were not statistically different in patients with bacterial co-infection; however, higher levels were found in the older population. Plasma LBP levels were higher in patients with bacterial co-infection when compared to patients without infection; however, when comparing plasma LBP levels in the older population with younger patients, no differences could be found. LBP, FABP, and cytokines can discriminate between bacterially infected patients and also discriminate elderly patients. The present study suggests that intestinal barrier dysfunction in SARS-CoV-2 infections is mainly due to damage to the intestinal tight junction complex with a disproportionately lower damage to enterocyte. In the older population, the authors also observed an increase in intestinal epithelial damage.

Figures