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

**Authors:** Hermes Vieira Barbeiro, Denise Frediani Barbeiro, Heraldo Possolo de Souza, Francisco Garcia Soriano, Marcel Cerqueira Machado, Ludhmila Abrahão Hajjar

PMC · DOI: 10.1016/j.clinsp.2025.100642 · 2025-04-23

## 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.

## Key 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.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IL1B (interleukin 1 beta)

## Full-text entities

- **Genes:** IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, FABP2 (fatty acid binding protein 2) [NCBI Gene 2169] {aka FABPI, I-FABP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, LBP (lipopolysaccharide binding protein) [NCBI Gene 3929] {aka BPIFD2}
- **Diseases:** intestinal barrier dysfunction (MESH:D007410), inflammatory (MESH:D007249), COVID-19 (MESH:D000086382), bacterially infected (MESH:D001424), bacterial co (MESH:D060085), infected (MESH:D007239)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12051628/full.md

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Source: https://tomesphere.com/paper/PMC12051628