Tumour necrosis factor-α induces macromolecule translocation in HIV-derived duodenal organoids.

ABSTRACT:

Background

Disease progression from human immunodeficiency virus (HIV) infection to acquired immunodeficiency syndrome (AIDS) is marked by chronic immune activation, partly due to increased translocation of gut-derived microbial antigens. Elevated mucosal tumour necrosis factor-α (TNF-α) and resulting epithelial cell apoptosis may be the etiology. However, studies using carcinoma cell lines have failed to find a causal link, possibly due to cellular abnormalities related to the malignant transformation of these immortal cell lines.

Methods

We established intestinal organoid monolayers from healthy controls and HIV-infected adults and characterized their growth dynamics and cellular composition. We then examined the effects of HIV-associated cytokines on transepithelial resis

SUBMITTER: Masete KV 

PROVIDER: S-EPMC11959035 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature