Silymarin Reduces the Inflammatory Response and the Burden of Mycobacterium tuberculosis H37Ra Infection in Human Lung A549 Cells

TL;DR

Silymarin reduces inflammation and infection by Mycobacterium tuberculosis in human lung cells, suggesting it could help treat tuberculosis.

Contribution

This study reveals silymarin's effect on controlling tuberculosis infection and inflammation in pulmonary epithelial cells.

Findings

Silymarin at 50 μM reduces M. tuberculosis H37Ra infection in A549 cells.

Silymarin lowers inflammatory response and pNF-κB activation in infected cells.

Silymarin affects miRNA expression linked to immune signaling pathways.

Abstract

Silymarin is a natural polyphenol known for its broad range of biological effects, and research conducted in macrophages and mice infected with Mycobacterium tuberculosis have highlighted its potential as a complementary treatment for tuberculosis. Silymarin modulates multiple cellular signaling pathways associated with various aspects of the immune response. However, its effect on the control of M. tuberculosis infection in pulmonary epithelial cells is still not well understood. In this study, we evaluated the effect of silymarin on the infection control and immune response of A549 pulmonary epithelial cells infected with M. tuberculosis H37Ra. Our findings showed that the A549 cell line was more sensitive to the cytotoxic effects of silymarin, particularly to silibinin. The treatment of A549 cells with a dose of 50 μM favors the control of infection caused by M. tuberculosis H37Ra. The treatment resulted in a reduction of the inflammatory response, which correlates with lower activation of pNF‐κB. Additionally, the treatment affects the expression of miRNAs that may target several genes involved in immune response signaling pathways, including the MAPK signaling pathway, the apoptosis pathway, the JAK‐STAT signaling pathway, the TNF signaling pathway, and the NF‐κB signaling pathway. Our results suggest that silymarin treatment contributes to the control of infection and protects the pulmonary epithelium by decreasing the inflammatory response.

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