JOURNAL ARTICLE

Heparin-Binding Hemagglutinin of Mycobacterium tuberculosis Inhibits Autophagy via Toll-like Receptor 4 and Drives M2 Polarization in Macrophages.

  • Published In: Journal of Infectious Diseases, 2024, v. 230, n. 2. P. 323 1 of 3

  • Database: Academic Search Ultimate 2 of 3

  • Authored By: Zheng, Qing; Li, Zhi; Zhou, Yu; Li, Yuru; Gong, Meiliang; Sun, Heqiang; Deng, Xinli; Ma, Yueyun 3 of 3

Abstract

This article focuses on the role of heparin-binding hemagglutinin (HBHA), a mycobacterial surface antigen, in modulating macrophage responses during Mycobacterium infection. The study demonstrates that HBHA inhibits autophagy in both murine RAW264.7 and human THP-1–derived macrophages via the Toll-like receptor 4 (TLR4)–dependent PI3K-AKT-mTOR signaling pathway, thereby promoting intracellular bacterial survival. Additionally, HBHA induces macrophage polarization toward the M2 anti-inflammatory phenotype, which may facilitate immune evasion by suppressing antimicrobial responses. These findings suggest that HBHA contributes to Mycobacterium tuberculosis pathogenesis by impairing macrophage-mediated clearance and highlight potential targets for novel tuberculosis therapies.

Additional Information

  • Source:Journal of Infectious Diseases. 2024/08, Vol. 230, Issue 2, p323
  • Document Type:Article
  • Subject Area:Health and Medicine
  • Publication Date:2024
  • ISSN:0022-1899
  • DOI:10.1093/infdis/jiae030
  • Accession Number:179042534
  • Copyright Statement:Copyright of Journal of Infectious Diseases is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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