English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Airway epithelial cell is often the initial site of attack by pathogens, and cell death is commonly caused by internalization of  Mycobacterium tuberculosis  ( Mtb ). However, the mechanism of interaction between epithelial cells and  Mtb  is not well understood. In this study, we investigated the role of the heparin-binding hemagglutinin (HBHA) protein of  Mtb  in the function of epithelial cells. In particular, the autophagy of A549 cells was determined based on microtubule-associated protein 1 light chain 3 alpha (LC3) activity. Autophagosome formation was detected by Monodansylcadaverine (MDC) staining and immune fluorescence staining of LC3. Autophagy could be significantly suppressed by HBHA protein. In addition, the LDH assay results showed that HBHA treatment could induce death on A549 cells. To explore the form of cell death, we detected the activity of caspase-3 and LDH release of A549 cells in the presence or absence of caspase inhibitor Z-VAD-FMK. Results demonstrated that HBHA treatment could induce apoptosis of A549 cells. To further confirm these results, we constructed the recombinant  Mycobacterium smegmatis  ( MS ) expressing HBHA ( rMS-HBHA ) and explored the influence of  rMS-HBHA  on the function of A549 cells.  rMS-HBHA  infection significantly inhibited LC3 expression and the maturation of autophagosomes in A549 cells. Subsequently, we infected A549 cells with  MS  and detected the viability of intracellular  MS  by CFU counts.  rMS-HBHA  showed higher survival and replication capacity in A549 cells than those of the wild-type  MS . Finally, infection of A549 cells with  rMS-HBHA  caused further apoptosis. These findings suggested that  rMS-HBHA  could inhibit autophagy, promote its survival and replication within A549 cells, and subsequently induce apoptosis on infected cells to facilitate infection.

Heparin-binding Hemagglutinin of Mycobacterium tuberculosis Is an Inhibitor of Autophagy