AI Article Synopsis

  • Acinetobacter baumannii is a major cause of hospital-acquired infections, and while the process of adhesion to host cells is understood, how it moves and survives inside those cells is less clear.
  • TFEB, a transcription factor, becomes activated after infection with A. baumannii in human lung cells and is essential for the bacteria's invasion and ability to persist in those cells.
  • Additionally, the study shows that TFEB's orthologue in C. elegans, HLH-30, is crucial for the nematode's survival during A. baumannii infection, indicating that these factors play a key role in how this pathogen operates within hosts.

Article Abstract

Acinetobacter baumannii is a significant human pathogen associated with hospital-acquired infections. While adhesion, an initial and important step in A. baumannii infection, is well characterized, the intracellular trafficking of this pathogen inside host cells remains poorly studied. Here, we demonstrate that transcription factor EB (TFEB) is activated after A. baumannii infection of human lung epithelial cells (A549). We also show that TFEB is required for the invasion and persistence inside A549 cells. Consequently, lysosomal biogenesis and autophagy activation were observed after TFEB activation which could increase the death of A549 cells. In addition, using the Caenorhabditis elegans infection model by A. baumannii, the TFEB orthologue HLH-30 was required for survival of the nematode to infection, although nuclear translocation of HLH-30 was not required. These results identify TFEB as a conserved key factor in the pathogenesis of A. baumannii. Adhesion is an initial and important step in Acinetobacter baumannii infections. However, the mechanism of entrance and persistence inside host cells is unclear and remains to be understood. In this study, we report that, in addition to its known role in host defense against Gram-positive bacterial infection, TFEB also plays an important role in the intracellular trafficking of A. baumannii in host cells. TFEB was activated shortly after A. baumannii infection and is required for its persistence within host cells. Additionally, using the C. elegans infection model by A. baumannii, the TFEB orthologue HLH-30 was required for survival of the nematode to infection, although nuclear translocation of HLH-30 was not required.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5874439PMC
http://dx.doi.org/10.1128/mSphere.00106-18DOI Listing

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