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A Microscopic Phenotypic Assay for the Quantification of Intracellular Mycobacteria Adapted for High-throughput/High-content Screening
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Mycobacteria exploit host hyaluronan for efficient extracellular replication.

Yukio Hirayama1, Mamiko Yoshimura, Yuriko Ozeki

  • 1Department of Bacteriology, Osaka City University Graduate School of Medicine, Osaka, Osaka, Japan.

Plos Pathogens
|October 31, 2009
PubMed
Summary
This summary is machine-generated.

Pathogenic mycobacteria utilize host hyaluronan as a nutrient source for growth in the lungs. Inhibiting hyaluronidase, an enzyme critical for this process, shows promise for treating mycobacterial diseases.

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Area of Science:

  • * Microbiology and Immunology
  • * Host-Pathogen Interactions
  • * Respiratory Infections

Background:

  • * Hyaluronan is crucial for host defense in the lungs.
  • * The role of hyaluronan in mycobacterial infections was previously unknown.
  • * Mycobacteria were observed to interact with hyaluronan on lung epithelial cells.

Purpose of the Study:

  • * To investigate the role of hyaluronan in established mycobacterial infections.
  • * To determine if mycobacteria can utilize hyaluronan as a nutrient.
  • * To explore potential therapeutic strategies targeting hyaluronan metabolism.

Main Methods:

  • * Analysis of hyaluronan utilization by mycobacteria using HAS-transfected cells.
  • * Quantification of hyaluronan synthase (HAS) expression in infected lungs.
  • * Histochemical analysis of hyaluronan accumulation in lung granulomas.
  • * Detection and characterization of mycobacterial hyaluronidase activity.
  • * In vivo testing of a hyaluronidase inhibitor (L-Ascorbic acid 6-hexadecanoate).

Main Results:

  • * Pathogenic mycobacteria can grow using hyaluronan as a carbon source.
  • * Hyaluronan synthases HAS1 and HAS3, but not HAS2, support mycobacterial growth.
  • * HAS1 is the predominant hyaluronan synthase in the lung and its expression increases post-infection.
  • * Hyaluronan accumulates significantly in lung granulomas of infected hosts.
  • * Mycobacterial hyaluronidase activity is essential for hyaluronan-dependent growth.
  • * A hyaluronidase inhibitor suppressed mycobacterial growth in vivo.

Conclusions:

  • * Pathogenic mycobacteria exploit host hyaluronan for growth in the respiratory tract.
  • * Hyaluronan, a host-protective molecule, is repurposed by mycobacteria.
  • * Hyaluronidase inhibitors represent a potential therapeutic avenue for mycobacterial diseases.