Mechanism of invasion of lung epithelial cells by filamentous legionella pneumophila

Akriti Prashar, Sonam Bhatia, Zohreh Tabatabaeiyazdi, Carla Duncan, Rafael A. Garduño, Patrick Tang, Donald E. Low, Cyril Guyard, Mauricio R. Terebiznik

Résultat de recherche: Articleexamen par les pairs

32 Citations (Scopus)

Résumé

Legionella, the aetiological agent responsible for Legionellosis, is an opportunistic pathogen that infects humans upon the inhalation of contaminated aerosolized water droplets. Legionella is pleomorphic and its different morphotypes exhibit varying degrees of virulence. While the filamentous forms of Legionella pneumophila (Lp) have been reported in patient samples since the first description of legionellosis, their role in disease has not been studied. Our results show that both E-cadherin and β1 integrin receptors mediate filamentous Lp (FLp) attachment to lung epithelial cells (LECs). The activation of these receptors induces the formation of actin enriched membrane surface structures that we designated 'hooks' and 'membrane wraps'. These structures entrap the filaments on the cell surface leading to their gradual internalization through a zipper mechanism of phagocytosis dependent on actomyosin activity. The supply of E-cadherin receptors from the recycling pathway and β1 integrins released from focal adhesion turnover are required to sustain this process. Intracellular FLp inhabits a vacuolar compartment where filaments differentiate into short rods and replicate to produce infective progeny. Here we are reporting a first description of the invasion mechanism used by FLp to invade LECs. Therefore, filamentous morphotype of Lp can induce its own uptake by LECs and has the potential ability to cause disease.

Langue d'origineEnglish
Pages (de-à)1632-1655
Nombre de pages24
JournalCellular Microbiology
Volume14
Numéro de publication10
DOI
Statut de publicationPublished - oct. 2012

ASJC Scopus Subject Areas

  • Microbiology
  • Immunology
  • Virology

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't

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