Tobacco smoke induces persistent infection of Chlamydophila pneumoniae in HEp-2 cells

Jean A Wiedeman, Ravi Kaul, Luke S. Heuer, Nao N. Thao, Kent E Pinkerton, Wanda M. Wenman

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

We examined tobacco smoke exposure and its effect on the life cycle of Chlamydophila pneumoniae (C. pneumoniae) in HEp-2, a human respiratory epithelial cell line. Using noncytotoxic concentrations of smoke medium, chlamydiae were grown in tissue culture and infectious particles were quantitated indirectly by immunocytometry of infected indicator cells. Chlamydial genome copy number was assessed with real-time polymerase chain reaction, and ultrastructure was examined by transmission electron microscopy. There was a significant reduction (56-64%; p<0.05) in the number of infectious elementary bodies following smoke exposure compared to untreated cultures. Under the same conditions, at late time points, smoke-exposed cultures showed significantly fewer chlamydial DNA copies (p<0.04). Moreover, smoke exposure induced large aberrant bodies that predominated within the inclusion. Following in vitro smoke exposure, alterations in the developmental cycle of C. pneumoniae included: inhibition of productive infection, reduced bacterial cell division, and formation of aberrant bodies. Thus, using this novel system, we were able to induce chlamydial persistence. Tobacco smoke exposure may represent a risk for establishment of a chronic reservoir of C. pneumoniae infection within respiratory epithelium.

Original languageEnglish (US)
Pages (from-to)141-148
Number of pages8
JournalMicrobial Pathogenesis
Volume37
Issue number3
DOIs
StatePublished - Sep 2004

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Keywords

  • Chlamydophila pneumoniae
  • Electron microscopy
  • HEp-2 cells
  • Immunocytometry of infected cells
  • Real time PCR
  • Tobacco smoke

ASJC Scopus subject areas

  • Microbiology
  • Infectious Diseases

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