Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

The UspA1 protein of Moraxella catarrhalis induces CEACAM-1-dependent apoptosis in alveolar epithelial cells.

Författare

  • PD. N'Guessan
  • M. Vigelahn
  • S. Bachmann
  • S. Zabel
  • B. Opitz
  • B. Schmeck
  • S. Hippenstiel
  • J. Zweigner
  • Kristian Riesbeck
  • BB. Singer
  • N. Suttorp
  • H. Slevogt

Summary, in English

Moraxella catarrhalis is a major cause of exacerbations of chronic obstructive pulmonary disease (COPD) and emphysema. M. catarrhalis–specific UspA1 and the epithelial carcinoembryonic antigen-related cell adhesion molecule (CEACAM1) were required to induce apoptosis. M. catarrhalis–induced apoptosis was significantly enhanced in HeLa cells stably transfected with CEACAM1, compared with HeLa cells not expressing CEACAM1. Infected cells showed increased activity of caspases 3, 6, and 9 but not of caspase 8. Reduced expression of Bcl-2, translocation of Bax into the mitochondria, and cytosolic increase of apoptosis-inducing factor in M. catarrhalis–infected cells implicated the involvement of mitochondrial death pathways. In conclusion, M. catarrhalis induced apoptosis in pulmonary epithelial cells—a process that was triggered by interaction between CEACAM1 and UspA1. Thus, M. catarrhalis–induced apoptosis of pulmonary epithelial cells may contribute to the development of COPD and emphysema.

Publiceringsår

2007

Språk

Engelska

Sidor

1651-1660

Publikation/Tidskrift/Serie

Journal of Infectious Diseases

Volym

195

Issue

11

Dokumenttyp

Artikel i tidskrift

Förlag

Oxford University Press

Ämne

  • Microbiology in the medical area

Status

Published

Forskningsgrupp

  • Clinical Microbiology, Malmö

ISBN/ISSN/Övrigt

  • ISSN: 1537-6613