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Mannose-receptor positive and negative mouse macrophages differ in their susceptibility to infection by Chlamydia

Cho-chou Kuo1, Mirja Puolakkainen, Tsun-Mei Lin

  • 1Department of Pathobiology, University of Washington, Seattle, Washington, Washington 98195, USA. cckuo@u.washington.edu

Microbial Pathogenesis
|January 10, 2002
PubMed

Insights

Mannose receptors influence chlamydiae infection differently depending on the species. Chlamydia trachomatis prefers mannose-receptor positive cells, while Chlamydia pneumoniae prefers negative cells, indicating varied host cell interactions.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • N-linked high mannose oligosaccharides inhibit chlamydiae attachment and infectivity in HeLa cells.
  • Mannose moieties may play a role in chlamydiae infectivity, necessitating further investigation.

Purpose of the Study:

  • To investigate the involvement of mannose moieties in chlamydiae infectivity.
  • To evaluate the susceptibility of mannose-receptor negative and positive mouse macrophages to different Chlamydia species.

Main Methods:

  • Comparison of Chlamydia trachomatis, Chlamydia psittaci, and Chlamydia pneumoniae infection rates in J774A (mannose-receptor negative) and J774E (mannose-receptor positive) mouse macrophages.
  • Utilizing a macrophage model to assess chlamydial entry and survival based on mannose receptor expression.

Main Results:

  • Chlamydia trachomatis demonstrated enhanced infection of mannose-receptor positive J774E cells compared to J774A cells.
  • Chlamydia psittaci infected both J774A and J774E cells with equal efficiency.
  • Chlamydia pneumoniae showed a preference for mannose-receptor negative J774A cells over J774E cells.

Conclusions:

  • The role of mannose receptors in chlamydial infection varies significantly among different Chlamydia species.
  • This study provides a model system to explore the specific mechanisms of mannose receptor involvement in chlamydial attachment, entry, and intracellular survival within macrophages.

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