4.6 Article

Trafficking of chlamydial antigens to the endoplasmic reticulum of infected epithelial cells

Journal

MICROBES AND INFECTION
Volume 10, Issue 14-15, Pages 1494-1503

Publisher

ELSEVIER
DOI: 10.1016/j.micinf.2008.09.001

Keywords

Chlamydia trachomatis; Inclusion membrane protein (Inc); Lipopolysaccharide (LPS); Endoplasmic reticulum; Antigen presentation

Funding

  1. National Institutes of Health
  2. National Institute of Allergy and Infectious Diseases [R01-A113446]

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Confinement of the obligate intracellular bacterium Chlamydia trachomatis to a membrane-bound vacuole, termed an inclusion, within infected epithelial cells neither prevents secretion of chlamydial antigens into the host cytosol nor protects chlamydiae from innate immune detection. However, the details leading to chlamydial antigen presentation are not clear. By immunoelectron microscopy of infected endometrial epithelial cells and in isolated cell secretory compartments, chlamydial major outer membrane protein (MOMP), lipopolysaccharide (LPS) and the inclusion membrane protein A (IncA) were localized to the endoplasmic reticulum (ER) and co-localized with multiple ER markers, but not with markers of the endosomes, lysosomes, Golgi nor mitochondria. Chlamydial LPS was also co-localized with CD1d in the ER. Since the chlamydial antigens, contained in everted inclusion membrane vesicles, were found within the host cell ER, these data raise additional implications for antigen processing by infected uterine epithelial cells for classical and non-classical T cell antigen presentation. (C) 2008 Elsevier Masson SAS. All rights reserved.

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