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Perforin-2 Restricts Growth of Chlamydia trachomatis in Macrophages
- Source :
- Infection and Immunity. 81:3045-3054
- Publication Year :
- 2013
- Publisher :
- American Society for Microbiology, 2013.
-
Abstract
- Chlamydia trachomatis is a Gram-negative obligate intracellular bacterium that preferentially infects epithelial cells. Professional phagocytes provide C. trachomatis only a limited ability to survive and are proficient killers of chlamydiae. We present evidence herein that identifies a novel host defense protein, perforin-2, that plays a significant role in the eradication of C. trachomatis during the infection of macrophages. Knockdown of perforin-2 in macrophages did not alter the invasion of host cells but did result in chlamydial growth that closely mirrored that detected in HeLa cells. C trachomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-mediated killing. Interestingly, induction of perforin-2 expression in epithelial cells is blocked during productive chlamydial growth, thereby protecting chlamydiae from bactericidal attack. Ectopic expression of perforin-2 in HeLa cells, however, does result in killing. Overall, our data implicate a new innate resistance protein in the control of chlamydial infection and may help explain why the macrophage environment is hostile to chlamydial growth.
- Subjects :
- Pore Forming Cytotoxic Proteins
Immunoblotting
Immunology
Chlamydiae
Chlamydia trachomatis
Biology
Transfection
medicine.disease_cause
Microbiology
Microscopy, Electron, Transmission
RNA interference
medicine
Humans
Macrophage
Gene knockdown
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Reverse Transcriptase Polymerase Chain Reaction
Macrophages
Chlamydia Infections
biology.organism_classification
Virology
Infectious Diseases
Microscopy, Fluorescence
Perforin
Gene Knockdown Techniques
biology.protein
RNA Interference
Parasitology
Ectopic expression
HeLa Cells
Subjects
Details
- ISSN :
- 10985522 and 00199567
- Volume :
- 81
- Database :
- OpenAIRE
- Journal :
- Infection and Immunity
- Accession number :
- edsair.doi.dedup.....401a587202b69a54a8b998f206ad52df