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A Human Fallopian Tube Model for Investigation of C. trachomatis Infections
Published on: August 11, 2012
Perforin-2 restricts growth of Chlamydia trachomatis in macrophages
K A Fields1, R McCormack, L R de Armas
1Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida, USA. Kfields@med.miami.edu
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.
Insights
A novel host defense protein, perforin-2, helps macrophages kill Chlamydia trachomatis. Blocking perforin-2 allows chlamydia to grow, revealing its role in controlling this infection.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Chlamydia trachomatis is an obligate intracellular bacterium infecting epithelial cells.
- Professional phagocytes like macrophages are generally proficient at killing chlamydiae.
- The mechanisms underlying macrophage-mediated Chlamydia eradication are not fully understood.
Purpose of the Study:
- To identify novel host defense mechanisms involved in controlling Chlamydia trachomatis infection.
- To investigate the role of perforin-2 in the innate immune response against Chlamydia.
Main Methods:
- Macrophage cell cultures were used to study Chlamydia trachomatis infection.
- Perforin-2 expression was modulated using knockdown techniques.
- Chlamydial growth and viability were assessed in infected cells.
- Epithelial cells (HeLa) were used to study perforin-2 induction and ectopic expression.
Main Results:
- Knockdown of perforin-2 in macrophages led to increased Chlamydia trachomatis growth, similar to epithelial cells.
- Perforin-2-mediated killing was effective against multiple Chlamydia trachomatis serovars and C. muridarum.
- Chlamydia trachomatis actively blocked perforin-2 induction in epithelial cells during infection.
- Ectopic expression of perforin-2 in epithelial cells conferred resistance to Chlamydia.
Conclusions:
- Perforin-2 is a novel host defense protein crucial for macrophage-mediated eradication of Chlamydia trachomatis.
- Chlamydia trachomatis employs strategies to evade perforin-2-mediated killing.
- Understanding perforin-2's role offers insights into innate immunity against bacterial infections.
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