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Updated: Feb 11, 2026
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Forward Genetic Approaches in Chlamydia trachomatis
Published on: October 23, 2013
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Complement C3 opsonization of Chlamydia trachomatis facilitates uptake in human monocytes
Mads Lausen1, Gunna Christiansen2, Nichlas Karred1
1Department of Health Science and Technology, Aalborg University, Fredrik Bajers Vej 3b, 9220, Aalborg Ø, Denmark.
Microbes and Infection
|May 6, 2018
Summary
Chlamydia trachomatis evades immune responses, but complement C3 opsonization enhances monocyte uptake. This interaction promotes bacterial elimination, not survival or cytokine release, offering insights into chlamydial infection control.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Chlamydia trachomatis causes severe infections, leading to infertility and ectopic pregnancy.
- The bacterium evades host immune responses, establishing chronic infections.
- The complement system and monocytes are crucial for antibacterial defense.
Purpose of the Study:
- Investigate the interaction between the complement system and Chlamydia trachomatis.
- Understand how complement influences chlamydial uptake by monocytes.
- Determine the role of complement in host defense against C. trachomatis.
Main Methods:
- Used complement-competent and C3-depleted serum.
- Utilized immunoelectron microscopy to visualize complement deposition.
- Quantified chlamydial uptake and intracellular survival in monocytes.
Main Results:
- Complement-competent serum facilitated rapid uptake of C. trachomatis serovars D and L2 into monocytes.
- Complement C3 was deposited on the bacterial surface as the opsonin iC3b.
- Complement-facilitated uptake did not affect intracellular bacterial survival or cytokine secretion.
Conclusions:
- C. trachomatis activates the complement system, leading to iC3b opsonization.
- Monocytes efficiently phagocytose and eliminate complement-opsonized C. trachomatis.
- This interaction highlights a key mechanism in the innate immune response to chlamydial infections.
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