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Published on: July 9, 2014
Amphiphysin IIm is required for survival of Chlamydia pneumoniae in macrophages
Elizabeth S Gold1, Randi M Simmons, Timothy W Petersen
1Institute for Systems Biology, 1441 N. 34th St., Seattle, WA 98103, USA.
Abstract:
Macrophages play a critical role in both innate and acquired immunity because of their unique ability to internalize, kill, and degrade bacterial pathogens through the process of phagocytosis. The adaptor protein, amphiphysin IIm, participates in phagocytosis and is transiently associated with early phagosomes. Certain pathogens, including Chlamydia pneumoniae, have evolved mechanisms to subvert macrophage phagosome maturation and, thus, are able to survive within these cells. We report here that, although amphiphysin IIm is usually only transiently associated with the phagosome, it is indefinitely retained on vacuoles containing C. pneumoniae. Under these wild-type conditions, C. pneumoniae do not elicit significant nitric oxide (NO) production and are not killed. Abrogation of amphiphysin IIm function results in C. pneumoniae-induced NO production and in the sterilization of the vacuole. The data suggest that C. pneumoniae retains amphiphysin IIm on the vacuole to survive within the macrophage.
Insights
Chlamydia pneumoniae subverts macrophage immunity by retaining amphiphysin II m on vacuoles, preventing bacterial killing. Disrupting this protein triggers nitric oxide production, eliminating the pathogen.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Macrophages are key immune cells employing phagocytosis to eliminate bacterial pathogens.
- The adaptor protein amphiphysin II m is involved in phagocytosis, transiently binding to early phagosomes.
- Pathogens like Chlamydia pneumoniae can evade macrophage defenses by disrupting phagosome maturation.
Purpose of the Study:
- To investigate the role of amphiphysin II m in the survival of Chlamydia pneumoniae within macrophages.
- To determine how Chlamydia pneumoniae interacts with amphiphysin II m during vacuole maturation.
Main Methods:
- Observing the association of amphiphysin II m with C. pneumoniae-containing vacuoles.
- Assessing nitric oxide (NO) production in macrophages infected with C. pneumoniae.
- Evaluating the survival of C. pneumoniae upon abrogation of amphiphysin II m function.
Main Results:
- Amphiphysin II m is retained indefinitely on vacuoles containing C. pneumoniae, unlike its transient association with typical phagosomes.
- In the presence of retained amphiphysin II m, C. pneumoniae survives and does not induce significant nitric oxide production.
- Disrupting amphiphysin II m function leads to C. pneumoniae-induced nitric oxide production and vacuole sterilization.
Conclusions:
- Chlamydia pneumoniae appears to exploit the retention of amphiphysin II m on its vacuole as a survival mechanism within macrophages.
- Amphiphysin II m retention is crucial for C. pneumoniae to evade immune responses like nitric oxide production.
- Targeting the interaction between C. pneumoniae and amphiphysin II m could be a strategy to enhance bacterial clearance by macrophages.
