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Published on: May 24, 2011
Chlamydia muridarum Causes Persistent Subclinical Infection and Elicits Innate and Adaptive Immune Responses in
Noah Mishkin1, Sebastian E Carrasco1,2, Michael Palillo1
1Tri-Institutional Training Program in Laboratory Animal Medicine and Science, Memorial Sloan Kettering Cancer Center, Weill Cornell Medicine, and The Rockefeller University, New York, NY.
Abstract:
Chlamydia muridarum (Cm) has reemerged as a moderately prevalent infectious agent in research mouse colonies. Despite its' experimental use, few studies evaluate Cm's effects on immunocompetent mice following its natural route of infection. A Cm field isolate was administered (orogastric gavage) to 8-week-old female BALB/cJ (C) mice. After confirming shedding (through 95d), these mice were cohoused with naïve C57BL/6J (B6), C, and Swiss (J:ARC[S]) mice (n=28/strain) for 30 days. Cohoused mice (n=3-6 exposed and 1-6 control/strain) were evaluated 7, 14, 21, 63, 120, and 180 days post-cohousing (DPC) via hemograms, serum biochemistry analysis, fecal qPCR, histopathology, and Cm MOMP immunohistochemistry. Immunophenotyping was performed on spleen (B6, C, S; n=6/strain) and intestines (B6; n=6) at 14 and 63 DPC. Serum cytokine concentrations were measured (B6; n=6 exposed and 2 control) at 14 and 63 DPC. All B6 mice were shedding Cm by 3 through 180 DPI. One of 3 C and 1 of 6 S mice began shedding Cm at 3 and 14 DPC, respectively, with the remaining shedding thereafter. Clinical pathology was nonremarkable. Minimal-to-moderate enterotyphlocolitis and gastrointestinal associated lymphoid tissue (GALT) hyperplasia was observed in 15 and 47 of 76 Cm-infected mice, respectively. Cm antigen was frequently detected in GALT-associated surface intestinal epithelial cells. Splenic immunophenotyping revealed increased monocytes and shifts in T cell population subsets in all strains/timepoints. Gastrointestinal immunophenotyping (B6) revealed sustained increases in total inflammatory cells and elevated cytokine production in innate lymphoid cells and effector T cells (large intestine). Elevated concentrations of pro-inflammatory cytokines were detected in the serum (B6). Results demonstrate that while clinical disease was not appreciated, 3 commonly utilized strains of mice are susceptible to chronic enteric Cm infection which may alter various immune responses. Considering the widespread use of mice to model GI disease, institutions should consider excluding Cm from their colonies.
Insights
Chlamydia muridarum (Cm) causes chronic enteric infection in mice, impacting immune responses without obvious disease. This highlights the need to manage Cm in research colonies to ensure accurate GI disease modeling.
Area of Science:
- Microbiology
- Immunology
- Veterinary Science
Background:
- Chlamydia muridarum (Cm) is a reemerging infectious agent in mouse research colonies.
- Limited studies assess Cm's impact on immunocompetent mice via natural infection routes.
Purpose of the Study:
- To evaluate the effects of natural Chlamydia muridarum infection on immunocompetent mice.
- To assess the susceptibility and immune response of different mouse strains to enteric Cm infection.
Main Methods:
- BALB/cJ mice were infected with Cm via orogastric gavage and subsequently cohoused with naïve C57BL/6J, BALB/cJ, and Swiss mice.
- Evaluations included fecal qPCR, histopathology, immunohistochemistry, hemograms, serum biochemistry, immunophenotyping (spleen and intestine), and serum cytokine analysis.
- Infection duration and immune cell changes were monitored over 180 days post-cohousing.
Main Results:
- All C57BL/6J mice shed Cm throughout the study; BALB/cJ and Swiss mice also became infected and shed Cm.
- Minimal-to-moderate enterotyphlocolitis and gastrointestinal associated lymphoid tissue (GALT) hyperplasia were observed in infected mice.
- Splenic and intestinal immunophenotyping revealed altered immune cell populations and elevated pro-inflammatory cytokines, particularly in C57BL/6J mice.
Conclusions:
- Three common mouse strains are susceptible to chronic enteric Chlamydia muridarum infection.
- While clinical disease was not apparent, Cm infection alters immune responses in mice.
- Institutions should consider excluding Cm from mouse colonies used for modeling gastrointestinal diseases.
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