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Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut
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
11Tri-Institutional Training Program in Laboratory Animal Medicine and Science, Memorial Sloan Kettering Cancer Center, Weill Cornell Medicine, and The Rockefeller University, New York, New York.
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-wk-old female BALB/cJ (C) mice. After shedding was confirmed (through 95 d), these mice were cohoused with naïve C57BL/6J (B6), C, and Swiss (J:ARC[S]) mice (n = 28/strain) for 30 d. Cohoused mice (n = 3 to 6 exposed and 1 to 6 control/strain) were evaluated 7, 14, 21, 63, 120, and 180 d post-cohousing (DPC) via hemograms, serum biochemistry analysis, fecal quantitative PCR, histopathology, and Cm major outer membrane protein immunohistochemistry. Immunophenotyping was performed on spleen (B6, C, and 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 were 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/time points. Gastrointestinal immunophenotyping (B6) revealed sustained increases in total inflammatory cells and elevated cytokine expression in innate lymphoid and effector T cells (large intestine). Elevated concentrations of proinflammatory cytokines were detected in the serum (B6). Results demonstrate that while clinical disease was not appreciated, 3 commonly used strains of mice are susceptible to chronic enteric Cm infection which may alter various immune responses. Considering the widespread use of mice to model gastrointestinal disease, institutions should consider excluding Cm from their colonies.
Insights
Chlamydia muridarum (Cm) causes chronic enteric infection in common mouse strains, altering immune responses without obvious clinical signs. Researchers should consider excluding Cm from mouse colonies to ensure accurate gastrointestinal disease modeling.
Area of Science:
- Veterinary Microbiology
- Immunology
- Infectious Diseases
Background:
- Chlamydia muridarum (Cm) is a reemerging pathogen in research mouse colonies.
- Few studies investigate Cm's impact on immunocompetent mice via natural infection routes.
Purpose of the Study:
- To evaluate the effects of chronic enteric Chlamydia muridarum infection on immunocompetent mice.
- To assess the susceptibility and immune response of different mouse strains to Cm.
Main Methods:
- BALB/cJ mice were orogastrically inoculated with Cm and subsequently cohoused with naïve C57BL/6J, BALB/cJ, and Swiss mice.
- Mice were monitored for shedding, clinical signs, and analyzed via hemograms, serum biochemistry, qPCR, histopathology, immunohistochemistry, immunophenotyping, and cytokine assays.
- Evaluations occurred at multiple time points post-cohousing (DPC) and post-infection (DPI).
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 GALT hyperplasia were observed in infected mice.
- Splenic and intestinal immunophenotyping revealed altered immune cell populations and elevated pro-inflammatory cytokines in infected mice.
Conclusions:
- Commonly used mouse strains are susceptible to chronic enteric Cm infection.
- Cm infection can alter immune responses in mice, even without apparent clinical disease.
- Excluding Cm from mouse colonies may be necessary for accurate gastrointestinal disease modeling.
