Related Experiment Video
Updated: Mar 19, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Effects of Murine Norovirus on Chlamydia pneumoniae-Accelerated Atherosclerosis in ApoE(-/-) Mice
Karuna Patil1, Lee Ann Campbell2, Michael E Rosenfeld3
1Departments of Comparative Medicine, University of Washington, Seattle, Washington, USA kpatil@uw.edu.
Abstract:
Chlamydia pneumoniae (Cpn), a common respiratory pathogen of humans, is associated with human cardiovascular disease and the acceleration of atherosclerosis in hyperlipidemic animal models. Our laboratory has demonstrated that murine norovirus (MNV), a prevalent infection of laboratory mice, can unpredictably alter atherosclerosis in hyperlipidemic Ldlr(-/-) and ApoE(-/-) mice. Given that MNV has a tropism for macrophages and may exacerbate atherogenesis, we investigated whether coinfection with MNV and Cpn might alter macrophage phenotypes in vitro and atherosclerosis in ApoE(-/-) mice. In the presence of oxidized low-density lipoprotein, coinfection of ApoE(-/-) bone marrow-derived macrophages (BMDM) with MNV and Cpn resulted in significant increases in gene expression of IL6, MCP1, iNOS, and TNFα compared with Cpn-monoinfected BMDM. On the basis of these findings, we hypothesized that concurrent MNV-Cpn infection might increase plaque lesion size in vivo. As expected, Cpn monoinfection of ApoE(-/-) mice increased mean plaque size by 62% compared with that in uninfected mice. However, MNV did not significantly alter plaque lesion size in MNV-Cpn-coinfected mice compared with Cpn-monoinfected mice. There were no differences in aortic cytokines locally at the site of plaque development or in peritoneal macrophages at 1 wk after infection in MNV-Cpn-coinfected mice compared with Cpn-monoinfected mice. MNV was not detected in the aortic tissue of MNV-infected mice at 1 or 8 wk after infection regardless of Cpn status. These data suggest that MNV infection does not appreciably alter plaque development in Cpn-accelerated atherosclerosis in ApoE(-/-) mice.
Insights
Murine norovirus (MNV) coinfection did not worsen atherosclerosis accelerated by Chlamydia pneumoniae (Cpn) in mice. This study found MNV does not significantly impact plaque development in this cardiovascular disease model.
Area of Science:
- Immunology
- Cardiovascular Research
- Infectious Disease
Background:
- Chlamydia pneumoniae (Cpn) is linked to cardiovascular disease and atherosclerosis.
- Murine norovirus (MNV), a common mouse infection, can unpredictably affect atherosclerosis.
- MNV targets macrophages, potentially worsening atherosclerosis.
Purpose of the Study:
- To investigate if coinfection with MNV and Cpn alters macrophage phenotypes in vitro.
- To determine if concurrent MNV-Cpn infection affects atherosclerosis progression in ApoE(-/-) mice.
Main Methods:
- ApoE(-/-) bone marrow-derived macrophages (BMDM) were coinfected with MNV and Cpn in the presence of oxidized low-density lipoprotein.
- Gene expression of inflammatory markers (IL6, MCP1, iNOS, TNFα) was analyzed.
- Atherosclerosis plaque size and aortic cytokines were assessed in ApoE(-/-) mice with Cpn monoinfection versus MNV-Cpn coinfection.
Main Results:
- Coinfection increased inflammatory gene expression in BMDM compared to Cpn monoinfection.
- Cpn monoinfection significantly increased plaque size (62%) in ApoE(-/-) mice.
- MNV coinfection did not significantly alter plaque lesion size compared to Cpn monoinfection.
- No differences in aortic cytokines or peritoneal macrophages were observed between groups at 1 week post-infection.
- MNV was undetectable in aortic tissue regardless of Cpn status.
Conclusions:
- MNV infection does not significantly alter atherosclerosis progression accelerated by Cpn in ApoE(-/-) mice.
- Despite in vitro inflammatory responses, MNV does not exacerbate Cpn-driven atherogenesis in vivo.
- The findings suggest MNV's role in Cpn-accelerated atherosclerosis is minimal in this model.
