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Updated: Feb 22, 2026

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Porphyromonas Gingivalis Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice
Rungtiwa Srisuwantha1,2, Yuka Shiheido2, Norio Aoyama2
1Department of Conservative Dentistry and Prosthodontics, Faculty of Dentistry, Srinakharinwirot University.
Insights
Periodontal pathogen Porphyromonas gingivalis infection after myocardial infarction (MI) in mice increased high mobility group box 1 (HMGB1) expression. This suggests periodontitis may worsen post-MI inflammation via HMGB1.
Area of Science:
- Cardiovascular Research
- Infectious Diseases
- Immunology
Background:
- High mobility group box 1 (HMGB1) is released from necrotic cells, driving inflammation.
- Periodontitis and cardiovascular diseases (CVDs) share potential links, with HMGB1 implicated in post-myocardial infarction (MI) inflammation.
- The role of periodontitis in exacerbating myocardial damage post-MI remains unclear.
Purpose of the Study:
- To investigate the impact of Porphyromonas gingivalis (P.g.) infection on myocardial HMGB1 expression following MI in a mouse model.
Main Methods:
- C57BL/6J mice underwent MI and were inoculated with P.g. or PBS.
- Plasma and heart tissue samples were collected at days 5 and 14 post-MI.
- HMGB1 expression was quantified using ELISA and immunohistochemistry.
Main Results:
- P.g.-inoculated mice showed significantly elevated HMGB1 protein levels on day 5 post-MI compared to controls.
- Immunohistochemistry revealed broader HMGB1 distribution in P.g.-infected hearts, including degenerated cardiomyocytes and extracellular spaces.
- A significant increase in HMGB1-positive cells was observed in the P.g.-inoculated group.
Conclusions:
- Porphyromonas gingivalis infection post-MI enhances myocardial HMGB1 expression.
- Periodontitis may contribute to post-infarction myocardial inflammation through HMGB1 signaling.
Abstract:
High mobility group box 1 (HMGB1) is a nuclear protein released from necrotic cells, inducing inflammatory responses. Epidemiological studies suggested a possible association between periodontitis and cardiovascular diseases (CVDs). Due to tissue damage and necrosis of cardiac cells following myocardial infarction (MI), HMGB1 is released, activating an inflammatory reaction. However, it remains unclear whether periodontitis is also involved in myocardial damage. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis (P.g.) after MI in mice.C57BL/6J wild type mice in post-MI were inoculated with P.g. in the infected group (P.g.-inoculated MI group) and with phosphate buffer saline (PBS) in the control group (PBS-injected MI group). Plasma samples and twelve tissue samples from mice hearts after MI were obtained. We determined the expression of HMGB1 by ELISA and immunohistochemistry.The level of HMGB1 protein in the P.g.-inoculated MI group was significantly higher than in the PBS-injected MI group on day 5, but not on day 14. Immunohistochemistry analysis revealed that HMGB1 was mainly expressed in cardiomyocytes, immune cells, and vascular endothelial cells in the PBS-injected MI group, while HMGB1 was seen broadly in degenerated cardiomyocytes, extracellular fields, immune cells, and vascular endothelial cells in the P.g.-inoculated MI group. A significant increase in the number of HMGB1 positive cells was observed in the P.g.-inoculated MI group compared to the PBS-injected MI group.Infection with P.g. after MI enhanced myocardial HMGB1 expression. There is a possible relationship between periodontitis and post-infarction myocardial inflammation through HMGB-1.

