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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Tissue destruction induced by Porphyromonas gingivalis infection in a mouse chamber model is associated with host
Yuh-Yih Lin1, Jan-Hung Huang, Yo-Yin Lai
1Department of Dentistry, Chung Shan Medical University, No. 110 Chien-Kuo N. Road, Taichung, 402, Taiwan. yuhyih@csmu.edu.tw
Abstract:
Intrachamber challenge with Porphyromonas gingivalis strain 381 in a mouse subcutaneous chamber model results in a local infection that progresses to exfoliation of the chambers within 15 days. This study was designed to elucidate the contribution of host reactions to tissue destruction manifested by chamber exfoliation in animals infected with P. gingivalis. Chamber fluids showed increasing levels of prostaglandin E(2) with infection, and the levels of tumor necrosis factor (TNF) in chamber fluids peaked just before chamber exfoliation. Intraperitoneal injection of a TNF inhibitor, thalidomide (TH), reduced the number of exfoliated chambers, while indomethacin had no effect. Exogenous TNF in chambers without bacterial infection did not cause chamber exfoliation but induced neutrophil infiltration. In a dual-chamber model, two chambers were implanted in the same mouse. One chamber was infected with P. gingivalis, and 9 days later exogenous TNF was added to the other chamber. Altogether, 66.67% of uninfected chambers were exfoliated between day 11 and day 16, although no bacteria were recovered from uninfected chambers. TH treatment alleviated both infected and uninfected chamber exfoliation. In this study, tissue destruction caused by P. gingivalis 381 infection was due to the elevation of the TNF levels and not due to local bacterial activities. Our results further indicate that local infection by P. gingivalis 381, a nondisseminating strain, actually has systemic effects on the host pathological outcome.
Insights
Porphyromonas gingivalis infection causes tissue destruction via elevated tumor necrosis factor (TNF), not direct bacterial action. Inhibiting TNF with thalidomide reduced chamber exfoliation, suggesting systemic host responses drive pathology.
Area of Science:
- Oral Microbiology
- Immunology
- Pathology
Background:
- Porphyromonas gingivalis infection in a mouse subcutaneous chamber model leads to chamber exfoliation within 15 days.
- Host immune responses contribute significantly to tissue destruction during P. gingivalis infection.
Purpose of the Study:
- To investigate the role of host reactions, specifically prostaglandin E(2) and tumor necrosis factor (TNF), in P. gingivalis-induced tissue destruction and chamber exfoliation.
- To elucidate the mechanisms underlying chamber exfoliation in response to P. gingivalis infection.
Main Methods:
- Utilized a mouse subcutaneous chamber model to induce localized P. gingivalis infection.
- Measured prostaglandin E(2) and TNF levels in chamber fluids.
- Administered TNF inhibitor thalidomide (TH) and indomethacin to assess their effects on chamber exfoliation.
- Employed a dual-chamber model to evaluate the systemic effects of localized infection and exogenous TNF.
Main Results:
- Chamber fluids showed increased prostaglandin E(2) and peaked TNF levels preceding exfoliation.
- Thalidomide treatment reduced chamber exfoliation, while indomethacin had no significant effect.
- Exogenous TNF induced neutrophil infiltration but not exfoliation in uninfected chambers.
- Infection in one chamber led to exfoliation of a concurrently implanted, uninfected chamber, which was also alleviated by TH treatment.
Conclusions:
- Tissue destruction and chamber exfoliation in P. gingivalis infection are primarily mediated by elevated TNF levels, not solely by local bacterial activity.
- Local P. gingivalis infection can elicit systemic host responses that contribute to pathological outcomes, even in non-infected sites.
- TNF plays a critical role in the pathogenesis of P. gingivalis-induced tissue damage and chamber exfoliation.
