The effect of stress on the inflammatory response to Porphyromonas gingivalis in a mouse subcutaneous chamber model.
BACKGROUND
The impact of emotional stress on the outcome of infectious diseases was studied in animal models and humans, but data related to the effect of stress on periodontal infection are limited. Using the subcutaneous chamber model in mice, the present study was carried out to investigate the effect of stress on the host response to Porphyromonas gingivalis.


METHODS
Mice with subcutaneous chambers (2 per animal) were divided into 4 treatment groups: cold-stress; isolation-stress; corticosterone (CS)-injected; and controls. On the third day of stress conditions, heat-killed P. gingivalis were injected into the chambers. The chambers were sampled 1 and 5 days later and analyzed for leukocyte number, tumor necrosis factor (TNF)-alpha levels, and interferon (IFN)-gamma levels.


RESULTS
Injection of P. gingivalis induced the migration of leukocytes into the chambers and increased the intrachamber levels of IFN-gamma and TNF-alpha. There were no significant differences in cell number and IFN-gamma levels between the different treatment groups, but the levels of TNF-alpha were significantly lower in the isolation-stress and cold-stress groups compared to control animals. CS-injected animals were not different from controls. In addition, the levels of TNF-alpha in the stressed animals were lower on the fifth day post-injection than on the first day, but not in the CS and control group.


CONCLUSIONS
The results suggest that the levels of TNF-alpha induced by P. gingivalis in the infection site are downregulated in stressed animals, and CS is not the sole mediator responsible. The stress-induced reduction in TNF-alpha levels might have an impact on the pathogenesis of periodontal disease in humans experiencing emotional stress.
Shapira
L
L
Department of Periodontology, Hebrew University - Hadassah School of Dental Medicine, Jerusalem, Israel. shapiral@cc.huji.ac.il
Houri-Haddad
Y
Y
Frolov
I
I
Halabi
A
A
Ben-Nathan
D
D
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D016866:Bacteroidaceae Infections / Q000276:immunology*; D002465:Cell Movement / Q000276:immunology; D003080:Cold Temperature / Q000009:adverse effects; D003345:Corticosterone / Q000494:pharmacology; D015194:Diffusion Chambers, Culture; D004195:Disease Models, Animal; D015536:Down-Regulation; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology; D007371:Interferon-gamma / Q000032:analysis; D007958:Leukocyte Count; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D010510:Periodontal Diseases / Q000209:etiology / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D012934:Social Isolation; D013312:Stress, Physiological / Q000276:immunology* / Q000503:physiopathology; D013315:Stress, Psychological / Q000276:immunology* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D003345:Corticosterone