Converging findings from linkage between periodontal pathogen with atopic and allergic immune response.

This study aims to explore a relationship between exposures of whole-cell Porphyromonas gingivalis in various doses with atopic inflammatory responses at experimental mice. A pretest-posttest controlled group design, with 16 Wistar rats (Rattus novergicus) randomized into four groups. Group 1 was the control group. Group 2 was given low-dose (9 × 107 colony-forming unit) of P. gingivalis. Group 3 was given medium-dose (9 × 109 colony-forming unit) of P. gingivalis. Group 4 was given high-dose (9 × 1011 colony-forming unit) of P. gingivalis. Interleukin-4, Interleukin-5, Interleukin-17F, Interleukin-21, Immunoglobulin-E, Immunoglobulin-G4 , and γ-Interferon were measured by direct-sandwich ELISA just before the treatments began, day-4, and day-11 after treatments. There is a sudden increase of Interleukin-4 in the group 4 (23.79 ± 0.91 pg/ml to 54.17 ± 0.79 pg/ml; p = 0.01) and slight increase of Interleukin-5 in the group 4 (207.60 ± 11.15 pg/ml to 243.40 ± 9.33 pg/ml; p = 0.03). No change was observed for Interleukin-17F in all groups. Serum concentration of Immunoglobulin-E was decreased in group 2 (-10.44 ± 8.13 pg/ml), but increased in group 4 (+1.03 ± 4.57 pg/ml). Taken together, some cytokines are up-regulated and others are down-regulated after exposure to whole-cell P. gingivalis. Moreover, study of host responses during periodontal infection may offer critical key insight that contribute to the development of atopy.

CLINICAL IMPLICATIONS: We introduced and explained the potential role of periodontal pathogen Porphyromonas gingivalis in systemic immune responses, along with its virulence factor inside the oral cavity. Our results consider several changes and differences of cytokines and immunoglobulins following whole-cell Porphyromonas gingivalis exposure. However, results of the study need to be interpreted with caution due to its limitations.

CAPSULE SUMMARY: Interleukin (IL)-4 and IL-5 had been found increase after exposure to the periodontal pathogens Porphyromonas gingivalis, whereas no or minimal change had been found in the level of IL-17F, Ig-G4 , and IFN-γ. The various cytokines and immunoglobulins shown in this study do not prove a causal relationship, and the precise role of Porphyromonas gingivalis in the regulation of atopic immune response warrants further investigation. Nevertheless, these findings may provide some critical key insight into the host responses following Porphyromonas gingivalis infection.