Cytokine production in response to endodontic infection in germ-free mice

A P Ribeiro Sobrinho1, S M de Melo Maltos, L M Farias

  • 1Institute of Microbiology Professor Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

Insights

This study investigated immune responses to root canal bacteria in germ-free mice. Gemella morbillorum triggered type 1 cytokines in vitro, but suppressed them in vivo, while other bacteria modulated responses via interleukin-4.

Area of Science:

  • Microbiology
  • Immunology
  • Endodontics

Background:

  • Endodontic periapical infections involve complex microbial communities.
  • Understanding the host immune response, particularly cytokine profiles, is crucial for managing these infections.
  • Germ-free animal models offer a controlled environment to study host-microbe interactions.

Purpose of the Study:

  • To evaluate the cytokine profiles (type 1 and type 2) triggered by and modulating endodontic periapical infections.
  • To compare the immune responses induced by single-species (Gemella morbillorum) versus polymicrobial infections (Bifidobacterium adolescentis, Fusobacterium nucleatum, Clostridium butyricum).
  • To investigate the in vitro and in vivo cytokine modulation in a germ-free mouse model.

Main Methods:

  • Inoculation of germ-free mice with specific oral microorganisms isolated from patients with pulpal necrosis.
  • Assessment of cytokine profiles, including interleukin-12 (IL-12) and interferon-gamma (IFN-gamma) for type 1, and interleukin-4 (IL-4) for type 2 responses.
  • Comparison of in vitro cytokine induction with in vivo modulation of immune responses.

Main Results:

  • In vitro, Gemella morbillorum induced type 1 cytokine synthesis.
  • In vivo, G. morbillorum modulated immune responses, reducing basal levels of IL-12 and IFN-gamma in an IL-4-independent manner.
  • Polymicrobial infections in vitro reduced type 1 cytokine levels, modulated by IL-4, while in vivo responses showed a predominance to one species.

Conclusions:

  • The in vitro and in vivo immune responses to endodontic pathogens can differ significantly.
  • Specific bacterial species and their combinations elicit distinct cytokine profiles, influencing the host's immune strategy.
  • Further research is needed to elucidate the complex interplay between oral microbiota and host immunity in endodontic infections.

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