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La colonización ectópica de bacterias orales en el intestino impulsa la inducción y la inflamación de las células TH1
Koji Atarashi1,2, Wataru Suda1,3,4, Chengwei Luo5,6
1Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Science (New York, N.Y.)
|October 21, 2017
Resumen
Las bacterias orales como Klebsiella pueden colonizar el intestino y desencadenar una inflamación severa, especialmente en personas con disbiosis. Esto pone de relieve la cavidad oral como un reservorio potencial para los biontes patógenos intestinales.
Área de la Ciencia:
- Microbiología
- Inmunología
- Gastroenterología
Sus antecedentes:
- La disbiosis intestinal está relacionada con varios problemas de salud, incluida la enfermedad inflamatoria intestinal (EII).
- El papel de las bacterias orales en la causa de enfermedades intestinales no se entiende completamente.
Objetivo del estudio:
- Para investigar el potencial patógeno de las bacterias orales en el intestino.
- Para determinar si las bacterias orales pueden inducir respuestas inflamatorias en el intestino.
Principales métodos:
- Utilizó técnicas gnotobióticas para estudiar la colonización bacteriana en el intestino.
- Especies de Klebsiella aisladas de la saliva humana.
- Las respuestas inmunes evaluadas, específicamente la inducción de células T auxiliares 1 (TH1).
Principales resultados:
- Las cepas orales de Klebsiella indujeron fuertemente las respuestas celulares TH1 en el intestino.
- Estas cepas de Klebsiella exhibieron resistencia a varios antibióticos.
- La colonización fue más frecuente en la microbiota intestinal disbiótica.
- Se observó una inflamación intestinal grave en huéspedes genéticamente susceptibles.
Conclusiones:
- La cavidad oral alberga biontes patógenos que pueden colonizar el intestino.
- Las bacterias orales, como la Klebsiella, pueden agravar la inflamación intestinal.
- Los hallazgos sugieren un vínculo entre la microbiota oral y la salud intestinal, contribuyendo potencialmente a la patogénesis de la EII.
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