Gut microbiota-immune system crosstalk and pancreatic disorders

D. Pagliari, Angela Saviano, E. E. Newton, Michele Lorenzo Serricchio, Antonio Angelo Dal Lago, Antonio Gasbarrini, Rossella Cianci

Risultato della ricerca: Contributo in rivistaArticolo in rivista

28 Citazioni (Scopus)

Abstract

Gut microbiota is key to the development and modulation of the mucosal immune system. It plays a central role in several physiological functions, in the modulation of inflammatory signaling and in the protection against infections. In healthy states, there is a perfect balance between commensal and pathogens, and microbiota and the immune system interact to maintain gut homeostasis. The alteration of such balance, called dysbiosis, determines an intestinal bacterial overgrowth which leads to the disruption of the intestinal barrier with systemic translocation of pathogens. The pancreas does not possess its own microbiota, and it is believed that inflammatory and neoplastic processes affecting the gland may be linked to intestinal dysbiosis. Increasing research evidence testifies a correlation between intestinal dysbiosis and various pancreatic disorders, but it remains unclear whether dysbiosis is the cause or an effect. The analysis of specific alterations in the microbiome profile may permit to develop novel tools for the early detection of several pancreatic disorders, utilizing samples, such as blood, saliva, and stools. Future studies will have to elucidate the mechanisms by which gut microbiota is modulated and how it tunes the immune system, in order to be able to develop innovative treatment strategies for pancreatic disorders.
Lingua originaleEnglish
pagine (da-a)N/A-N/A
RivistaMediators of Inflammation
Volume2018
DOI
Stato di pubblicazionePubblicato - 2018

Keywords

  • Animals
  • Gastrointestinal Microbiome
  • Humans
  • Immune System
  • Microbiota
  • Pancreatic Diseases

Fingerprint

Entra nei temi di ricerca di 'Gut microbiota-immune system crosstalk and pancreatic disorders'. Insieme formano una fingerprint unica.

Cita questo