Gut Microbiota-Immune System Crosstalk and Pancreatic Disorders

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.

High-Salt Diet Gets Involved in Gastrointestinal Diseases through the Reshaping of Gastroenterological Milieu

“…L. murinus in host intestinal could modulate the Th17 cells and is vital in the formation of some autoimmune diseases [46]. Moreover, gut commensals protect the intestinal against pathogenic microbes by maintaining gut integrity and regulating intestinal barrier permeability [63]. Reciprocally, the host immune state plays a key role in the composition of gut microbiota, such as the intestinal IgA, which was found to influence the gut microbiota composition [41].…”

Factors That Worsen Disease Severity in Acute Pancreatitis: Implications for More Innovative Nutrition Therapy

“…There is evidence of a shift in the population of inflammatory cells emerging from the gut in response to pancreatitis, with the activation and recruitment of T‐cell subpopulations that participate in further pancreatic inflammation . Specifically, in chronic pancreatitis, systemic increases in Th1 and Th17 cells have been documented . Further proof of this interaction leading to disease severity is documented by the fact that administration of TLR‐4 and TLR‐9 ligands has been shown to induce pancreatic injury in mice .…”

“…A systemic vascular disorder occurs in large vessels and in the microcirculation surrounding the pancreas in response to the inflammation. Large fluid losses from third‐spacing, redistribution of blood away from the splanchnic circulation, autoregulatory abnormalities, and vasoconstriction of mesenteric afferent arterioles infusing the pancreas cause a classic ischemia/reperfusion injury . The ischemia damages the intestinal mucosa .…”

“…Large fluid losses from third‐spacing, redistribution of blood away from the splanchnic circulation, autoregulatory abnormalities, and vasoconstriction of mesenteric afferent arterioles infusing the pancreas cause a classic ischemia/reperfusion injury . The ischemia damages the intestinal mucosa . With fluid resuscitation, the splanchnic circulation is usually the last to be reperfused.…”

“…The levels of these DAMPs, which are acutely elevated in pancreatitis, correlate with disease severity . There is evidence of a shift in the population of inflammatory cells emerging from the gut in response to pancreatitis, with the activation and recruitment of T‐cell subpopulations that participate in further pancreatic inflammation . Specifically, in chronic pancreatitis, systemic increases in Th1 and Th17 cells have been documented .…”