Pancreatic Ductal Adenocarcinoma and Nutrition: Exploring the Role of Diet and Gut Health

Abstract

The incidence of pancreatic cancer is increasing worldwide. The most common form is represented by pancreatic ductal adenocarcinoma (PDAC) which has been shown to be linked to chronic inflammation. Notably, the gut microbiota has emerged as a critical player in regulating immune responses and inflammation. Indeed, intestinal dysbiosis, characterized by an imbalance in the gut microbiota composition, can contribute to the initiation of chronic inflammation. Sterile chronic inflammation can occur, probably activated by the translocation of bacterial components, such as lipopolysaccharide (LPS), the major component of Gram-negative microbiota, with the consequent induction of innate mucosal immunity, through the activation of Toll-like receptors (TLRs). Furthermore, the interaction between LPS and TLRs could enhance cancer progression. Recent research has shed light on the pivotal role of nutrition, as a modifiable risk factor, in PDAC immunological processes, particularly focusing on the immuno-modulatory effects of the gut microbiota. Different dietary regimens, fiber intake, immunonutrients, and antioxidants have the potential to either exacerbate or mitigate chronic inflammation, thereby influencing the pathogenesis and natural history of PDAC. These dietary components may affect the gut microbiota composition and, consequently, the level of inflammation, either promoting or protecting against PDAC. In this review of reviews, we discuss the modulatory role of nutrition and the gut microbiota in PDAC’s immunological processes to explore a translational therapeutic approach that could improve the survival and quality of life of these patients.

Obesity Is Associated with Distal Migration of Pancreatic Adenocarcinoma to Body and Tail: A Multi-Center Study

“…A previous prospective study revealed a decline in gut microbiome diversity and a specific microbial profile in Chinese patients with pancreatic cancer [31]. An imbalance in the distribution of gut microbiota, named intestinal dysbiosis, can lead to the initiation of chronic inflammation that is mediated by a bacterial translocation component, such as lipopolysaccharide, which activates Toll-like receptors, inducing innate immunity and enhancing cancer progression [32]. Additionally, lipopolysaccharide plays an important role in the initiation of a pro-inflammatory cascade by activating the nuclear factor-κappa B (NF-κB) pathway, leading to the production of pro-inflammatory cytokines [tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-1] and leading to oxidative stress and an inflammatory state [33]; and (3) pancreatic microbiota, as a previous study demonstrated the presence of various bacterial taxa in the pancreatic tissue, and some of these bacteria were found to be inhabitants in the oral cavity [34].…”