Food-Induced Acute Pancreatitis

Abstract

Food allergy, a commonly increasing problem worldwide, defined as an adverse immune response to food. A variety of immune-related effector cells such as mast cells, eosinophils, neutrophils, and T cells are involved in food-related allergic responses categorized as IgE mediated, non-IgE mediated, and mixed (IgE and non-IgE) depending upon underlying immunological mechanisms. The dietary antigens mainly target the gastrointestinal tract including pancreas that gets inflamed due to food allergy and leads acute pancreatitis. Reports indicate several food proteins induce pancreatitis; however, detailed underlying mechanism of food-induced pancreatitis is unexplored. The aim of the review is to understand and update the current scenario of food-induced pancreatitis. A comprehensive literature search of relevant research articles has been performed through PubMed, and articles were chosen based on their relevance to food allergen-mediated pancreatitis. Several cases in the literature indicate that acute pancreatitis has been provoked after the consumption of mustard, milk, egg, banana, fish, and kiwi fruits. Food-induced pancreatitis is an ignored and unexplored area of research. The review highlights the significance of food in the development of pancreatitis and draws the attention of physicians and scientists to consider food allergies as a possible cause for initiation of pancreatitis pathogenesis.

Keywords: Eosinophils; Food allergy; Mast cells; Neutrophils; Pancreatitis.

Figure 1. The possible operational mechanism in food allergen-induced acute pancreatitis

Food allergens internalized and processed by antigen presenting cells (APCs) with the help of proteosomal complex and presented by major histocompatibility complex class-II (MHC-II) to the naive CD4⁺ T cells that differentiate into the Th2 cells in the presence of IL-4 and produce IL-5 and IL-13 that activate downstream allergic pathways and induces food allergen associated acute pancreatitis. The food allergen–induced allergic response in the pancreas may be IgE or non-IgE mediated. In IgE mediated response, Th2 cells secrete IL-4 and IL-13 that causes B cell activation and IgE class switching. IgE antibodies bind to FcεRI surface receptors present on mast cells and basophils that lead degranulation and release of several allergic mediators. These allergic mediators probably cause trypsinogen activation and development of pancreatitis. However, this hypothesis needs to be explored further for the designing treatment strategies. In contrast, the non-IgE mediated response may also occur that includes the role of IL-5 and eosinophil active chemokines eotaxins that recruit, activate and releases several inflammatory mediators and lead trypsinogen activation. Increased level of trypsin consecutively setup the episode of acute pancreatitis. In addition, neutrophils are forming neutrophil extracellular traps (NETs) of de-condensed DNA and histones, which is sufficient to induce trypsin activation to promote pancreatitis pathogenesis.