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Glutine e infiammazione intestinale

by luciano

Il glutine induce infiammazione intestinale non solo nei soggetti celiaci ma anche in quelli sani

L’infiammazione intestinale è una condizione del sistema gastro-intestinale che riguarda una platea di persone molto vasta e in continuo costante aumento. Questa condizione rappresenta per l’ndividuo non solo uno stato di malessere che incide sulla qualità della vita ma può -se sottovalutata o trascurata- favorire l’insorgere o l’aggravare malattie gravi.
Un ruolo importante ma ancora da esplorare a fondo lo riveste il glutine in quanto pro-infiammatorio.
Lo studio” The Role of Gluten in Gastrointestinal Disorders: A Review. Sabrina Cenni. Gastrointestinal Disorders: A Review. Nutrients 2023” fornisce un’utile panoramica della sua efficacia nella prevenzione e nella gestione di questi disturbi.

Il glutine è soltanto parzialmente digerito dagli enzimi intestinali e può generare peptidi che alterano la permeabilità intestinale

“Abstract: Gluten is only partially digested by intestinal enzymes and can generate peptides that can alter intestinal permeability, facilitating bacterial translocation, thus affecting the immune system. Few studies addressed the role of diet with gluten in the development of intestinal inflammation and in other gastrointestinal disorders. The aim of this narrative review was to analyse the role of gluten in several gastrointestinal diseases so as to give a useful overview of its effectiveness in the prevention and management of these disorders.”

“Introduction. Gluten is a protein mass made of a complex network of gliadins and glutenins, which are proteins rich in glutamines and prolines found in most grains, such as barley, wheat, and rye [1 ,2]. Due to its high-water binding capacity and its consequent malleability and elasticity, gluten induces the formation of viscoelastic membranes, thus determining the proper consistency of dough, which allows it to be processed in bread and other foods [ 3– 5]. The high content of glutamines and prolines in gliadins make them difficult to cleave, making them able to escape degradation from gastric, pancreatic, and intestinal proteolytic enzymes [3, 4]. Therefore, gluten is what remains after the removal of starch, water-soluble proteins, and albumins [1]. In Western countries, the gluten dietary intake is approximately 5 to 20 g per day [3 , 4]. In the last decades, the literature reports an increased number of reactions following a widespread exposure to gluten [ 6]. Gluten-related diseases affect up to 10% of the general population and can be classified as three different disorders: IgE-mediated wheat allergy, Celiac disease (CD), and non-celiac gluten sensitivity (NCGS) [2, 6]. However, there is increasing evidence that gluten can trigger an innate and adaptative immune response responsible for intestinal inflammation [7]. Notably, along with other dietary elements, gluten may contribute to the development of inflammatory intestinal disorders, such as inflammatory bowel disease (IBD), as well as functional gastrointestinal disorders (FGIDs) and concur in symptom exacerbation, although its exact role is still under investigation.”

“Gluten and intestinsl inflammation. Inflammation is the natural response of the innate immune system to external stimuli, such as microbial pathogens and injuries [8 ]. When the trigger persists and the immune cells are constantly activated, the inflammatory response may become chronic and self-sustainable [8]. The aetiology of inflammation is clear and easily detectable in some health conditions, while in others it can be difficult to identify [ 8]. The pathogenesis of inflammation is multifactorial. Nevertheless, genetic vulnerability, psychological stress, environmental factors, and some dietary patterns have been described as potentially implicated in the development of inflammatory phenotypes [ 8]. There are at least 50 different types of gliadin epitopes that can have an immunomodulatory and cytotoxic role or that can impact the gut permeating activities [ 8 ]; in fact, some of these can stimulate a pro-inflammatory innate immune response and others can activate specific T cells [8]. Gliadins immune cells’ activation is not only observed in celiac patients, as described by Lammers et al. [9, 10]. Indeed, their study concluded that gliadin induced an inflammatory response and, in particular, an important production of pro-inflammatory cytokines (IL-6, IL-13, and interferon-gamma) both in Celiac patients and in healthy controls, even if proinflammatory cytokine levels were higher in Celiac patients [9, 10]. Similarly, Harris et al. showed that incubated peripheral blood mononuclear cells (PMBC) obtained from healthy HLA-DQ2 positive individuals produced proinflammatory cytokines, such as IL-23, IL-1beta, and TNF-α, when exposed to gliadin peptides [ 8, 11]. These cytokines’ production was significantly higher in Celiac patients compared to healthy controls [8,11]. Accordingly, Cinova et al., in their case-control study, demonstrated that gliadin could stimulate a substantial TNF-α and IL-8 production by monocytes, principally in celiac patients, but also, to a lesser extent, in healthy control individuals [12]. Gliadin also has an important role in modifying intestinal permeability through the reorganization of actin filaments and the modified expression of junctional complex proteins [ 8,13 ]. As demonstrated by Drago et al. and Lammers et al., gliadin’s binding to the chemokine receptor CXCR3 determines a release of zonulin, an active protein, which compromises the integrity of the intestinal barrier through the rearrangements of actin filaments, ultimately leading to an altered intestinal permeability both in Celiac and non-Celiac patients [ 9, 10, 14 ]. In conclusion, Ziegler et al. and Junker et al. reported that amylase trypsin inhibitors, found in gluten-containing cereals, have the capacity to activate toll-like receptors, thus stimulating the release of inflammatory cytokines and inducing a T-cell immune response in both celiac and non-celiac patients [15,16].”

Einkorn wheat is the exception in relation to gluten-induced intestinal inflammation

Einkorn bread evidenced an anti-inflammatory effect. Integrated Evaluation of the Potential Health Benefits of Einkorn-Based Breads A. Gobetti et al. 2017.

Protective effects of ID331 Triticum monococcum. Protective effects of ID331 Triticum monococcum gliadin on in vitro models of the intestinal epithelium. Giuseppe Iacomino et al. (PMID: 27374565 DOI: 10.1016/j.foodchem.2016.06.014 ).

Keywords: glutine, IBS, disordini gastro-intestinali, celiachia