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Barone, M.V.;  Auricchio, R.;  Nanayakkara, M.;  Greco, L.;  Troncone, R.;  Auricchio, S. Pivotal Role of Inflammation in Celiac Disease. Encyclopedia. Available online: (accessed on 20 June 2024).
Barone MV,  Auricchio R,  Nanayakkara M,  Greco L,  Troncone R,  Auricchio S. Pivotal Role of Inflammation in Celiac Disease. Encyclopedia. Available at: Accessed June 20, 2024.
Barone, Maria Vittoria, Renata Auricchio, Merlin Nanayakkara, Luigi Greco, Riccardo Troncone, Salvatore Auricchio. "Pivotal Role of Inflammation in Celiac Disease" Encyclopedia, (accessed June 20, 2024).
Barone, M.V.,  Auricchio, R.,  Nanayakkara, M.,  Greco, L.,  Troncone, R., & Auricchio, S. (2022, July 19). Pivotal Role of Inflammation in Celiac Disease. In Encyclopedia.
Barone, Maria Vittoria, et al. "Pivotal Role of Inflammation in Celiac Disease." Encyclopedia. Web. 19 July, 2022.
Pivotal Role of Inflammation in Celiac Disease

Celiac disease (CD) is an immune mediate disease characterised by gluten dependent T-cell mediated activation, autoimmunity and derangement of the intestinal mucosa in a specific genetic background. Although the activation of the T-cells has been studied in dept, the central question remains still unanswered, namely, why a pro-inflammatory T cell response to gluten is generated instead of a regulatory response, which normally promotes oral tolerance to dietary protein antigens. There is an inflamed environment in CD intestine, enriched in cytokines, such as IL-15, or type I interferons, in which T cells tend to acquire a pro- inflammatory phenotype. The factors that create a pro-inflammatory environment in the CD intestine, leading to an expansion of gliadin-specific T cells in genetically susceptible individuals and further shifting them towards a pro-inflammatory phenotype, remain to be identified. Gluten exacerbates these constitutive alterations, by increasing the same markers already altered before the gluten introduction, both in vitro and in vivo. All these new observations add this disease tout court” to the big family of increasing chronic inflammatory diseases where nutrients can have pro-inflammatory or anti-inflammatory effects, directly or indirectly mediated by the intestinal microbiota, where the intestine functions as a cross road for the control of the inflammation both local and at distance.

celiac disease gluten inflammation microbiota

1. Celiac Disease as an Inflammatory Chronic Disease

The recent literature describes in celiac disease (CD) a meeting of several different factors such as cellular vulnerability, pro-inflammatory effects of gluten and other wheat proteins, Western diet, and other environmental triggers such as viruses that prepare and/or amplify the T cell-mediated response to gluten. The factors that create a pro-inflammatory environment in the CD intestines, leading to an expansion of gliadin-specific T cells in genetically susceptible individuals and further shifting them toward a pro-inflammatory phenotype, could have multiple origins: the pro-inflammatory environment (exogenous stimuli), such as diet, viruses and other pro-inflammatory factors; and the constitutive cellular alterations (endogenous predisposition) that by themselves induce and/or render the cells more sensitive to pro-inflammatory stimuli. All these factors, both exogenous and endogenous, can contribute to the generation of “sterile” inflammation in CD (Figure 1). 
Figure 1. Both exogenous and endogenous factors can generate low-grade chronic inflammation in CD, initiating a series of events that will eventually induce an intestinal lesion.

2. Endogenous Alterations in CD Independent of Gluten

Endogenous alterations, defining a celiac cellular phenotype, have been described in different tissues and cells from CD patients, including intestinal organoids [1]. Gluten exacerbates these constitutive alterations by increasing the same markers already altered in the absence of gluten, both in vitro and in vivo. This phenotype confers the vulnerability to the CD cells to several different triggers that have effects on different pathways, including innate immunity activation. Many of these constitutive alterations are now regarded as biomarkers of clinical relevance, as they can be used to intervene in the “at risk” population before the onset of the disease [1][2].
The recent literature is starting to address the question of endogenous alterations, independent of gluten, in CD by in vivo studies and in cellular models. From these studies, it clearly appears that subtle alterations of the CD cells are also present in the absence of gluten as well as in the absence of T cell activation.
There are many literatures including the population studies, such as patients at risk of CD, CD patients with GFD–CD (gluten-free diet–celiac disease) and in vitro studies on biopsies, intestinal organoids and CD cells from compartments different from the intestines (Table 1).
Table 1. Endogenous, constitutive alterations of several pathways have been described in different cellular models of CD. Most of these endogenous alterations can predispose one to inflammation. Some of these constitutive alterations can be regarded as biomarkers of CD. CD: celiac disease; Wnt: Wingless and Int 1; NFkB: nuclear factor kappa-light-chain-enhancer of activated B cells; EGFR: epithelial growth factor receptor; ERK: extracellular signal-regulated kinases; ECM: extracellular matrix; pNFkB: phosphorylated (active) form of NFkB; pERK: phosphorylated (active) form of ERK; IL1 beta: interleukin beta 1; IL6: interleukin 6; LPP: lipoma-preferred partner; IL15: interleukin 15; IL15R alpha: IL15 receptor alpha; tTg: tissue transglutaminase.


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