How infection can incite sensitivity to food

  title={How infection can incite sensitivity to food},
  author={Elena F. Verd{\'u} and Alberto Caminero},
  pages={29 - 30}
Microbes can trigger chronic immune disorders to dietary antigens, such as in celiac disease Immune tolerance to dietary antigens is key to preventing undesirable responses to innocuous antigens ingested with food. On page 44 of this issue, Bouziat et al. (1) report how viral infection may break oral tolerance to dietary proteins. The findings provide an explanation for the known epidemiological association between viral infections and the onset of food sensitivities, such as celiac disease… 

Mechanisms by which gut microorganisms influence food sensitivities

This Review discusses the clinical and experimental evidence for enteric infections and/or alterations in the gut microbiota in inciting food sensitivity, and focuses on mechanisms by which microorganisms might provide direct pro-inflammatory signals to the host promoting breakdown of oral tolerance to food antigens or indirect pathways that involve the metabolism of protein antigen and other dietary components by gut microorganisms.

Celiac disease: Should we care about microbes?

  • A. CamineroE. Verdú
  • Biology
    American journal of physiology. Gastrointestinal and liver physiology
  • 2019
Evidence is discussed regarding the role of microbes in promoting CeD, and the specific pathways triggered by microbes that could participate in CeD pathogenesis, to develop optimal microbiota modulating strategies to help prevent CeD.

Duodenal bacterial proteolytic activity determines sensitivity to dietary antigen through protease-activated receptor-2

It is shown that duodenal biopsies from patients with active CeD have increased proteolytic activity against gluten substrates that correlates with increased Proteobacteria abundance, including Pseudomonas aeruginosa.

Contribution of Infectious Agents to the Development of Celiac Disease

Modulation of microbiota composition and function and the potential beneficial effects of probiotics in celiac disease are discussed and attention is paid to the mechanisms by which microbes and their components affect mucosal immunity, including tolerance to food antigens.

Celiac Disease: What Do We Know in 2017

  • J. Amil Dias
  • Medicine
    GE - Portuguese Journal of Gastroenterology
  • 2017
Observations still do not provide final answers about the pathophysiology of celiac disease but certainly lead to progress in the knowledge of gluten sensitization and the role of some environmental factors.

Celiac Disease: What Do We Know in 2017?

Observations still do not provide final answers about the pathophysiology of celiac disease but certainly lead to progress in the knowledge of gluten sensitization and the role of some environmental factors.

Coeliac disease

The risk factors and immune mechanisms of coeliac disease are discussed, future treatment options beyond the gluten-free diet are highlighted and the diet is restrictive and gluten is difficult to avoid.

Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father

Overall, it is argued for a significant paternal role in the development of PE through microbial infection of the mother via insemination through microbes from the gut, oral and female urinary tract microbiomes as the main sources of the infection.

The possible link between coeliac and Kawasaki diseases in Brazil: a cross-sectional study

The detected CD prevalence does not confirm the existence of an association between KD and CD since this prevalence is similar to that found in the general population (≃1%).



Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease

A viral infection model that makes use of two reovirus strains that infect the intestine but differ in their immunopathological outcomes discovered that it can nonetheless disrupt intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion and promoting TH1 immunity to dietary antigen.

Triggers and drivers of autoimmunity: lessons from coeliac disease

It is proposed that other exogenous factors might be identified as drivers of autoimmune processes, in particular when evidence for T cells with specificity for self antigens driving the disease is lacking.

Novel players in coeliac disease pathogenesis: role of the gut microbiota

The importance of utilizing animal models and long-term clinical studies to gain insight into the mechanisms through which host–microbial interactions can influence host responses to gluten and how the interplay between host genetics, environmental factors and the intestinal microbiota might contribute to its pathogenesis is highlighted.

Duodenal Bacteria From Patients With Celiac Disease and Healthy Subjects Distinctly Affect Gluten Breakdown and Immunogenicity.

This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie the reported association of dysbiosis and CD.

Identification of tissue transglutaminase as the autoantigen of celiac disease

Tissue transglutaminase is identified as the unknown endomysial autoantigen of celiac disease, and gliadin is a preferred substrate for this enzyme, giving rise to novel antigenic epitopes.

Rotavirus Infection Frequency and Risk of Celiac Disease Autoimmunity in Early Childhood: A Longitudinal Study

This prospective study provides the first indication that a high frequency of rotavirus infections may increase the risk of celiac disease autoimmunity in childhood in genetically predisposed individuals.

Enhanced Expression of Interferon Regulatory Factor-1 in the Mucosa of Children with Celiac Disease

Analysis of the expression of interferon (IFN) regulatory factor (IRF)-1 in Celiac disease suggests that IFN-γ/IRF-1 signaling pathway can play a key role in maintaining and expanding the local Th1 inflammatory response in this disease.

Evidence for the role of interferon-alfa production by dendritic cells in the Th1 response in celiac disease.

These data suggest that IFN-alfa-producing DCs contribute to the Th1 response in celiac disease.

IL-15 functions as a danger signal to regulate tissue-resident T cells and tissue destruction

It is proposed that expression of IL-15 in tissues promotes T helper 1 cell-mediated immunity and provides co-stimulatory signals to effector cytotoxic T cells to exert their effector functions and drive tissue destruction.