Alcohol-induced gastritis prevents oral tolerance induction in mice

Andrade, Mariléia Cháves; Menezes, José Elmo de; Cassali, G. D.; Martins‐Filho, Olindo Assis; Cara, Denise Carmona; Faria, Ana Maria Caetano

doi:10.1111/j.1365-2249.2006.03207.x

Cited by 32 publications

(38 citation statements)

References 44 publications

(51 reference statements)

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“…A bulk of data suggests an important role for IL-4 in the induction of CCR9 expression by T cells primed in the GALT (23,25,29), and we do not rule out the possibility that, under physiological conditions, IL-4 effect may be also autocrine on MLN-DC.…”

Section: Discussionmentioning

confidence: 99%

Imprinting of CCR9 on CD4 T Cells Requires IL-4 Signaling on Mesenteric Lymph Node Dendritic Cells

Elgueta

Sepulveda

Vilches

et al. 2008

The Journal of Immunology

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Section: Discussionmentioning

confidence: 99%

Imprinting of CCR9 on CD4 T Cells Requires IL-4 Signaling on Mesenteric Lymph Node Dendritic Cells

Elgueta

Sepulveda

Vilches

et al. 2008

The Journal of Immunology

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“…Furthermore, alcohol may influence gastric acid levels, which in turn influences degradation and allergenicity of food proteins [33]. Interestingly, experimental studies have shown that alcohol-induced gastritis decreases oral tolerance [34]. …”

Section: Discussionmentioning

confidence: 99%

Immunoglobulin E Sensitization to Cross-Reactive Carbohydrate Determinants: Epidemiological Study of Clinical Relevance and Role of Alcohol Consumption

Linneberg¹,

Fenger²,

Husemoen³

et al. 2010

Int Arch Allergy Immunol

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Background: The determinants and biologic significance of IgE-mediated sensitization to cross-reactive carbohydrate determinants (CCDs) are not entirely known. An association between alcohol consumption and CCD sensitization has been reported in studies from Spain and Portugal. Objective: To investigate the relationship of alcohol consumption with CCD sensitization, the role of alcohol dehydrogenase gene polymorphisms, and the clinical consequences of CCD sensitization. Methods: Serum-specific IgE sensitization (≧0.1 kU/l) to a CCD (the N-glycan from bromelain) was assessed in 1,197 adults participating in a population-based study in Copenhagen, Denmark. Alcohol consumption and atopic symptoms (rhinitis, asthma and oral allergy syndrome) were assessed by questionnaire. Examinations included skin prick tests (SPTs), qualitative multiallergen IgE test (Phadiatop®), methacholine bronchial hyperreactivity, eosinophil cationic protein and alcohol dehydrogenase (ADH) gene polymorphisms. Results: Alcohol consumption was significantly associated with CCD sensitization and this was particularly evident in SPT-negative individuals. The fast-metabolizing allele of the ADH1b polymorphism was significantly associated with CCD sensitization in alcohol drinkers. CCD sensitization was associated with atopic symptoms, but associations attenuated markedly when adjusting for SPT reactivity. Conclusions: Our results suggest that the positive association between alcohol consumption and CCD sensitization is universal and not specific to certain populations. The observed association between the ADH1b polymorphism and CCD sensitization may support that alcohol is causally related to the risk of CCD sensitization. The observed association between CCD sensitization and atopic phenotypes did not appear to be independent of SPT reactivity indicating limited significance of CCD sensitization per se.

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“…It is well known that alcohol consumption is able to trigger inflammatory effects on gastrointestinal tract interfering with mucosal homeostasis (Andrade et al, 2006;Cook, 1998;Coombes and Maloy, 2007;Lau et al, 2008;Watson et al, 1994). Previous reports from our group demonstrated that high-dose ethanol (EtOH) administration is able to induce an allergic-type inflammatory response in function of enhanced levels of seric IgE, high levels of gastric interleukin (IL)-4 and increased IL-4 synthesis by splenic T cells after in vitro unspecific stimulus (concanavalin A) (Andrade et al, 2006(Andrade et al, , 2008(Andrade et al, , 2009).…”

mentioning

confidence: 95%

“…Previous reports from our group demonstrated that high-dose ethanol (EtOH) administration is able to induce an allergic-type inflammatory response in function of enhanced levels of seric IgE, high levels of gastric interleukin (IL)-4 and increased IL-4 synthesis by splenic T cells after in vitro unspecific stimulus (concanavalin A) (Andrade et al, 2006(Andrade et al, , 2008(Andrade et al, , 2009). This allergic-type reaction in the GALT can disturb pathways involved in the establishment of regulatory mechanisms, hindering oral tolerance.…”

mentioning

confidence: 98%

Previous Ingestion ofLactococcus lactisby Ethanol-Treated Mice Preserves Antigen Presentation Hierarchy in the Gut and Oral Tolerance Susceptibility

Perez

Gomes-Santos

Miyoshi

et al. 2015

Alcohol Clin Exp Res

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Alcohol-induced gastritis prevents oral tolerance induction in mice

Cited by 32 publications

References 44 publications

Imprinting of CCR9 on CD4 T Cells Requires IL-4 Signaling on Mesenteric Lymph Node Dendritic Cells

Imprinting of CCR9 on CD4 T Cells Requires IL-4 Signaling on Mesenteric Lymph Node Dendritic Cells

Immunoglobulin E Sensitization to Cross-Reactive Carbohydrate Determinants: Epidemiological Study of Clinical Relevance and Role of Alcohol Consumption

Previous Ingestion ofLactococcus lactisby Ethanol-Treated Mice Preserves Antigen Presentation Hierarchy in the Gut and Oral Tolerance Susceptibility

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