Akademska digitalna zbirka SLovenije - logo
E-resources
Peer reviewed Open access
  • Helicobacter pylori cagA + ...
    Lucero, Yalda; Oyarzún, Amaya; O'Ryan, Miguel; Quera, Rodrigo; Espinosa, Nelly; Valenzuela, Romina; Simian, Daniela; Alcalde, Elisa; Arce, Claudio; Farfán, Mauricio J; Vergara, Alejandra F; Gajardo, Iván; Mendez, Jocelyn; Carrasco, Jorge; Errázuriz, Germán; Gonzalez, Mónica; Ossa, Juan C; Maiza, Eduardo; Perez-Bravo, Francisco; Castro, Magdalena; Araya, Magdalena

    Frontiers in cellular and infection microbiology, 08/2017, Volume: 7
    Journal Article

    What is already known about this subject?Celiac disease (CD) has a high clinical and histological diversity and the mechanisms underlying this phenomenon remain elusive. is a bacterium that chronically infect gastric and duodenal mucosa activating both a Th1/Th17 and T-reg pathways.The role of (and the effect of their virulence factors) in CD have not yet completely elucidated.What are the new findings? + strains are associated to milder histological damage in infected CD patients.In active-CD patients the presence of + is associated to an increase in T-reg markers, contrasting with a downregulation in + infected potential-CD individuals.How might it impact on clinical practice in the foreseeable future?The identification of microbiological factors that could modulate inflammation and clinical expression of CD may be used in the future as preventive strategies or as supplementary treatment in patients that cannot achieve complete remission, contributing to the better care of these patients. Mechanisms underlying the high clinical and histological diversity of celiac disease (CD) remain elusive. (Hp) chronically infects gastric and duodenal mucosa and has been associated with protection against some immune-mediated conditions, but its role (specifically of + strains) in CD is unclear. To assess the relationship between gastric Hp infection ( + strains) and duodenal histological damage in patients with CD. Case-control study including patients with active-CD, potential-CD and non-celiac individuals. Clinical presentation, HLA genotype, Hp/ gene detection in gastric mucosa, duodenal histology, Foxp3 positive cells and TGF-β expression in duodenal lamina propria were analyzed. We recruited 116 patients, 29 active-CD, 37 potential-CD, and 50 non-CD controls. Hp detection was similar in the three groups (~30-40%), but + strains were more common in infected potential-CD than in active-CD (10/11 vs. 4/10; = 0.020) and non-CD (10/20; = 0.025). Among active-CD patients, Foxp3 positivity was significantly higher in subjects with + Hp+ compared to Hp+ ( < 0.01) and Hp- ( < 0.01). In cagA+ Hp+ individuals, Foxp3 positivity was also higher comparing active- to potential-CD ( < 0.01). TGF-β expression in duodenum was similar in active-CD with + Hp+ compared to Hp- and was significantly downregulated in + potential-CD subjects compared to other groups. Hp infection rates were similar among individuals with/without CD, but infection with + strains was associated with milder histological damage in celiac patients infected by Hp, and in active-CD cases with higher expression of T-reg markers. Results suggest that infection by + Hp may be protective for CD progression, or conversely, that these strains are prone to colonize intestinal mucosa with less severe damage.