Review paper on Helicobacter pylori on front page of FEBS Letters

The article provides an overview on how Helicobacter pylori interacts with the epithelial cells of the gastric mucosa via modification of the adherens junctions. These alterations may be beneficial for the establishment of H. pylori colonization and persistence in the stomach, and simultaneously activate signaling pathways in the host cells that can induce disease. H. pylori is considered the most prevalent chronic infection in the world and is a risk factor for peptic ulcer disease and gastric carcinoma. The interaction between H. pylori and the molecules involved in the maintenance of gastric epithelial integrity is a relevant research field that will contribute to better understand H. pylori pathogenesis and the molecular mechanisms underlying disease development.

Authors and affiliations:

Angela Margarida Costa^1,2, Marina Leite¹, Raquel Seruca¹, Ceu Figueiredo^1,2,*

¹ Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), Porto, Portugal;

² Faculdade de Medicina da Universidade do Porto, Porto, Portugal;

^*Autora sénior e correspondente

Abstract:

Adherens junctions as targets of microorganisms: A focus on Helicobacter pylori

Mucosal epithelia are targeted by several microorganisms as a way of adhesion, internalization, and/ or exploitation of the host properties to induce disease. Helicobacter pylori are worldwide prevalent bacteria that colonize the human stomach. Persistent infection of the gastric mucosa with H. pylori and concurrent chronic gastritis are risk factors for ulcer disease and gastric carcinoma. Therefore, interactions at the H. pylori–epithelial interface are important to understand the pathogenesis of these bacteria and the host responses that contribute to disease development. Here, we provide an overview of the interactions between microorganisms and the adherens junctions with an emphasis on H. pylori.

Journal:

FEBS Letters 587: 259-65, 2013

Link:

http://www.febsletters.org/article/S0014-5793(12)00924-6/abstract