Inflammatory effects of Helicobacter pylori on lung.

ARISMENDI SOSA AC; SALINAS IBAÑEZ AG; FERRAMOLA FF; PEREZ CHACA MV; GÓMEZ NN, ; VEGA AE.

Mendoza

Congreso; XXXIV Reunión Científica Anual Sociedad Biología de Cuyo.; 2016

Sociedad de Biología de Cuyo

Helicobacter pylori infection has been associated with respiratory illness; however, the impact of this bacterium on lung is not well understood. Inflammatory response is mediated by the release of chemokines, cytokines, interferon, and enzymes such as metalloproteinases (MMPs). Interleukin-1β (IL-1β) and tumor necrosis factor (TNF-α) stimulate the fibroblast proliferation, and ROS and the nitrogen metabolites modulate fibronectin-induced fibroblast migration. This may contribute to collagen accumulation during the early phase of infection. MMPs are proteolytic enzymes involved in degradation of extracellular matrix and MMP9 is a majority in lung. This work was aimed to study the inflammatory effects of H. pylori on lung. Balb/c mice were infected by orotracheal instillation with 20 μl of a H. pylori reference strain 1×108 suspension once per day for 3 days. Infected animals and controls were sacrificed at 3, 7, 14, 21 and 30 days. Expression level of multiple markers implicated in inflammation TNF-α, IL-1β, IL-4, IL-6, IL-8, IL-10, MMP9 and endothelial dysfunction markers (I-CAM and V-CAM) were determined from mRNA of lung tissues by RT-PCR. Gene relative expression was calibrated by the β-actin housekeeping gene expression. Results showed that mRNA of IL-1β and TNF-α, MMP9, I-CAM and V-CAM increased at 3-7 days of infection. Also, iNOS, IL8 and phosphocholine cytidylyltransferase (CT) increased with lung injury. Anti-inflammatory IL-4 and IL-10 increased at 7 days of infection. We demonstrated previously that H. pylori induced morphological changes in the lung tissue with recruitment of inflammatory cells and lung parenchymal dysfunction. Results obtained in this study suggest that the pathophysiological mechanism of H. pylori on lung might be strongly associated with lung injury as measured by elevation in the expression of inflammatory mediators and endothelial dysfunction markers.