Helicobacter pylori
infection has been reported to be associated with extra-digestive disorders such as
respiratory diseases; however, the impact of H. pylori on lung is incompletely understood. Inflammatory response is mediated by the release of
cytokines,
interferon, and
enzymes such as
metalloproteinases (
MMPs). This may contribute to
collagen accumulation during the early phase of
infection.
MMP expression is an important factor for the proliferation and infiltration of lung cells in the process of
fibrosis formation. The aim of this work was to study the impact of the
infection with H. pylori on lung using a mouse model. We looked for histological lesions of lung infected with the microorganism as well as the expression of inflammatory and of endothelial dysfunction markers. C57BL/6 wild type (WT) mice were infected by orotracheal instillation with 20 μl of 1 × 108H. pylori reference strain
suspension once per day for 3 days. Animals infected and controls were sacrificed at 3, 7, 14, 21 and 30 days. The lung from mice were stained with
Hematoxylin-
Eosin (H-E), Masson's Trichromic and
Periodic Acid Schifft (PAS) for histological study. Also,
lipid hydroperoxides and enzime
catalase (CAT) activity were determined. Expression level of multiple markers implicated in
inflammation (
tumor necrosis factor (TNF)-α,
interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10;
metalloproteinase MMP-9) and markers of endothelial dysfunction (I-CAM and V-CAM) was determined from lung tissues
mRNA using RT-PCR. Results showed that H. pylori induced morphological changes in the lung tissue with recruitment of inflammatory cells and lung parenchymal cell degradation. The
mRNA of IL-1β and TNF-α; MMP-9, I-CAM and V-CAM increased at 3-7 days
infections. Also, iNOS,
IL-8 and
Phosphocholine cytidyltransferase (CCT) increased with
lung injury. Anti-inflammatory
interleukin as:
IL-4, and
IL-10 increased at 7 and 14 days post
infection respectively. The results obtained suggest that the pathogenic mechanism of H. pylori on lung could be strongly associated with
lung injury as indicate the expression increased of inflammatory mediators and markers of endothelial dysfunction.