chronic aspiration of gastric and duodenal contents and their effects on inflammatory cytokine production in respiratory system of rats.

نویسندگان

mitra samareh fekri department of pulmonology and physiology, kerman university of medical sciences, kerman, iran

hamid reza poursalehi animal physiology, physiology research center, kerman university of medical sciences, kerman, iran

hamid najafipour animal physiology, physiology research center, kerman university of medical sciences, kerman, iran

beydolah shahouzahi animal physiology, physiology research center, kerman university of medical sciences, kerman, iran

چکیده

gastroesophageal reflux disease (gerd)  is defined with clinical symptoms  of  heart burning and regurgitation. it may be associated with external esophageal symptoms such as chronic cough, asthma, laryngitis, chronic lung disease, sinusitis and pulmonary fibrosis. in the present study, rats with chronic aspiration of gastroduodenal contentswere studied for  cellular phenotypes  and  cytokine concentrations  in bronchoalveolar lavage and  lung tissue. thirty-six male  albino  n-mri  rats  were  randomly  divided  into  six  groups.  after anesthesia and tracheal intubation, the animals received either 0.5ml/kg of normal saline (control), gastric juice, pepsin, hydrochloric acid or bile salts by injection into their lungs twice a  week  for  8  weeks. in  sham  group  nothing  was  injected.  thereafter,  cellular phenotypes  and  cytokine  concentrations  of  interleukine  (il)-1α, il-1β,  transforming growth  factor  (tgf)-β,  tumor  necrosis  factor  (tnf)-α,  and  il-6  were assessed in bronchoalveolar lavage and lung tissue homogenates.  the numbers of epithelial cells, macrophages, neutrophils and lymphocytes in bal and levels of cytokines il-1α, il-6, tnf-α and tgf-β in bal and lung tissue of test groups were significantly higher  than  the  control  group.  aspiration  of  bile salts caused more cytokine levels and inflammatory cells compared to other reflux components. it can be concluded that gerd with increased cytokines and inflammatory cells in lung could cause or exacerbate asthma and pulmonary fibrosis.

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عنوان ژورنال:
iranian journal of allergy, asthma and immunology

جلد ۱۳، شماره ۱، صفحات ۴۰-۴۶

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