Background: Air pollution PM exposure associated with increased inflammation and decreased cellular immune function. The innate immune system is one of the first lines of defense against inhaled air pollution and is characterized by activation of lung key signaling pathways. One pathway is initiated by the activation of toll-like receptors (TLRs) that associated with airway cells culminates in the translocation of nuclear factor-kappa B and other transcription factors to the nucleus, and therefore initiation of altered signaling of pro-inflammatory mediators such as IL-1β and TNF-α. The purpose of this study was to investigate the effect of 4 weeks of aerobic training after long-term inhalation of black carbon black particulate matter on IL-β lung tissue in male rats.
Methods: The present study was conducted experimentally in October and November 2015 at the Sport Physiology Laboratory of Tarbiat Modares University of Tehran. 12 adult male Wistar rats (279.29±26.97) were divided to two groups: A: Daily, two hours inhalation of carbon black PM10, n=6), B: 60 minutes aerobic exercise activity, 50 percent average peak velocity, 15 minutes after inhalation of carbon black PM10. The gene expression of IL-1β was analyzed in lung tissue by real-time-PCR and Pfaffl formula. In order to determine the significant differences between groups independent t-test were used.
Results: Although, there were no significant differences among the A and B groups, however, the mean of relative gene expression of IL-1β in group B was slightly lower than group A.
Conclusion: Four weeks regular aerobic exercise activity did not worsen lung tissue inflammation after long-term inhalation of carbon black PM10. It seems regular exercise training mitigate pulmonary inflammatory responses and in part, decrease the risk of pulmonary diseases.
