Alterations in Regulatory Matrix Related to Inflammation in Lungs of Calcium Carbide Exposed Mice

Pulmonary disorders are established consequence of air pollution. Emissions from vehicles, factories and combustion of biomass are major contributors to air pollution. Accumulation of pollutants in lungs develops several respiratory diseases like asthma, chronic obstructive pulmonary disease (COPD). Persistent inflammation due to long term exposure to toxicants causes permanent pulmonary tissue damage and often arises serious medical emergency. Calcium carbide (CaC2) and its byproduct acetylene have been recognized as potential environmental toxicant. It is widely used in various commercial fields including fruit ripening and welding, cutting industries. In the present study we have investigated the inflammatory status and its consequences on lungs during inhalation of CaC2 generated toxicants by mimicking similar situation of people who occupationally get exposed with the same. After 40 days of exposure by calcium carbide generated gas, real-time qPCR has been performed to investigate the level of Cox2 and PGES mRNA. Apoptosis and TH17 as well as Treg percentage have been estimated flow cytometrically. Levels of Cox2 and PGES have been found to increase with the increase in CaC2 exposure. Apoptotic cell percentage has been declined with increasing dose of toxicant. TH17 and Treg cell percentage reduced as the dose of toxicant increased, indicating a balance between the two at 7gm CaC2 exposure. Balance between inflammatory and anti-inflammatory condition of lung tissue has been attempted after chronic CaC2 exposure, but it has been disrupted at the highest level likely due to accumulation of damaged cells as reflected by the spike of Cox2 mRNA level in 7gm CaC2 exposure.