Effect of cigarette smoke on TNF-a and IL-1b mRNA expression in lung tissues and cells of rats

Abstract

We investigated lung tissue expression of the pro-inflammatory cytokines TNF-a and IL-1b in response to cigarette smoke exposure and the ensuing effects on arterial oxygen and carbon dioxide as indices of respiratory function. Experimental group rats were exposed to cigarette smoke twice daily (30 min per exposure) for 28 consecutive days. Arterial partial pressure of oxygen (PO2), arterial partial pressure of carbon dioxide (PCO2), and both mRNA and protein expression levels of TNF-a and IL-1b were compared to a control group. Contents of TNF-a and IL-1b in bronchoalveolar lavage fluid (BALF) and lung homogenate were detected by enzyme linked immunosorbent assays while TNF-a mRNA and IL-1b mRNA expression levels in lung tissue were detected by reverse transcription-polymerase chain reaction. Arterial PO2 was significantly lower in the experimental group than the control group, while the arterial PCO2 was significantly higher. BALF levels of TNF-a and IL-1b were significantly higher in the experimental group than the control group, as were TNF-a mRNA and IL-1b mRNA expression levels in lung tissue. Cigarette smoke may activate inflammatory cells in the pulmonary circulation and increase the expression of the pro-inflammatory cytokines TNF-a and IL-1b in lung tissue, leading to lung injury and respiratory dysfunction.