BACKGROUNDFound in inflammatory zone 1 (FIZZ1) protein increased in pulmonary epithelial cells and in limited amounts of other lung cells. FIZZ1 increased in murine model of smoke induced chronic obstructive pulmonary disease. However, the direct role of FIZZ1 produced by pulmonary epithelium stimulated with cigarette smoke extraction has not been determined. We examined the expression and function of FIZZ1 in rat lung epithelial L2 cells.

METHODSThe rat lung epithelial L2 cells (CCL 149) were exposed to cigarette smoke extraction, expression of FIZZ1 mRNA was investigated by RT-PCR. Levels of FIZZ1 protein were detected by Western blotting and laser confocal microscope. CCL 149 cells were treated with different concentrations and for different time of recombinant protein FIZZ1. After treatment, the expression levels of interleukin 8 (IL-8) were detected by enzyme-linked immunosorbent assay (ELISA).

RESULTSWhen CCL 149 cells were exposed to cigarette smoke extraction, FIZZ1 mRNA and protein levels expressed significantly higher than control group. Recombinant protein FIZZ1 promoted the expression of IL-8 in a dose and time dependent manner in a certain range.

CONCLUSIONSCigarette smoke extraction activates FIZZ1 at mRNA and protein levels in CCL 149 cells. Recombinant protein FIZZ1 induces the expression of IL-8 and may thus participate in the process of chronic obstructive pulmonary disease airway inflammation and airflow obstruction. Generally, immune cells such as macrophages, neutrophils and lymphocytes are unavoidably involved in airway inflammatory and immune responses to cigarette smoke, but it is still unclear whether their involvement in the pathogenesis of chronic obstructive pulmonary disease is based on the specific expression in lung epithelial cells of FIZZ1.