The role of granzyme B in promoting tissue inflammation has attracted increasing attention, but whether it plays a role in pulmonary inflammation caused by PM_2.5 is still unclear. This study investigated the role of granzyme B in pulmonary inflammation caused by PM_2.5.

In the first step, the animal model of rat lung inflammation induced by intratracheal instillation of PM_2.5 suspension was established. The experiment was divided into PBS group, PM_2.5 (2 mg/kg) group, PM_2.5 (6 mg/kg) group and PM_2.5 (18 mg/kg) group. By setting the PM_2.5 instillation dose gradient, we detected the expression of granzyme B, pathology and inflammation scores in rat lung tissues under different PM_2.5 exposure doses to explore whether there is a correlation between the expression level of granzyme B and the severity of lung inflammation. In the second step, whether granzyme B plays a role in promoting pulmonary inflammation caused by PM_2.5 was investigated by blocking granzyme B. In the third step, whether granzyme B acts through IL-18 in PM_2.5-induced pulmonary inflammation was investigated by blocking IL-18.

As the PM_2.5 instillation dose increased, the expression of granzyme B in lung tissue increased, the degree of inflammatory cell infiltration and pulmonary edema, and the inflammation score in lung tissue pathological sections increased. PM_2.5 increased granzyme B expression and inflammation in the lungs. Blocking granzyme B inhibited IL-18 expression and NF-κB phosphorylation, and reduced lung inflammation caused by PM_2.5. Blocking IL-18 inhibited Phosphorylation of NF-κB and reduced lung inflammation caused by PM_2.5.

PM_2.5 aggravates lung inflammation by up-regulating granzyme B to promote IL-18 expression, and the mechanism may be related to the activation of NF-κB signaling pathway.