Objective To explore the molecular mechanisms of ROS expression induced by mycoplasma pneumoniae infection promoting NLRP3 activation in children.

Methods The data of 63 cases of mycoplasmal pneumonia (MPP) were retrospectively analyzed. According to the severity, the patients were divided into the mild group (n = 34) and severe group (n = 29). The serum levels of NLPR3, IL-18, IL-37, IL-1 beta and ROS in children were detected using the ELISA. At the same time, the animal model of mycoplasma pneumonia and inhibitor group (acetylcysteine) were established. HE staining was used to detect the changes in all groups. ELISA was used to detect the expression of NLRP3, IL-18, IL-37, IL-1β and ROS. Western blotting was used to detect the expression levels of NLRP3, IL - 18, IL – 37 and IL-1 beta.

Results Compared with the mild group, the expressions of NLRP3, IL-18, IL-1β, IL-37 and ROS in severe group increased (P ＜ 0.01). In the severe group, the expression of IL-18 increased in patients with pleural effusion (P ＜ 0.01). Compared with the cured group, the expressions of NLRP3, IL-1β and ROS in the non-cured group increased (P ＜ 0.05). The results of animal experiments showed that the infiltration of alveolar inflammatory cells increased in the model group compared with the control group. The inflammatory cell infiltration decreased in the ROS inhibitor group compared to the model group. ELISA results indicated that compared with the control group, the expressions of NLRP3, IL-18, IL-1β, IL-37 and ROS in the model group increased (P ＜ 0.05). Compared with the model group, the expressions of NLRP3, IL-18, IL-1β, IL-37 and ROS in the inhibitor group decreased (P ＜ 0.05). The results of Western blotting further verified this result.

Conclusions Mycoplasma pneumoniae infection induces the expression of ROS to promote the activation of NLRP3 inflammasome, which increases the secretion of cytokines to aggravate the progress of pneumonia.