The sterile
inflammation (SI) of the urinary tract is a common problem requiring serious consideration after
prostatectomy. This study mainly focuses on the role of the
reactive oxygen species-NLR family, pyrin domain-containing 3 (ROS-NLRP3) signaling pathway in SI after
thulium laser resection of the prostate (TmLRP). Urinary
cytokines were determined in patients who received TmLRP, and
heat shock protein 70 (HSP70) was detected in the resected tissues. The involvement of ROS signaling in HSP70-induced
inflammation was explored in THP-1 cells with or without
N-acetyl- l-cysteine (NAC) pretreatment. The function of NLRP3 and Caspase-1 was determined by Western blot analysis,
enzyme-linked
immunosorbent assay (ELISA), and polymerase chain reaction. These phenomena and mechanisms were verified by the beagle models that received TmLRP. Clinical urine samples after TmLRP showed high expression of inflammatory factors and peaked 3-5 days after surgery. The high expression of HSP70 in the resected tissues was observed. After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and
interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC. The expression of IL-1β and
IL-18 could be inhibited by NLRP3 or Caspase-1 inhibitors. In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1β, and
IL-18 were highly expressed in the
wound tissue or urine, and could also be reduced by NAC pretreatment. Activation of the ROS-NLRP3 signaling pathway induces SI in the
wound after
prostatectomy. Inhibition of this pathway may be effective for clinical prevention and treatment of SI and related complications after
prostatectomy.