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This study investigates the role of IL-1 in neutrophil influx during peritonitis and air pouch models. Using IL-1R1 knockout (KO) mice, we observe reduced peritoneal neutrophils in response to CPPD-induced crystal inflammation compared to wild-type (WT) controls. Additionally, administering mIL-1 Trap at 35 mg/kg demonstrated a significant reduction in neutrophil counts in CPPD-treated subjects. These findings highlight the critical role of IL-1 signaling in mediating neutrophil recruitment in inflammatory responses to crystalline agents.
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Fig. 1 IL-1R1 WT IL-1R1 KO Trap Vehicle 35 mg/kg mIL-1 Trap B A 5 5 4 4 Neutrophils (X106)/mouse Neutrophils (X106)/mouse 3 3 2 2 Supplementary Figure 1. Blocking IL-1 reduced neutrophil influx in crystal-induced peritonitis and air pouch models. (A) IL-1R1 KOs showed fewer CPPD-induced peritoneal neutrophils (PBS: n=4 WT; n=3 IL-1R1 KO / CPPD: n=8 per genotype). (B) mIL-1 Trap (35 mg/kg) reduced CPPD crystal-induced peritoneal neutrophils (PBS: n=4 Vehicle / CPPD: n=6 per group). + p< 0.01; # p < 0.001 compared to controls. Data expressed as means + SEM. WT: IL-1R1 WT mice; KO: IL-1R1 knockout mice. 1 # + 1 0 0 CPPD PBS PBS CPPD
