To explore the mechanism of Toll-like receptors (TLRs)/nuclear factor-kappaB (NF-κB) signaling pathway mediated by speckle-type POZ protein (SPOP) on lung tissue injury in rats with pneumonia.

Thirty Sprague Dawley rats were divided into a pneumonia group, an inhibitor group and a control group, with 10 rats in each group. A rat model of pneumonia was constructed, and the histopathological changes of lung tissue were observed. The lung tissue injury degree score and lung wet/dry specific gravity were calculated. The protein expression levels of SPOP, TLR4, TLR9, NF-κB and myeloid differentiation factor 88 (MyD88) were detected by western-blotting. The levels of serum interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) were detected by enzyme-linked immunosorbent assay.

The lung tissue structure of the rats in the control group was normal, without obvious lesions. In the pneumonia group, some alveolar walls were thickened, and inflammatory cell infiltration could be observed. The degree of alveolar destruction was greater, and the range and degree of inflammatory cell infiltration were more severe in the inhibitor group than in the pneumonia group. There were statistically significant differences in the lung tissue injury degree score, wet/dry specific gravity, protein expression levels of SPOP, TLR4, TLR9, NF-κB and MyD88 in lung tissue, and levels of serum IL-1β, IL-6 and TNF-α among the three groups (F = 178.049, 8.557, 15.489, 36.935, 37.490, 35.152, 91.250, 89.687, 361.539, 16.319; all P < 0.001). Further pairwise comparisons revealed that the lung tissue injury degree score, wet/dry specific gravity, and protein expression levels of SPOP, TLR4, TLR9, NF-κB, and MyD88 in lung tissue, as well as serum levels of IL-1β, IL-6 and TNF-α, in the pneumonia group and inhibitor group were all higher than those in the control group (all P < 0.05). Moreover, the lung tissue injury degree score, wet/dry specific gravity, and protein expression levels of TLR4, TLR9, NF-κB and MyD88 in lung tissue, as well as the levels of serum IL-1β, IL-6 and TNF-α, in the inhibitor group were all higher than those in the pneumonia group, while the protein expression of SPOP was lower (all P < 0.05).

SPOP regulates the TLRs/NF-κB signaling pathway through the interaction with MyD88, which in turn affects the inflammatory response of lung tissue in rats with pneumonia.