CRS is a multifactorial inflammatory disease characterized by high prevalence and morbidity. Unfortunately, adequate literature is not available about the mechanisms that underlie its pathogenesis. This study focuses on T-box 1 on the EMT and inflammation of CRS via the TGFβ-Smad2/3 signaling pathway.

CRS mice models were established by Merocel nasal packing material, followed by the streptococcus pneumonia cultivation. The expression levels of TBX1 were measured accordingly. The mice were injected with TBX1 mimic or TBX1 inhibitor and the TGFβ-Smad2/3 signaling pathway inhibitor to elucidate the influence of TBX1 on EMT and inflammation in CRS, with the expression of the EMT-related factors, Th1 cytokines, and Th2 cytokines assayed.

TBX1 expression exhibited upregulated levels in the sinus mucosa tissues of the mice. Besides, TBX1 downregulation was found to inhibit the expression of TGFβ and the extent of Smad2 and Smad3 phosphorylation.

The study concluded that taken together, the key findings of our study highlight the inhibitory role of TBX1 in the process of EMT and inflammation in CRS mice via the inhibition of the TGFβ-Smad2/3 signaling pathway, underlining the promise of TBX1 as a potential target for CRS therapy.