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Silencing TBX1 Exerts Suppressive Effects on Epithelial–Mesenchymal Transition and Inflammation of Chronic Rhinosinusitis Through Inhibition of the TGFβ-Smad2/3 Signaling Pathway in Mice

Background Chronic rhinosinusitis (CRS) is a multifactorial inflammatory disease characterized by high prevalence and morbidity, and little is known about the mechanisms that underlie its pathogenesis. Objective This study focuses on the effect of T-box 1 (TBX1) on the epithelial–mesenchymal transition (EMT) and inflammation of CRS via the transforming growth factor (TGF)β-Smad2/3 signaling pathway. Methods CRS mice models were established by Merocel nasal packing material, followed by the streptococcus pneumoniae cultivation. The expression levels of TBX1 in the sinus mucosa tissues of mice were measured accordingly. The successfully modeled mice were subsequently injected with TBX1 mimic or TBX1 inhibitor and the TGFβ-Smad2/3 signaling pathway inhibitor (SB-431542) to elucidate the influence of TBX1 on EMT and inflammation in CRS, with the expression of the EMT-related factors (E-cadherin, Vimentin, alpha-smooth muscle actin [α-SMA]), Th1 cytokines (interleukin [IL]-2, interferon-γ), and Th2 cytokines (IL-4, IL-8, total immunoglobulin E) assayed. Results TBX1 expression exhibited upregulated levels in the sinus mucosa tissues of the mice. In addition, TBX1 downregulation was found to inhibit the expression of TGFβ as well as the extent of Smad2 and Smad3 phosphorylation. Silencing TBX1 was shown to elevate the expression of Th1 cytokines and E-cadherin, while diminishing expression of Th2 cytokines, Vimentin and α-SMA. Conclusions 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.