半乳糖凝集素-3與介白素-22訊號傳遞對於腸表皮細胞表現抗菌胜肽之影響

Abstract

Galectin-3 (Gal-3) 在生理反應上調控許多生物活性功能。在腸炎症患者中，腸道中的Gal-3 表現量明顯較健康人低。在腸道發炎情況下，Interleukin-22 (IL-22) 能透過表現抗菌蛋白，如Reg3β/3γ 及 S100A8/A9，來保護腸道避免遭受病原菌侵犯。IL-22結合到IL-22受器後，會活化下游Jak1/Tyk2-STAT3、Akt 及 MAPK 訊號路徑。許多研究顯示 Gal-3 及 IL-22 對於維持腸道生理平衡扮演重要角色，故我們假設 Gal-3 也許參與在IL-22/IL-22R 訊號傳遞，並調控腸表皮細胞的功能。我們研究中發現，Gal-3似乎不參與在IL-22/IL-22R下游主要的三條訊號路徑。在動物實驗的大腸組織中，雖然Gal-3不參與在調控 Reg3b/3g 的表現，但Gal-3會負調控 IL-22 所誘導表現的 S100A8/A9。

Galectin-3 (Gal-3) is known to exert a lot of biological function. Expression of Gal-3 is significantly downregulated in the gut of patients with inflammatory bowel disease (IBD). Interleukin-22 (IL-22) is known to protect against colitis through enhancing the production of antimicrobial peptides (AMP), such as Reg3β/3γ and S100A8/A9. Binding of IL-22 to its receptor activates Jak1/Tyk2-STAT3, Akt and MAPK signaling pathways. It has been reported that Gal-3 and IL-22 are important to maintain the intestinal homeostasis. We hypothesize that Gal-3 may participate in IL-22 signaling and regulate the functions in intestinal epithelial cells (IECs). In our study, Gal-3 seems not regulate the three major IL-22 signaling pathways. Although Gal-3 is not involved in regulating Reg3b/3g expression, it negatively regulates IL-22-induced S100A8/A9 expression in colon.