Classical collectins (surfactant protein A and D) play a significant role in innate immunity and host defence in uropathogenic Escherichia coli (UPEC)-induced urinary tract infection (UTI). However, the functions of collectin-11 (CL-11) with respect to UPEC and UTI remain largely unexplored. This study aimed to investigate the effect of CL-11 on UPEC and its role in UTI. We further examined its modulatory effect on inflammatory reactions in proximal tubular epithelial cells (PTECs). The present study provides evidence for the effect of CL-11 on the growth, agglutination, binding, epithelial adhesion and invasion of UPEC. We found increased basal levels of phosphorylated p38 MAPK and human cytokine homologue (keratinocyte-derived chemokine) expression in CL-11 knockdown PTECs. Furthermore, signal regulatory protein α blockade reversed the increased basal levels of inflammation associated with CL-11 knockdown in PTECs. Additionally, CL-11 knockdown effectively inhibited UPEC-induced p38 MAPK phosphorylation and cytokine production in PTECs. These were further inhibited by CD91 blockade. We conclude that CL-11 functions as a mediator of innate immunity via direct antibacterial roles as well as dual modulatory roles in UPEC-induced inflammatory responses during UTI. Thus, the study findings suggest a possible function for CL-11 in defence against UTI.

经典的聚集素（表面活性剂蛋白 A 和 D）在泌尿致病性大肠杆菌的先天免疫和宿主防御中发挥重要作用(UPEC) 引起的尿路感染 (UTI)。然而，关于 UPEC 和 UTI 的 collectin-11 (CL-11) 的功能在很大程度上仍未探索。本研究旨在调查 CL-11 对 UPEC 的影响及其在 UTI 中的作用。我们进一步检查了它对近端肾小管上皮细胞 (PTECs) 炎症反应的调节作用。本研究为 CL-11 对 UPEC 的生长、凝集、结合、上皮粘附和侵袭的影响提供了证据。我们发现 CL-11 敲低 PTEC 中磷酸化 p38 MAPK 和人细胞因子同源物（角质形成细胞衍生趋化因子）表达的基础水平增加。此外，信号调节蛋白 α 阻断逆转了 PTEC 中与 CL-11 敲低相关的炎症基础水平升高。此外，CL-11 敲低有效抑制了 PTEC 中 UPEC 诱导的 p38 MAPK 磷酸化和细胞因子的产生。这些被 CD91 阻断进一步抑制。我们得出结论，CL-11 通过直接抗菌作用以及在 UTI 期间 UPEC 诱导的炎症反应中的双重调节作用作为先天免疫的介质。因此，研究结果表明 CL-11 可能具有防御 UTI 的功能。