曼氏血吸蟲可溶性蟲卵抗原藉由調節 JAK/STAT 訊息傳遞途徑抑制泌尿道致病性大腸桿菌對膀胱細胞的入侵

吳志緯¹、鄭柏青²、何承勳¹

1. 新光吳火獅紀念醫院外科部泌尿科

2. 臺北醫學大學醫學系分子寄生蟲暨熱帶疾病學科  

Schistosoma mansoni Soluble Egg Antigens Suppresses UPEC Invasion in Bladder Cells via Modulating the JAK/STAT Pathway

Chih-Wei Wu ¹, Po-Ching Cheng ², Chen-Hsun Ho ¹

1.Divisions of Urology, Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan;

2.Department of Molecular Parasitology and Tropical Diseases, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

Purpose:

Cystitis can be classified as bacterial or non-bacterial, with bacterial cystitis being the predominant form and commonly referred to as urinary tract infection (UTI). Uropathogenic Escherichia coli (UPEC) is recognized as the primary etiological agent and is associated with both acute and chronic inflammatory conditions of the urinary tract.

The JAK/STAT signaling cascade serves as a central downstream effector of numerous cytokines, hormones, and growth factors, and is essential for regulating apoptosis, cellular proliferation, immune responses, and inflammation. Previous studies have also reported that JAK/STAT signaling specifically modulates inflammatory reactions associated with metabolic abnormalities and infection in bladder cells. Consistent with these findings, our earlier work demonstrated that inhibition of the JAK/STAT pathway significantly alleviates UPEC-induced pathological changes in bladder epithelial cells.

Materials and Methods:

In this study, normal human bladder epithelial cells (SV-HUC-1) infected model were used to evaluate the immunomodulatory potential of Schistosoma mansoni soluble egg antigens (SEA).

Results:

SEA pretreatment markedly inhibited UPEC invasion, resulting in a substantial reduction in intracellular colony-forming units. Western blotting and quantitative PCR demonstrated that UPEC infection induced a notable upregulation of key JAK/STAT pathway key factors, whereas SEA pre-administration elicited a dose-dependent suppression of these responses. Flow cytometry further revealed that UPEC-induced elevation of TLR-4 and STAT1 expression was significantly attenuated following SEA pretreatment in the bladder cells.

Conclusion:

Collectively, these findings indicate that SEA mitigates UPEC invasion and inflammatory signaling in bladder epithelial cells by modulating the JAK/STAT pathway. This work highlights a previously unrecognized immunoregulatory mechanism and suggests that SEA may offer a promising adjunct or complementary strategy for managing UPEC-associated cystitis.