Author/Authors :
GUO، Yijie نويسنده Department of Pathogenic Microbiology and Immunology, School of Basic Medical Sciences, Xi’an Jiao Tong University, Xi’an, China , , Ding، Cuiping نويسنده Department of Pathogenic Microbiology and Immunology, School of Basic Medical Sciences, Xi’an Jiao Tong University, Xi’an, China , , Zhang، Bo نويسنده , , XU، Jun نويسنده Faculty of Science and Engineering, Iwate University, Iwate, Japan , , XUN، Meng نويسنده Department of Pathogenic Microbiology and Immunology, School of Basic Medical Sciences, Xi’an Jiao Tong University, Xi’an, China , , Xu، Jiru نويسنده The First Affiliated Hospital, Xi’an Jiaotong University Health Science Center, Xi’an, China ,
Abstract :
Bovine leptospirosis is a widespread zoonotic disease, leading to serious economic losses in animal production and causing potential hazards to human health. Leptospiral lipopolysaccharide (L-LPS) plays an important role in leptospirosis pathogenicity. With respect to L-LPS endotoxin-like activity, we examined bovine immune response to L-LPS and the inhibitory ability of bovine myeloid antimicrobial peptide-28 (BMAP-28) against L-LPS-induced immune activation in bovine cells. In this study, L-LPS-induced proinflammatory cytokine production in bovine cells was quantitatively measured with real-time PCR and ELISA, and we determined which cell membrane receptors (toll-like receptor [TLR]2 and TLR4) played a major role. In addition, the ability of BMAP-28 to inhibit L-LPS-induced endotoxin-like immune activation in bovine cells was determined by the decrease in cytokine secretion. L-LPS showed the ability to induce cytokine production in bovine cells, and its induction was TLR2-dependent. BMAP-28 was used to inhibit L-LPS-induced endotoxin-like activity. The function of BMAP-28 was to inhibit LPS-induced TLR2 expression and cytokine production. In this study, the L-LPS immune response of bovine cells was significant, indicating that TLR2 is the predominant receptor for L-LPS. Due to L-LPS endotoxin-like activity, we found a strategy through using BMAP-28 to prevent L-LPS-induced TLR2-dependent immune activation in bovine cells.
