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Jundishapur J Microbiol. 2016 Jun 21;9(6):e33926. doi: 10.5812/jjm.33926. eCollection 2016 Jun.

Inhibitory effect of BMAP-28 on Leptospiral Lipopolysaccharide-Induced TLR2-Dependent Immune Response in Bovine Cells.

Author information

1
Department of Pathogenic Microbiology and Immunology, School of Basic Medical Sciences, Xi'an Jiao Tong University, Xi'an, China; Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
2
Department of Pathogenic Microbiology and Immunology, School of Basic Medical Sciences, Xi'an Jiao Tong University, Xi'an, China.
3
Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
4
Faculty of Science and Engineering, Iwate University, Iwate, Japan.

Abstract

BACKGROUND:

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.

OBJECTIVES:

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.

MATERIALS AND METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

KEYWORDS:

BMAP-28; Cattle; Cytokines; LPS; Leptospira; Toll-Like Receptor 2

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