Saccharomyces boulardii attenuates inflammatory response induced by Clostridium perfringens via TLR4/TLR15-MyD8 pathway in HD11 avian macrophages

• Published in: Poultry science 2020-11, Vol.99 (11), p.5356-5365
• Main Authors: Wang, Baikui, Hussain, Altaf, Zhou, Yuanhao, Zeng, Zihan, Wang, Qi, Zou, Peng, Gong, Li, Zhao, Pengwei, Li, Weifen
• Format: Article
• Language: English
• Subjects: Animals; Antibiosis - immunology; Chickens; Clostridium Infections - immunology; Clostridium Infections - microbiology; Clostridium Infections - veterinary; Clostridium perfringens; HD11 macrophage; Immunology, Health and Disease; immunomodulation; Inflammation - immunology; Macrophages - immunology; Macrophages - microbiology; Myeloid Differentiation Factor 88 - immunology; Poultry Diseases - immunology; Poultry Diseases - microbiology; Saccharomyces boulardii; Saccharomyces boulardii - immunology; Toll-Like Receptor 4 - immunology; Toll-Like Receptors - immunology
• ISSN: 0032-5791; 1525-3171
• DOI: 10.1016/j.psj.2020.07.045

Macrophages are professional phagocytic cells that play a critical role in initiating immune responses by presenting antigen and phagocytic clearance. The macrophages can be targeted for immunomodulation by beneficial microbes, such as probiotics. The aim of this study is to investigate the protective effect of Saccharomyces boulardii against Clostridium perfringens infection in avian macrophage cell line HD11. In this study, HD11 macrophages were prestimulated with S. boulardii for 6 h and then infected with C. perfringens for 3 h. Results showed that S. boulardii enhanced phagocytosis and bactericidal capacity against C. perfringens by HD11 cells. The S. boulardii effectively promoted the mRNA expression of CD80, CD83, and CD197 cell-surface molecules in C. perfringens-infected HD11 cells. Moreover, we found that prestimulation with S. boulardii reduced the mRNA expression of CD40, toll-like receptor [TLR] 4, and TLR15 induced by C. perfringens and thereby downregulated the mRNA expression of myeloid differentiation primary response 88, TNF receptor associated factor 6, nuclear factor kappa-B p65 subunit, and c-Jun N-terminal kinase genes in HD11 cells. The upregulation of cytokines (interleukin [IL]-6, tumor necrosis factor alpha, and IL-10) and inducible nitric oxide synthase mRNA expression in C. perfringens-infected HD11 cells were noticeably inhibited by S. boulardii pretreatment. Conclusively, these results might provide a new insight into the role of S. boulardii in regulating avian immune defense against C. perfringens invasion and immune escape.