4.7 Article

Effects of Caulis Spatholobi Polysaccharide on Immunity, Intestinal Mucosal Barrier Function, and Intestinal Microbiota in Cyclophosphamide-Induced Immunosuppressive Chickens

Journal

FRONTIERS IN VETERINARY SCIENCE
Volume 9, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fvets.2022.833842

Keywords

Caulis Spatholobi polysaccharide; immunosuppression; intestinal microflora; intestinal mucosal barrier; cyclophosphamide; immune enhancer

Funding

  1. Key Research and Development Plan of Guangxi, China [AB19245037]
  2. Natural National Science Foundation of China [317607446]
  3. Major R&D Project of Nanning Qingxiu District [2020005]
  4. Major R&D Project of Nanning [20212138]

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The study demonstrates that Caulis Spatholobi polysaccharide (CSP) has protective effects on immune function, intestinal mucosal barrier, and intestinal microflora in cyclophosphamide-induced immunosuppressed chickens. CSP can increase body weight, immune organ index, and the secretion of cytokines and immunoglobulins in chickens. Additionally, it reduces intestinal injury, improves intestinal health, and enhances the abundance of Lactobacillus in the intestine.
The protective effects of Caulis Spatholobi polysaccharide (CSP) on immune function, intestinal mucosal barrier, and intestinal microflora in cyclophosphamide (CY)-induced immunosuppressed chickens have been rarely reported. This study was designed to investigate the cecal microbiota in chickens and to elucidate the immune mechanism involved in the CSP effect on CY induced-immunosuppressed chickens. A total of 288 cocks were equally divided into six groups and used to evaluate the immune effect of CSP. Results showed that the CSP increased the body weight and immune organ index of immunosuppressed chickens, significantly increased the secretion of cytokines (IL-4, IL-10) and immunoglobulins (IgG, IgM) in sera of chickens, and restored the body immune function. The CSP reduced intestinal injury of the jejunum and ileum, increased the ratio of the intestinal villus height to crypt depth (V/C), improved the expression of tight junction protein, and protected intestinal health. The CSP activated the toll-like receptor (TLR)/MyD88/NF-kappa B pathway and enhanced the expression of TLR4, MyD88, NF-kappa B, Claudin1, and Zo-1, protecting the intestinal tract. High-throughput sequencing of the 16S rRNA gene showed that CSP increased species richness, restored CY-induced intestinal microbiome imbalance, and enhanced the abundance of Lactobacillus in the intestinal tract. In conclusion, our study provided a scientific basis for CSP as an immune enhancer to regulate intestinal microflora and protect intestinal mucosal damage in chickens.

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