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Research Article | Open Access

Nocardia rubra cell-wall skeleton mitigates whole abdominal irradiation-induced intestinal injury via regulating macrophage function

Lingling Wu1,2, Long Chen2, Huijuan Li2, Yawei Wang2, Kexin Xu2,3, Wanchao Chen2, Aihua Zhang1, Yu Wang2( ), Chunmeng Shi1,2 ( )
Department of Toxicology, School of Public Health, Guizhou Medical University, Guiyang, 550025, China
State Key Laboratory of Trauma and Chemical Poisoning, Third Military Medical University (Army Medical University), 400038, Chongqing, China
College of Biological Engineering, Chongqing University 400044, Chongqing, China
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Highlights

• Nocardia rubra cell wall skeleton, as an approved National Category II New Drug, was proven to possess beneficial properties against radiation-induced intestinal injury.

• Nocardia rubra cell wall skeleton can effectively ameliorate WAI-induced intestinal barrier structural and functional injury and promote the regeneration of the intestinal epithelium.

• Nocardia rubra cell wall skeleton can improve intestinal bacterial flora homeostasis and alter the composition of the gut microbiota in WAI mice.

• Nocardia rubra cell wall skeleton protects the morphology and function of the spleen against radiation-induced spleen damage.

• Nocardia rubra cell wall skeleton-induced radioprotection is macrophage dependent. Nr-CWS activated the NF-κB signaling pathway and promoted the phagocytosis and migration of macrophages.

Abstract

Background

Ionizing radiation (IR)-induced intestinal injury is a major side effect and dose-limiting toxicity in patients receiving radiotherapy. There is an urgent need to identify an effective and safe radioprotectant to reduce radiation-induced intestinal injury. Immunoregulation is considered an effective strategy against IR-induced injury. The purpose of this article was to investigate the protective effect of Nocardia rubra cell wall skeleton (Nr-CWS), an immunomodulator, on radiation-induced intestinal damage and to explore its potential mechanism.

Methods

C57BL/6 J male mice exposed to 12 Gy whole abdominal irradiation (WAI) were examined for survival rate, morphology and function of the intestine and spleen, as well as the gut microbiota, to comprehensively evaluate the therapeutic effects of Nr-CWS on radiation-induced intestinal and splenetic injury. To further elucidate the underlying mechanisms of Nr-CWS-mediated intestinal protection, macrophages were depleted by clodronate liposomes to determine whether Nr-CWS-induced radioprotection is macrophage dependent, and the function of peritoneal macrophages stimulated by Nr-CWS was detected in vitro.

Results

Our data showed that Nr-CWS promoted the recovery of intestinal barrier function, enhanced leucine-rich repeat-containing G protein-coupled receptor 5+ intestinal stem cell survival and the regeneration of intestinal epithelial cells, maintained intestinal flora homeostasis, protected spleen morphology and function, and improved the outcome of mice exposed to 12 Gy WAI. Mechanistic studies indicated that Nr-CWS recruited macrophages to reduce WAI-induced intestinal damage. Moreover, macrophage depletion by clodronate liposomes blocked Nr-CWS-induced radioprotection. In vitro, we found that Nr-CWS activated the nuclear factor kappa-B signaling pathway and promoted the phagocytosis and migration ability of peritoneal macrophages.

Conclusions

Our study suggests the therapeutic effect of Nr-CWS on radiation-induced intestinal injury, and provides possible therapeutic strategy and potential preventive and therapeutic drugs to alleviate it.

Keywords

Nocardia rubra cell wall skeletonIonizing radiationRadiation-induced intestinal injuryIntestinal floraRadiation protectionPeritoneal macrophages

References

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Burns & Trauma
Volume 12,
December 2024
Article number: tkad045
DOI: 10.1093/burnst/tkad045

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Cite this article:
Wu L, Chen L, Li H, et al. Nocardia rubra cell-wall skeleton mitigates whole abdominal irradiation-induced intestinal injury via regulating macrophage function. Burns & Trauma, 2024, 12: tkad045. https://doi.org/10.1093/burnst/tkad045

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Received: 13 December 2022
Revised: 13 April 2023
Accepted: 16 August 2023
Published: 10 October 2026
© The Author(s) 2024. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.