Different activities of antitumor immunomodulators to induce neutrophil adherence response

Tanaka, Motoharu; Abe, Shigeru

doi:10.5582/ddt.2019.01065

Cited by 3 publications

(2 citation statements)

References 31 publications

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“…It has been reported that Nr-CWS is not only an immunomodulator but also an anti-tumor agent [ 27 ], consisting of arabinogalactan, mycolic acid and mucopeptide and enhancing the ability of the host to clear infection. Studies have demonstrated that Nr-CWS has antitumor [ 14 ], immune response regulation [ 23 , 29 , 50 ], angiogenesis and cutaneous wound healing promoting properties [ 51 ]. A study proved that treatment with Nr-CWS could reduce Programmed cell death 1 ligand 1 (PD-L1) in tumor tissues and provide the possibility for the combination of Nr-CWS with PD-1/PD-L1 antibodies [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

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

Wu,

Chen,

et al. 2024

Burns &Amp; Trauma

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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.

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Section: Discussionmentioning

confidence: 99%

“…The Nocardia rubra cell wall skeleton (Nr-CWS), an innate immunomodulatory and antitumor agent [ 14 , 21 ], was first reported in 1976 by Azuma et al . [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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

Wu,

Chen,

et al. 2024

Burns &Amp; Trauma

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Augmented anti-tumour effect of lipopolysaccharide with G-CSF without enhancing body weight loss in mice bearing MH134 hepatoma

Tanaka

Abe

2022

European Journal of Pharmacology

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Gastric cancer cell-derived exosomal miR-541-5p induces M2 macrophage polarization through DUSP3/JAK2/STAT3 pathway

Xiao,

Fu,

Liu

et al. 2024

BMC Cancer

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Purpose Exosomal microRNAs have been identified as important mediators of communication between tumor cells and macrophages in the microenvironment. miR-541-5p was reported to be involved in hepatocellular carcinoma progression, but its role in gastric cancer (GC) and in GC cell-macrophage crosstalk is unknown. Methods Cell proliferation, migration and invasion were respectively assessed by CCK-8 assay, scratch and Transwell assays. RT-qPCR was used to detect the level of miR-541-5p, macrophage markers and DUSP3. The percentage of CD11b + CD206 + cell population was analyzed by flow cytometry. Western blotting was employed to evaluate DUSP3-JAK2/STAT3 pathway proteins and exosome markers. The interaction between miR-541-5p and DUSP3 was verified by luciferase assay. Results The results showed that miR-541-5p was upregulated in GC tissues and cells, and stimulated GC cell growth, migration and invasion in vitro. GC cells induce M2 macrophage polarization by secreting the exosomal miR-541-5p. Exosomal miR-541-5p maintained JAK2/STAT3 pathway activation in macrophages by targeting negative regulation of DUSP3. Inhibiting miR-541-5p significantly limited tumor growth in vivo. Conclusion In conclusion, miR-541-5p promotes GC cell progression. GC cells may induce macrophage M2 polarization through the exosomal miR-541-5p-mediated DUSP3/JAK2/STAT3 pathway. miR-541-5p may be a potential therapeutic target for GC. Supplementary Information The online version contains supplementary material available at 10.1186/s12885-024-12672-1.

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Different activities of antitumor immunomodulators to induce neutrophil adherence response

Cited by 3 publications

References 31 publications

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

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

Augmented anti-tumour effect of lipopolysaccharide with G-CSF without enhancing body weight loss in mice bearing MH134 hepatoma

Gastric cancer cell-derived exosomal miR-541-5p induces M2 macrophage polarization through DUSP3/JAK2/STAT3 pathway

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