Deficiency in interleukin‐10 production by M2 macrophages in eosinophilic chronic rhinosinusitis with nasal polyps

Wang, Zhichao; Yao, Yin; Wang, Nan; Liu, Jinxin; Ma, Jin; Chen, Cailing; Deng, Yi‐Ke; Wang, Meng-Chen; Liu, Yang; Zhang, Xin‐Hao; Liu, Zheng

doi:10.1002/alr.22218

Cited by 29 publications

(24 citation statements)

References 44 publications

(121 reference statements)

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“…In contrast to the finding in eosinophilic nasal polyps, we did not detect CCL24 expression in macrophages in non‐eosinophilic polyps. Our previous studies demonstrated a predominant M2 phenotype of macrophages in eosinophilic nasal polyps and skewed M1 phenotype of macrophages in non‐eosinophilic nasal polyps . In the present study, we found the macrophages in both eosinophilic and non‐eosinophilic polyps exhibited expression of NK1R.…”

Section: Discussionsupporting

confidence: 70%

Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Deng

Wang

et al. 2019

Int Forum Allergy Rhinol

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Background:The mechanisms underlying mucosal eosinophilia in chronic rhinosinusitis with nasal polyps (CRSwNP) remain poorly clarified. The nervous system and neuropeptides play an important role in the regulation of immune response. Herein we explore the expression and function of hemokinin-1 (HK-1), a newly identified tachykinin, along with its receptor neurokinin 1 receptor (NK1R) in CRSwNP. Methods:HK-1, NK1R, and C-C motif chemokine ligand 24 (CCL24) expression in nasal tissues (53 eosinophilic CRSwNP, 32 non-eosinophilic CRSwNP, and 33 controls) was investigated by quantitative reverse transcript polymerase chain reaction (RT-PCR) and immunofluorescence staining. THP-1, a human monocytic leukemia cell line, and eosinophilic polyp tissues were stimulated with HK-1. Cells, tissues, and culture supernatants were subsequently collected for detection of the production of various inflammatory cytokines and chemokines by quantitative RT-PCR and enzyme-linked immunoassay.Results: HK-1 and NK1R mRNA and protein expression were upregulated in eosinophilic and non-eosinophilic nasal polyps compared with control tissues, with eosinophilic polyps demonstrating a higher upregulation compared with that of non-eosinophilic polyps. Eosinophils constituted the major source of HK-1, whereas macrophages were the predominant cell type exhibiting NK1R in eosinophilic polyps. HK-1 induced CCL24 production from macrophages differentiated from THP-1 cells; this was abolished by an NK1R antagonist. HK-1 also induced CCL24 production from ex vivo-cultured eosinophilic nasal polyps. CCL24 was expressed by macrophages in eosinophilic but not noneosinophilic polyps. The expression level of HK-1 correlated with CCL24 expression and tissue eosinophilia in eosinophilic nasal polyps. Conclusion:Eosinophil-derived HK-1 induces CCL24 production from macrophages and therefore exaggerates eosinophilic inflammation in CRSwNP. C 2019 ARS-AAOA, LLC.

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Section: Discussionsupporting

confidence: 70%

Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Deng

Wang

et al. 2019

Int Forum Allergy Rhinol

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“…A histological study on a large sample of CRS tissues demonstrated that CRSwNP presented a higher amount of immune cell infiltration compared with CRSsNP, and there were higher levels of cell infiltration of cytotoxic CD8 + T cells, B cells and macrophages in CRSwNP, as determined by immunohistochemistry (14). In addition, ECRSwNP has been reported to be associated with fewer M1 macrophages and more M2 macrophages compared with non-ECRSwNP, and the number of IL-10 + CD68 + macrophages was decreased in ECRSwNP (15). Specific chemokines and cytokines, such as MIP-1α, IL-5 and RANTES, are crucial to eosinophil recruitment, survival and differentiation (16)(17)(18).…”

Section: Introductionmentioning

confidence: 97%

Immune cell infiltration and related core genes expression characteristics in eosinophilic and non‑eosinophilic chronic rhinosinusitis with nasal polyps

et al. 2020

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Chronic rhinosinusitis with nasal polyps (CRSwNP) refers to chronic inflammation of the sinonasal mucosa. It can either be eosinophilic (ECRSwNP) or non-eosinophilic (non-ECRSwNP). However, immune cell infiltration in the microenvironment and pathogenesis of ECRSwNP and non-ECRSwNP are still unclear. The aim of the present study was to assess the immune cell infiltration and molecular mechanisms of ECRSwNP and non-ECRSwNP. In the present study, 22 immune cell types in ECRSwNP and non-ECRSwNP were investigated by CIBERSORT based on transcriptome data. The core gene related pathophysiology of CRSwNP was analyzed using Weighted Gene Correlation Network Analysis according to the phenotype of the infiltrated eosinophils and nasal polyps (NP). A total of four types of immune cells (mast cells, activated dendritic cells, M2 macrophages and activated natural killer cells) were demonstrated to have a direct and indirect correlation with eosinophilic infiltration in ECRSwNP. M1 macrophages and activated CD4 + memory T cells were correlated with major immune cell types in non-ECRSwNP. NP could affect the expression of 'olfactory receptor activity' and 'channel activity' genes to impair the olfactory signaling pathway and neuroactive ligand receptor pathway. 'Cell adhesion molecule binding', 'cytokine receptor binding' and 'glucocorticoid receptor binding' were significantly enriched in ECRSwNP, whereas epithelial cell injury, autophagy and the mTOR pathway (hsa04140 and hsa04150) may serve an important role in the pathogenesis of non-ECRSwNP. There were significantly different immune cell infiltration and related core genes expression characteristics between ECRSwNP and non-ECRSwNP. The results of the present study provide an improved basis for elucidation of the mechanism and treatment of CRSwNP.

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“…This suggests no difference in the number of differentiated M1 and M2 macrophage cells between the two groups. Then, we measured the mRNA expression levels of CCR7 and IL-10 as markers for M1 and M2 macrophages, respectively (41,42). The mRNA expression level of CCR7 was higher in M1 than in M2 macrophages (U = 27, p = 0.0079), whereas that of IL-10 was higher in M2 than in M1 macrophages (U = 0, p < 0.0001), thus con rming the differentiation into M1 and M2 macrophages (Suppl.…”

Section: Cytokine Expression In M1 and M2 Macrophages: Differences Bementioning

confidence: 99%

TNF-α expression ratio of M1/M2 macrophages is a potential adjunctive tool for the diagnosis of autism spectrum disorder

Yamauchi¹,

Makinodan²,

Toritsuka³

et al. 2020

Preprint

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Background The etiology of autism spectrum disorder (ASD) is complex. Its pathobiology is characterized by enhanced inflammatory activities; however, the exact ASD pathobiology remains unclear. Some cases of ASD are difficult to diagnose using existing psychological assessments because the careful exclusion of other psychiatric disorders is challenging. To distinguish between the appropriate targets for interventions and research, the demand for identifying efficient diagnostic biomarkers is increasing. This study aimed to find an inflammatory indicator beneficial for the diagnosis of ASD.Methods Cytokine mRNA expression, including tumor necrosis factor-α (TNF-α), was measured in the differentiated M1 and M2 macrophages of ASD patients (n = 29) and typically developed (TD) individuals (n = 30). TNF-α expression was also measured in the monocytes of ASD patients (n = 7) and TD individuals (n = 6).Results TNF-α expression in M1 macrophages and TNF-α expression ratio of M1/M2 macrophages were markedly higher in ASD patients than in TD subjects; however, this difference was not observed in M2 macrophages (M1: p < 0.01; ratio of M1/M2: p < 0.0001; M2: p > 0.05), suggesting that this indicator could be a useful tool for diagnosing ASD (M1: sensitivity = 34.5%, specificity = 96.7%, area under the curve (AUC) = 0.74, positive likelihood ratio (PLR) = 10.34; ratio of M1/M2: sensitivity = 55.2%, specificity = 96.7%, AUC = 0.79, PLR = 16.55). However, there was no significant difference in the TNF-α expression in monocytes between ASD and TD individuals (p > 0.05).Conclusion These findings suggest that TNF-α expression in differentiated macrophages represents a novel adjunctive tool for the diagnosis of ASD.

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Deficiency in interleukin‐10 production by M2 macrophages in eosinophilic chronic rhinosinusitis with nasal polyps

Cited by 29 publications

References 44 publications

Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Hemokinin‐1 stimulates C‐C motif chemokine ligand 24 production in macrophages to enhance eosinophilic inflammation in nasal polyps

Immune cell infiltration and related core genes expression characteristics in eosinophilic and non‑eosinophilic chronic rhinosinusitis with nasal polyps

TNF-α expression ratio of M1/M2 macrophages is a potential adjunctive tool for the diagnosis of autism spectrum disorder

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