Cold‐inducible RNA‐binding protein contributes to tissue remodeling in chronic rhinosinusitis with nasal polyps

Shi, Lili; Ma, Jin; Deng, Yi‐Ke; Chen, Cailing; Wang, Heng; Cao, Pingping; Xiang, Long; Zeng, Ming; Liu, Zheng

doi:10.1111/all.14287

Cited by 17 publications

(15 citation statements)

References 45 publications

(74 reference statements)

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“…30 Nasal epithelial cells and macrophages release cold-inducible RNAbinding protein, which induces oedema and tissue remodelling in eosinophilic and non-eosinophilic polyps. 31 Eosinophilic nasal polyps can also have significant levels of neutrophils and non-type 2 cytokines. 32 These patients with mixed-pattern inflammation tend to have higher symptom scores, greater cytokine burden and mucin hypersecretion than those with a single predominant endotype.…”

Section: Challenges With Endotypingmentioning

confidence: 99%

“…Hippo pathway components are upregulated in eosinophilic and non‐eosinophilic CRSwNP 30 . Nasal epithelial cells and macrophages release cold‐inducible RNA‐binding protein, which induces oedema and tissue remodelling in eosinophilic and non‐eosinophilic polyps 31 . Eosinophilic nasal polyps can also have significant levels of neutrophils and non‐type 2 cytokines 32 .…”

Section: Crs Endotypesmentioning

confidence: 99%

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Highlights in the advances of chronic rhinosinusitis

Reitsma

Wang

et al. 2021

Allergy

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Chronic rhinosinusitis (CRS) is a protracted inflammatory condition with global societal and financial burden. [1][2][3] Its prevalence is estimated to be 10-28% based on self-reported symptoms alone, 4,5 and about 4-9% when endoscopy 6 or imaging is applied. 7,8 Real world data suggest that nearly half of CRS patients have uncontrolled disease based on visual analogue scale for rhinosinusitis. 9 This subgroup has significant disease burden as these patients require longterm follow-up, medication and often repeat sinus surgeries. 10 Traditionally, CRS is classified based on the presence or absence of nasal polyps. It is evident that this classification based on a visual trait is probably an overly simplistic representation of a heterogenous condition with a spectrum of clinical presentations and severity. Hence in recent years, there is increasing interest in uncovering the inflammatory mechanisms, or endotypes, of CRS. With the advent of novel treatment options, including biologicals, the ability to accurately define endotypes and predict response to specific treatments via biomarkers is important in order to provide individualised patient care. 11 Research in CRS is a continually evolving field. The objective of this review is to update readers on the recent, important developments in the field of CRS in adults. This includes the changes in the latest edition of the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS2020), novel biomarkers, biologicals in the treatment of CRSwNP and the implications of the COVID-19 on the

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Section: Challenges With Endotypingmentioning

confidence: 99%

Section: Crs Endotypesmentioning

confidence: 99%

Highlights in the advances of chronic rhinosinusitis

Reitsma

Wang

et al. 2021

Allergy

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“…Previous studies demonstrated that TGF-b1, MMP2, MMP7, and MMP9 could induce EMT in nasal polyps and can be synthesized and secreted by macrophages (11,31). In the OVA+SEB group, the TGF-b1, MMP2, MMP7, and MMP9 levels were significantly increased in nasal lavage fluid, but only the TGF-b1 levels were decreased after TIM-4 mAb treatment.…”

Section: Tim-4 Mab Influences the Tgf-b1 Protein Level In Nasal Secre...mentioning

confidence: 99%

“…The chronic inflammatory state induces the loss of the epithelial adhesion molecule E-cadherin and accelerates nasal polypogenesis (9). Several inflammatory mediators have been implicated in the regulation of EMT in CRSwNP, such as transforming growth factor-beta 1 (TGF-b1) (10), matrix metalloproteinases (MMPs) (11)(12)(13), and vascular endothelial growth factor (14). These mediators can be secreted by macrophages and play an important role in EMT.…”

Section: Introductionmentioning

confidence: 99%

TIM-4 in macrophages contributes to nasal polyp formation through the TGF-β1–mediated epithelial to mesenchymal transition in nasal epithelial cells

et al. 2022

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is caused by prolonged inflammation of the paranasal sinus mucosa. The epithelial to mesenchymal transition (EMT) is involved in the occurrence and development of CRSwNP. The T-cell immunoglobulin domain and the mucin domain 4 (TIM-4) is closely related to chronic inflammation, but its mechanism in CRSwNP is poorly understood. In our study, we found that TIM-4 was increased in the sinonasal mucosa of CRSwNP patients and, especially, in macrophages. TIM-4 was positively correlated with α-SMA but negatively correlated with E-cadherin in CRS. Moreover, we confirmed that TIM-4 was positively correlated with the clinical parameters of the Lund-Mackay and Lund-Kennedy scores. In the NP mouse model, administration of TIM-4 neutralizing antibody significantly reduced the polypoid lesions and inhibited the EMT process. TIM-4 activation by stimulating with tissue extracts of CRSwNP led to a significant increase of TGF-β1 expression in macrophages in vitro. Furthermore, coculture of macrophages and human nasal epithelial cells (hNECs) results suggested that the overexpression of TIM-4 in macrophages made a contribution to the EMT process in hNECs. Mechanistically, TIM-4 upregulated TGF-β1 expression in macrophages via the ROS/p38 MAPK/Egr-1 pathway. In conclusion, TIM-4 contributes to the EMT process and aggravates the development of CRSwNP by facilitating the production of TGF-β1 in macrophages. Inhibition of TIM-4 expression suppresses nasal polyp formation, which might provide a new therapeutic approach for CRSwNP.

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“…Zheng et al reported the clinical characteristics of allergic rhinitis (AR) patients in 13 metropolitan cities of China and outlined the regional differences in the pathogenesis of AR in China 1 . Shi et al also showed that the production and release of cold‐inducible RNA‐binding protein (CIRP) was upregulated in the nasal epithelial cells and macrophages, contributing to edema formation in both eosinophilic and non‐eosinophilic chronic rhinosinusitis with nasal polyps (CRSwNP) by inducing matrix metalloproteinases (MMPs) and vascular endothelial growth factor A (VEGF‐A) production in these cells 2 . Furthermore, Zhong et al elucidated the mechanism by which hypoxia‐inhibitory factor‐1α (HIF‐1α) induces the nucleotide‐binding oligomerization domain (NOD)–like receptor family and pyrin domain‐containing 3 (NLRP3) expression in M1 macrophages in non‐eosinophilic CRSwNP 3 .…”

Section: Figurementioning

confidence: 99%