Clara cell protein 16 and eosinophil cationic protein production in chronically inflamed sinonasal mucosa

Špadijer-Mirković, Cveta; Perić, Aleksandar; Belic, Branislav; Vojvodić, Danilo

doi:10.1002/alr.21710

Cited by 13 publications

(36 citation statements)

References 32 publications

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“…22 In addition, the CC16 levels were significantly lower in patients with PAR and allergic chronic rhinosinusitis with nasal polyp patients compared to healthy controls. 23 Thus, we expected the inverse correlation between nasal fluid CC16 and symptoms in PAR patients.…”

Section: Discussionmentioning

confidence: 88%

Correlation of Nasal Fluid Biomarkers and Symptoms in Patients with Persistent Allergic Rhinitis

Kim

Kwon

Park

et al. 2020

Ann Otol Rhinol Laryngol

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Objectives: This study investigated whether the biomarkers present in nasal fluid reflect the severity of symptoms in patients with persistent allergic rhinitis (PAR). Methods: We enrolled 29 PAR patients complaining of nasal symptoms and testing positive to skin prick test. Patients’ total nasal symptom score (TNSS) was measured and their nasal lavage fluid (NALF) was collected. The levels of biomarkers including Clara cell protein 16 (CC16), tryptase, and interleukin 5 (IL-5) in NALF were determined via enzyme-linked immunosorbent assay (ELISA). Results: PAR patients were classified into persistent mild and persistent moderate-to-severe groups according to the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines. The CC16 alone was significantly negatively correlated with TNSS ( P < .05). Further, the CC16 level was significantly lower in persistent moderate-to-severe group than persistent mild group of patients ( P < .05). Conclusions: The levels of CC16 alone among several NALF biomarkers showed an inverse correlation with symptoms of PAR patients.

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Section: Discussionmentioning

confidence: 88%

Correlation of Nasal Fluid Biomarkers and Symptoms in Patients with Persistent Allergic Rhinitis

Kim

Kwon

Park

et al. 2020

Ann Otol Rhinol Laryngol

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“…Glucocortocoids [23] and proin ammatory cytokines such as INF-γ [24] and TNF-α [25] promote CC16 expression in the airways, whilst exposing to air toxicants such as cigarette smoking(CS) [26], nitrogen dioxide [27],and ozone [28] reduce the synthesis of CC16 by Clara cells. Additionally, CC16 is regarded as a useful biomarker of airway epithelial damage in chronic upper and lower respiratory diseases [29,30]. Accumulating evidence have con rmed that the number of Clara cell protein-positive epithelial cells is diminished in allergic airway diseases such as asthma, allergic rhinitis and chronic rhinosinusitis [31], leading to lower level of CC16 production in BALF and airway mucosa.…”

Section: Discussionmentioning

confidence: 99%

Clara cell 16KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition.

Liu

Zhang

et al. 2021

Preprint

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Background: House dust mite (HDM) inhalation can cause airway epithelial damage which is implicated in the process of airway inflammation in asthma. High mobility group box 1 (HMGB1) is critically required for cellular damage and apoptosis as an important endogenous danger signal. Recently, Clara cell 16KDa protein (CC16) has been identified to exert anti-inflammatory and immunomodulatory influence in various injury-related diseases model. However, little is known about its ability to protect against airway epithelial injury in allergic asthma. This study was aimed to clarify the protective roles of CC16 on airway epithelia in HDM-induced asthma and the regulation of HMGB1 by CC16.Methods: Mice were sensitized and challenged by HDM extract and administrated intranasally with CC16 (5ug/g or 10ug/g) or saline in the challenged period. The BEAS-2B human airway epithelial cell line were cultured with CC16 or the control vehicle and then exposed to HDM. Knockdown or overexpression of HMGB1 was induced by cell transfection or intratracheal injection of recombinant adenovirus.Results: CC16 treatment decreased airway inflammation and histological damage of airway epithelium dose-dependently in HDM-induced asthma model. Airway epithelia apoptosis upon HDM stimulation was noticeably abrogated by CC16 in vivo and in vitro. In addition, upregulation of HMGB1 expression and its related signaling were also detected under HDM conditions, while silencing HMGB1 significantly inhibited the apoptosis of BEAS-2B cells. Furthermore, the activity of HMGB1-mediated signaling was restrained after CC16 treatment whereas HMGB1 overexpression abolished the protective effect of CC16 on HDM-induced airway epithelia apoptosis.Conclusions: Our data confirm that CC16 attenuates HDM-mediated airway inflammation and damage via suppressing airway epithelial cell apoptosis in a HMGB1-dependent manner, suggesting the role of CC16 as a potential protective option for HDM-induced asthma.

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“…In an experimental investigation, Roth et al (13) demonstrated that long-term exposure to perennial allergens caused most Clara cells to transform into large secretory goblet cells, which resulted in lower CC16 and higher mucus production in the bronchoalveolar mucosa. Studies with patients with PAR and CRSwNP demonstrated similar inhibition of CC16 nasal mucosa production by eosinophil inflammation (11,14). One study (15) showed significantly lower mean CC16 levels in the nasal secretions of patients with SAR, PAR, and (allergic and non-allergic) than controls whose nasal mucosa was not inflamed (15).…”

Section: The Role Of Cc16 In Ar and Crsmentioning

confidence: 94%

Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants

Perić

Mirković

Vojvodić

2018

Archives of Industrial Hygiene and Toxicology

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Clara cell protein 16 (CC16) is a small protein mainly produced by non-ciliated Clara cells in the respiratory epithelium. It has an anti-inflammatory role in chronic upper and lower airway eosinophilic inflammations. Decreased levels of CC16 are found in the nasal secretions and plasma of patients with chronic eosinophilic inflammatory disorders, such as asthma, allergic rhinitis, and chronic rhinosinusitis with or without nasal polyps, as well as in people exposed to high levels of air pollutants. Intranasal corticosteroid administration suppresses chronic inflammation of the nasal mucosa driven by eosinophils and stimulates local CC16 production. CC16 can be a reliable biomarker of the beneficial effects of perennial allergic rhinitis and chronic rhinosinusitis therapy and of the functional recovery of the nasal mucosa after treatment with topical glucocorticoids.

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Clara cell protein 16 and eosinophil cationic protein production in chronically inflamed sinonasal mucosa

Abstract: CC16 and ECP measured in nasal secretions could be reliable markers for assessment of the recovery function of sinonasal mucosa during corticosteroid treatment.

Cited by 13 publications

References 32 publications

Correlation of Nasal Fluid Biomarkers and Symptoms in Patients with Persistent Allergic Rhinitis

Correlation of Nasal Fluid Biomarkers and Symptoms in Patients with Persistent Allergic Rhinitis

Clara cell 16KDa protein mitigates house dust mite-induced airway inflammation and damage via regulating airway epithelial cell apoptosis in a manner dependent on HMGB1-mediated signaling inhibition.

Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants

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