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

Perić, Aleksandar; Mirković, Cveta Špadijer; Vojvodić, Danilo

doi:10.2478/aiht-2018-69-3081

Cited by 9 publications

(22 citation statements)

References 30 publications

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“…Indeed, number of studies have proposed associations between air pollutants, including DEPs, and nasal inflammatory diseases, such as rhinitis and rhinosinusitis. 38,39 However, our in vivo research suggests that DEP nasal exposure may have a much stronger association with rhinitis than rhinosinusitis based on the pathway analysis of DEG data. Further studies required for determining the exact mechanisms involved, though, our data suggest that key genes such as TNFRSF9, CD80, S100A9, IL20, and CAMP might have a close relationship with rhinitis and may involve other indirect networks.…”

Section: Discussionmentioning

confidence: 84%

Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

Kim

Park

et al. 2019

Ann Otol Rhinol Laryngol

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Objectives: Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response in vitro, but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially in vivo. Methods: In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity. Results: Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8. Conclusions: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our in vivo results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.

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Section: Discussionmentioning

confidence: 84%

Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

Kim

Park

et al. 2019

Ann Otol Rhinol Laryngol

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“…It, also known as uteroglobin, secretoglobin-1a1, club cell secretory protein, plays an anti-inflammatory and anti-oxidant role in airway eosinophilic inflammations such as AR and asthma. 20,21 An inverse relation was reported between nasal fluid CC16 and rhinitis symptoms in IAR patients. 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.…”

Section: Discussionmentioning

confidence: 98%

“…On the other hand, intranasal glucocorticoids decrease the number of antigen-presenting cells, lymphocytes, mast cells, and eosinophils in the nasal mucosa, resulting in stimulation of CC16 production. 21 Thus, we told subjects to stop taking the allergic medication including topical steroid for 2 weeks before the collection of NALF to rule out the effects of medication.…”

Section: Discussionmentioning

confidence: 99%

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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“…CC16 is a small anti-in ammatory protein mainly expressed by nonciliated Clara cells in airway epithelium [22] and also a useful biomarker of airway epithelial damage in chronic upper and lower respiratory diseases [23,24]. Accumulating evidence have con rmed that the number of Clara cell proteinpositive epithelial cells is diminished in allergic airway diseases such as asthma, allergic rhinitis and chronic rhinosinusitis [25], leading to lower level of CC16 production in BALF and airway mucosa. Another study documented that OVA-challenged CC16 −/− mice exhibited more severe airway dysfunction than wild mice [26].…”

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

Cited by 9 publications

References 30 publications

Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

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.

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