ArticlePloS one2013
Antibody to mCLCA3 suppresses symptoms in a mouse model of asthma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Calcium-activated chloride channel regulator 1 (CLCA1): More than a regulator of chloride transport and mucus production.The World Allergy Organization journal · 2019Article
- Niflumic Acid Reverses Airway Mucus Excess and Improves Survival in the Rat Model of Steroid-InducedFrontiers in microbiology · 2019Article
- Soluble mucus component CLCA1 modulates expression of leukotactic cytokines and BPIFA1 in murine alveolar macrophages but not in bone marrow-derived macrophages.Histochemistry and cell biology · 2018Article
- Article
- New Role of Adult Lung c-kitMediators of inflammation · 2016Article
- Host proteome correlates of vaccine-mediated enhanced disease in a mouse model of respiratory syncytial virus infection.Journal of virology · 2015Article
- Article
- Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway Diseases.Mediators of inflammation · 2015Review
- mCLCA3 modulates IL-17 and CXCL-1 induction and leukocyte recruitment in murine Staphylococcus aureus pneumonia.PloS one · 2014Article
- The Chloride Channel Regulator, Calcium-Activated-1 Is Expressed in Synoviocytes and Articular Chondrocytes in Health and Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry SocietyArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthma is a complex and heterogeneous chronic inflammatory disorder that is associated with mucous cell metaplasia and mucus hypersecretion. Functional genomic analysis indicates that mucous cell metaplasia and mucus hypersecretion depend on members of the calcium-activated chloride channel (CLCA) gene family. It has been reported that the inhibition of CLCAs could relieve the symptoms of asthma. Thus, the mCLCA3 antibody may be a promising strategy to treat allergic diseases such as asthma.
methodsWe constructed asthmatic mouse models of OVA-induced chronic airway inflammatory disorder to study the function of the mCLCA3 antibody. Airway inflammation was measured by HE staining; goblet cell hyperplasia and mucus hypersecretion were detected by PAS staining; muc5ac, IL-13, IFN-γ levels in bronchoalveolar lavage fluid (BALF) were examined by ELISA; Goblet cell apoptosis was measured by TUNEL assay and alcian blue staining; mCLCA3, Bcl-2 and Bax expression were detected by RT-PCR, Western blotting and immunohistochemical analysis.
resultsIn our study, mice treated with mCLCA3 antibody developed fewer pathological changes compared with control mice and asthmatic mice, including a remarkable reduction in airway inflammation, the number of goblet cells and mCLCA3 expression in lung tissue. The levels of muc5ac and IL-13 were significantly reduced in BALF. We also found that the rate of goblet cell apoptosis was increased after treatment with mCLCA3 antibody, which was accompanied by an increase in Bax levels and a decrease in Bcl-2 expression in goblet cells.
conclusionsTaken together, our results indicate that mCLCA3 antibody may have the potential as an effective pharmacotherapy for asthma.
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