ArticleInfection and immunity2014
Epithelial anion transporter pendrin contributes to inflammatory lung pathology in mouse models of Bordetella pertussis infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Epithelial plasma membrane transporters as drug targets.Physiological reviews · 2026Review
- Pendrin inhibition is associated with protective effect of prone positioning in a ventilator-induced lung injury mouse model.Scientific reports · 2025Article
- MASP1 modulation as a novel therapeutic target in severe pediatric pertussis: insights from a multi-omics approach.Infection and immunity · 2025Article
- Solute Carrier Family 26 Member 4 (SLC26A4), A Potential Therapeutic Target for Asthma.Journal of respiratory biology and translational medicine · 2024Article
- Mechanism of anion exchange and small-molecule inhibition of pendrin.Nature communications · 2024Article
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- DNA-Dependent Interferon Induction and Lung Inflammation inJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Article
- Live attenuated pertussis vaccine for prevention and treatment of allergic airway inflammation in mice.NPJ vaccines · 2022Article
- Atmospheric Reactive Oxygen Species and Some Aspects of the Antiviral Protection at the Respiratory Epithelium.Biochemistry (Moscow) Supplement. Series B, Biomedical chemistry · 2022Article
- Pharmacological targeting of host chaperones protects from pertussis toxin in vitro and in vivo.Scientific reports · 2021Article
- Article
- Age-Dependent Effects of Type I and Type III IFNs in the Pathogenesis ofJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Inhibition of Pendrin by a small molecule reduces Lipopolysaccharide-induced acute Lung Injury.Theranostics · 2020Article
- Synthesis and evaluation of tetrahydropyrazolopyridine inhibitors of anion exchange protein SLC26A4 (pendrin).Bioorganic & medicinal chemistry letters · 2019Article
- Review
- Airway surface liquid acidification initiates host defense abnormalities in Cystic Fibrosis.Scientific reports · 2019Article
- Interleukin-Mediated Pendrin Transcriptional Regulation in Airway and Esophageal Epithelia.International journal of molecular sciences · 2019Review
- Role of Major Toxin Virulence Factors in Pertussis Infection and Disease Pathogenesis.Advances in experimental medicine and biology · 2019Article
- Fatal Pertussis in the Neonatal Mouse Model Is Associated with Pertussis Toxin-Mediated Pathology beyond the Airways.Infection and immunity · 2017Article
- Interleukin-13 increases pendrin abundance to the cell surface in bronchial NCI-H292 cells via Rho/actin signaling.Pflugers Archiv : European journal of physiology · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Pertussis disease, characterized by severe and prolonged coughing episodes, can progress to a critical stage with pulmonary inflammation and death in young infants. However, there are currently no effective treatments for pertussis. We previously studied the role of pertussis toxin (PT), an important Bordetella pertussis virulence factor, in lung transcriptional responses to B. pertussis infection in mouse models. One of the genes most highly upregulated in a PT-dependent manner encodes an epithelial transporter of bicarbonate, chloride, and thiocyanate, named pendrin, that contributes to asthma pathology. In this study, we found that pendrin expression is upregulated at both gene and protein levels in the lungs of B. pertussis-infected mice. Pendrin upregulation is associated with PT production by the bacteria and with interleukin-17A (IL-17A) production by the host. B. pertussis-infected pendrin knockout (KO) mice had higher lung bacterial loads than infected pendrin-expressing mice but had significantly reduced levels of lung inflammatory pathology. However, reduced pathology did not correlate with reduced inflammatory cytokine expression. Infected pendrin KO mice had higher levels of inflammatory cytokines and chemokines than infected pendrin-expressing mice, suggesting that these inflammatory mediators are less active in the airways in the absence of pendrin. In addition, treatment of B. pertussis-infected mice with the carbonic anhydrase inhibitor acetazolamide reduced lung inflammatory pathology without affecting pendrin synthesis or bacterial loads. Together these data suggest that PT contributes to pertussis pathology through the upregulation of pendrin, which promotes conditions favoring inflammatory pathology. Therefore, pendrin may represent a novel therapeutic target for treatment of pertussis disease.
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