ArticlePhysiological reports2013
Effects of dipeptidyl peptidase-4 inhibition in an animal model of experimental asthma: a matter of dose, route, and time.
Article in Physiological reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- l-Arginine supplementation in severe asthma.JCI insight · 2020Trial
- Development of the dipeptidyl peptidase 4 family and its association with lung diseases: a narrative review.Journal of thoracic disease · 2023Review
- An update on the diagnostic biomarkers for asthma.Journal of family medicine and primary care · 2021Review
- Expansion of different subpopulations of CD26Scientific reports · 2019Article
- Association between Dipeptidyl Peptidase-4 Inhibitors and Allergic Rhinitis in Asian Patients with Diabetes.International journal of environmental research and public health · 2019Article
- CD26 and Asthma: a Comprehensive Review.Clinical reviews in allergy & immunology · 2019Review
- Asthma Biomarkers: Do They Bring Precision Medicine Closer to the Clinic?Allergy, asthma & immunology research · 2017Review
- Asthma biomarkers in the age of biologics.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2017Review
- Biomarkers in Severe Asthma.Immunology and allergy clinics of North America · 2016Review
- Cut to the chase: a review of CD26/dipeptidyl peptidase-4's (DPP4) entanglement in the immune system.Clinical and experimental immunology · 2016Review
- Dipeptidyl peptidase-4 is highly expressed in bronchial epithelial cells of untreated asthma and it increases cell proliferation along with fibronectin production in airway constitutive cells.Respiratory research · 2016Article
- A case of vildagliptin-induced interstitial pneumonia.Respiratory medicine case reports · 2016Article
- Exposure to Allergen Causes Changes in NTS Neural Activities after Intratracheal Capsaicin Application, in Endocannabinoid Levels and in the Glia Morphology of NTS.BioMed research international · 2015Article
- Sitagliptin-induced diffuse alveolar hemorrhage mimicking pulmonary edema.Journal of family medicine and primary careArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CD26-associated enzymatic activity of dipeptidyl peptidase-4 (DPP4) as well as the recruitment of CD26(+) T cells increase under allergic airway inflammation. Furthermore, genetic deficiency of CD26/DPP4 exerts protective effects in experimental asthma. Therefore, CD26/DPP4 might represent a novel therapeutic target in asthma. To study the effects of pharmacological inhibition of DPP4 on allergic airway inflammation the DPP4-inhibitor isoleucine thiazolidide was tested using different doses at different time points (at sensitization, immediately before and simultaneously with the allergen challenge, as well as continuously via drinking water), and different routes (intraperitoneal, oral, and by inhalation). Allergic-like airway inflammation was induced in Fischer 344 rats (Charles River) sensitized against ovalbumin (OVA) using OVA aerosols. Intraperitoneal application of the DPP4 inhibitor showed effects neither at sensitization nor at challenge, whereas a continuous application via drinking water using high doses of the inhibitor led to an aggravation of the histomorphological signs of airway inflammation. In contrast, aerosolization of the DPP4 inhibitor simultaneously with the allergen significantly reduced airway hyperresponsiveness and ameliorated histopathological signs compared to controls. In addition, this treatment resulted in increased mRNA levels of surfactant proteins, suggesting an involvement of DPP4 inhibitors in surfactant metabolism in OVA-challenged rats. Continuous systemic inhibition of DPP4 via the oral route aggravates allergic airway inflammation. In contrast, topical inhibition of DPP4 exerts potential protective effects, and further research in humans is needed.
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Registered trials
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