ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2019
Lung infection caused by Pseudomonas aeruginosa in a CD26/DPP4 deficient F344 rat model.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Bridging bench and bedside: translational omics ofEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Exploring microorganism-host interactions: Emerging organoid models and analytical approaches.mLife · 2026Review
- Genotypic and phenotypic characterization of Pseudomonas aeruginosa PAV112: a virulent clinical strain causing severe pneumonia and lethal sepsis in a murine infection model.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026Article
- Biofluid-derived exosomes as next-generation biotherapeutic platforms to combat multidrug-resistant bacterial infections.Regenerative biomaterials · 2026Review
- NK cell-derived exosomes improved lung injury in mouse model of Pseudomonas aeruginosa lung infection.The journal of physiological sciences : JPS · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPseudomonas aeruginosa (PA) is the most important opportunistic pathogen in causing nosocomial infections and, furthermore, poses a permanent threat for severe chronic infections in patients with cystic fibrosis or COPD. The transmembrane protein CD26 with dipeptidyl peptidase-4 (DPP4) activity shows an increased expression in inflamed tissue. We tested whether CD26/DPP4 deficiency leads to reduced inflammation and decreased structural damage when infected with PA.
methodsCD26/DPP4
resultsCompared to saline treated controls, in both infected groups (1) the acinar airspace was significantly increased, (2) the volume density of the alveolar epithelium was significantly decreased, (3) the septal thickness was significantly reduced, (4) more than 40% of the alveolar epithelial surface was damaged, and up to 36% of the epithelial surface was covered with edema. In infected CD26
conclusionsCD26/DPP4 deficiency resulted in reduced pulmonary edema under sublethal PA infection, implicating a role for CD26 in infection progression. The partly pronounced structural damage may mask further possible influences of CD26 on the inflammatory response.
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Registered trials
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