title: Differential OVA-induced pulmonary inflammation and unspecific reaction in Dark Agouti (DA) rats contingent on CD26/DPPIV deficiency.
abstract: Many disease models have shown that, within the species rat, different strains are differentially susceptible to asthma-induced inflammation depending on the genetic background. Likewise, CD26/DPPIV-deficiency in asthmatic F344 rats has been shown to result in a less pronounced inflammation and in increased Treg cell influx into the lung compared to wild-types. The aim of the present study was to investigate whether the genetic background of the animals interferes with CD26/DPPIV-deficiency in a model of allergic-like inflammation, or whether the deficiency per se is the predominant regulator of the inflammation. Therefore, we hypothesised that CD26/DPPIV-deficient Dark Agouti (DA) rats also exhibit a less pronounced ovalbumin (OVA)-induced inflammation compared to wild-types. After sensitisation with OVA, Al(OH)3 and heat-killed Bordetella pertussis bacilli, animals were challenged three times with 5% aerosolized OVA at intervals of 24h, i.e., on three consecutive days. 24h after the third challenge, animals were sacrificed and examined. In both wild-type and CD26/DPPIV-deficient rat groups, asthma induction led to (1) lung inflammation, (2) significantly increased eosinophil infiltration in the BALF, (3) significantly increased IgE serum levels, (4) a significant increase of inflammatory cytokines, (5) a significant increase of different T cell populations in the lungs and in their draining lymph nodes, as well as to (6) a significantly higher number of all T lymphocyte subtypes in the blood. Thus, the degree of the OVA-induced Th2-driven pulmonary inflammation was similarly pronounced in both wild-type and CD26/DPPIV-deficient DA rats.
authors.affiliation: Institute of Functional and Applied Anatomy, Hannover Medical School, Germany.
authors.forename: Tihana
authors.initials: T
authors.lastname: Tasic
authors.affiliation: Clinic for Psychosomatics and Psychotherapy, Hannover Medical School, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Stephan
authors.affiliation: Department for Experimental Therapy, Franz-Penzoldt-Center, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
authors.forename: Stephan
authors.initials: S
authors.lastname: von Hörsten
authors.affiliation: Institute of Immunomorphology, Hannover Medical School, Germany.
authors.forename: Reinhard
authors.initials: R
authors.lastname: Pabst
authors.affiliation: Institute of Functional and Applied Anatomy, Hannover Medical School, Germany. Electronic address: Schmiedl.Andreas@mh-hannover.de.
authors.forename: Andreas
authors.initials: A
authors.lastname: Schmiedl
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000235:genetics / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D018819:Dipeptidyl Peptidase 4 / Q000172:deficiency* / Q000235:genetics; D004195:Disease Models, Animal; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D018836:Inflammation Mediators / Q000378:metabolism; D008198:Lymph Nodes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018655:Lymphocyte Count; D010047:Ovalbumin / Q000009:adverse effects; D011014:Pneumonia / Q000139:chemically induced / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D051381:Rats; D055647:Rats, Transgenic; D012720:Severity of Illness Index; D013045:Species Specificity; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007073:Immunoglobulin E; D010047:Ovalbumin; D018819:Dipeptidyl Peptidase 4
keywords: Asthma; CD26/DPPIV; CD26/DPPIV-deficiency; Dark Agouti rats; OVA