title: Airway-specific recruitment of T cells is reduced in a CD26-deficient F344 rat substrain.
abstract: Asthma is a chronic inflammatory disease affecting the airways. Increased levels of T cells are found in the lungs after the induction of an allergic-like inflammation in rats, and flow cytometry studies have shown that these levels are reduced in CD26-deficient rats. However, the precise anatomical sites where these newly recruited T cells appear primarily are unknown. Therefore, we quantified the distribution of T cells in lung parenchyma as well as in large, medium and small airways using immunohistochemical stainings combined with morphometric analyses. The number of T cells increased after the induction of an allergic-like inflammation. However, the differences between CD26-deficient and wild-type rats were not attributable to different cell numbers in the lung parenchyma, but the medium- and large-sized bronchi revealed significantly fewer T cells in CD26-deficient rats. These sites of T cell recruitment were screened further using immunohistochemistry and quantitative real-time polymerase chain reaction with regard to two hypotheses: (i) involvement of the nervous system or (ii) expression of chemokines with properties of a T cell attractor. No topographical association was found between nerves and T cells, but a differential transcription of chemokines was revealed in bronchi and parenchyma. Thus, the site-specific recruitment of T cells appears to be a process mediated by chemokines rather than nerve-T cell interactions. In conclusion, this is the first report showing a differential site-specific recruitment of T cells to the bronchi in a CD26-deficient rat substrain during an asthma-like inflammation.
authors.affiliation: Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Schade
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
authors.forename: A
authors.initials: A
authors.lastname: Kehlen
authors.forename: T Z
authors.initials: TZ
authors.lastname: Veres
authors.forename: M
authors.initials: M
authors.lastname: Stephan
authors.forename: R
authors.initials: R
authors.lastname: Pabst
authors.forename: S
authors.initials: S
authors.lastname: von Hörsten
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology*; D001980:Bronchi / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D018819:Dipeptidyl Peptidase 4 / Q000172:deficiency* / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007150:Immunohistochemistry; D008168:Lung / Q000276:immunology*; D018655:Lymphocyte Count; D008297:Male; D023421:Models, Animal; D010047:Ovalbumin; D051381:Rats; D011916:Rats, Inbred F344; D011922:Rats, Mutant Strains; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D018709:Statistics, Nonparametric; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D007073:Immunoglobulin E; D010047:Ovalbumin; D018819:Dipeptidyl Peptidase 4