title: Steroid Treatment Reduces Allergic Airway Inflammation and Does Not Alter the Increased Numbers of Dendritic Cells and Calcitonin Gene-Related Peptide-Expressing Neurons in Airway Sensory Ganglia.
abstract: OBJECTIVE
  Our previous data demonstrated that allergic airway inflammation induces migration of dendritic cells (DC) into airway sensory jugular and nodose ganglia (jugular-nodose ganglion complex; JNC). Here we investigated the effects of steroid treatment regarding the expression and migration of DC and calcitonin gene-related peptide (CGRP)-immunoreactive neurons of vagal sensory ganglia during allergic airway inflammation.
  
  
  METHODS
  A house dust mite (HDM) model for allergic airway inflammation was used. The mice received 0.3 mg fluticasone propionate per kilogram of body weight in the last 9 days. JNC slices were analyzed on MHC II, the neuronal marker PGP9.5, and the neuropeptide CGRP.
  
  
  RESULTS
  Allergic airway inflammation increased the numbers of DC and CGRP-expressing neurons in the JNC significantly in comparison to the controls (DC/neurons: HDM 44.58 ± 1.6% vs. saline 33.29 ± 1.6%, p < 0.05; CGRP-positive neurons/total neurons: HDM 30.65 ± 1.9% vs. saline 19.49 ± 2.3%, p < 0.05). Steroid treatment did not have any effect on the numbers of DC and CGRP-expressing neurons in the JNC compared to HDM-treated mice.
  
  
  CONCLUSIONS
  The present findings indicate an important role of DC and CGRP-containing neurons in the pathogenesis of allergic airway inflammation. However, steroid treatment did not have an effect on the population of DC and neurons displaying CGRP in the JNC, whereas steroid treatment was found to suppress allergic airway inflammation.
authors.affiliation: Department of Internal Medicine V - Experimental Pneumology and Allergology, Saarland University Faculty of Medicine, Homburg, Germany.
authors.forename: Duc Dung
authors.initials: DD
authors.lastname: Le
authors.forename: Ulrike
authors.initials: U
authors.lastname: Funck
authors.forename: Sabine
authors.initials: S
authors.lastname: Wronski
authors.forename: Sebastian
authors.initials: S
authors.lastname: Heck
authors.forename: Thomas
authors.initials: T
authors.lastname: Tschernig
authors.forename: Markus
authors.initials: M
authors.lastname: Bischoff
authors.forename: Martina
authors.initials: M
authors.lastname: Sester
authors.forename: Christian
authors.initials: C
authors.lastname: Herr
authors.forename: Robert
authors.initials: R
authors.lastname: Bals
authors.forename: Tobias
authors.initials: T
authors.lastname: Welte
authors.forename: Armin
authors.initials: A
authors.lastname: Braun
authors.forename: Quoc Thai
authors.initials: QT
authors.lastname: Dinh
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism*; D003713:Dendritic Cells / Q000187:drug effects*; D004195:Disease Models, Animal; D005260:Female; D000068298:Fluticasone / Q000633:toxicity; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D066298:In Vitro Techniques; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000187:drug effects*; D009620:Nodose Ganglion / Q000473:pathology*; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D013256:Steroids / Q000627:therapeutic use*; D043222:Ubiquitin Thiolesterase / Q000378:metabolism
chemical_list: D000949:Histocompatibility Antigens Class II; D013256:Steroids; D000068298:Fluticasone; D043222:Ubiquitin Thiolesterase; C496976:Uchl1 protein, mouse; D015740:Calcitonin Gene-Related Peptide