Allergic airway inflammation induces migration of mast cell populations into the mouse airway.
Mast cells (MCs) and airway nerves play an important role in allergic asthma. However, little is known about the MCs and their interaction with airway nerves during allergic airway inflammation. This study aims to investigate the distribution and proliferation of MC populations in different lung compartments, along with the association of mast cells with nerve endings, using a house dust mite (HDM) model for allergic airway inflammation. BALB/c mice were exposed to HDM extract intranasally (25 μg/50 μl) for 5 consecutive days a week over 7 weeks. Immunofluorescence and Edu stains were used to examine the colocalisation of MCs and nerves and the proliferation of MCs, respectively. HDM treatment caused an increased migration of MCs into bronchi, alveolar parenchyma and airway vessels. The proportions of tryptase-chymase expressing MC (MCTC) increased significantly in the bronchi and the alveolar parenchyma but not in the vascular tissues, by allergic airway inflammation. The association of MCs with nerves was found only in the bronchi and there were no changes in comparison of controls to HDM-treated animals. The present study shows a strong migration of tryptase expressing MC (MCT) and MCTCinto the bronchi and the alveolar parenchyma, as well as of MCTin the vascular compartment under HDM treatment. This supports the hypothesis that these mast cell populations may contribute to allergic airway inflammation.
Department of Experimental Pneumology and Allergology, Saarland University Hospital and Saarland University Faculty of Medicine, Kirrberger Strasse, Geb. 61.4, 66421, Homburg/Saar, Germany.
David
D
Schmit
Department of Experimental Pneumology and Allergology, Saarland University Hospital and Saarland University Faculty of Medicine, Kirrberger Strasse, Geb. 61.4, 66421, Homburg/Saar, Germany.
Duc Dung
DD
Le
Department of Experimental Pneumology and Allergology, Saarland University Hospital and Saarland University Faculty of Medicine, Kirrberger Strasse, Geb. 61.4, 66421, Homburg/Saar, Germany.
Sebastian
S
Heck
Institute of Medical Microbiology and Hygiene, Saarland University Hospital, Homburg, Germany.
Markus
M
Bischoff
Institute of Anatomy and Cell Biology, Saarland University Hospital, Homburg, Germany.
Thomas
T
Tschernig
Department of Internal Medicine V, Saarland University Hospital, Homburg, Germany.
Christian
C
Herr
Department of Internal Medicine V, Saarland University Hospital, Homburg, Germany.
Christoph
C
Beisswenger
Center for Internal Medicine and Dermatology, Division of General Internal and Psychosomatic Medicine, Charité - Universitätsmedizin, Berlin, Germany.
Peter
P
Kobelt
Department of Internal Medicine V, Saarland University Hospital, Homburg, Germany.
Phillipp Moritz
PM
Lepper
Thoracic Medicine, National Heart & Lung Institute, Imperial College, London, UK.
Kian Fan
KF
Chung
Department of Internal Medicine V, Saarland University Hospital, Homburg, Germany.
Robert
R
Bals
Department of Experimental Pneumology and Allergology, Saarland University Hospital and Saarland University Faculty of Medicine, Kirrberger Strasse, Geb. 61.4, 66421, Homburg/Saar, Germany. Thai.Dinh@uniklinikum-saarland.de.|Department of Internal Medicine V, Saarland University Hospital, Homburg, Germany. Thai.Dinh@uniklinikum-saarland.de.
Quoc Thai
QT
Dinh
D000818:Animals; D002465:Cell Movement; D049109:Cell Proliferation; D005260:Female; D006967:Hypersensitivity / Q000469:parasitology / Q000473:pathology*; D007249:Inflammation / Q000473:pathology*; D008168:Lung / Q000294:innervation / Q000469:parasitology / Q000473:pathology*; D008807:Mice, Inbred BALB C; D009417:Nerve Tissue / Q000473:pathology; D039981:Pyroglyphidae / Q000502:physiology
Allergic airway inflammation; Chymase; Mast cells; Neuroimmune Interaction; Tryptase