Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (15)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Kozma, G. T.
Right arrow Articles by Szalai, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kozma, G. T.
Right arrow Articles by Szalai, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 15, No. 8, pp. 963-973, August 2003
© 2003 Japanese Society for Immunology

Histamine deficiency in gene-targeted mice strongly reduces antigen-induced airway hyper-responsiveness, eosinophilia and allergen-specific IgE

Gergely T. Kozma1, György Losonczy2, Márton Keszei1, Zsolt Komlósi2, Edit Buzás1, Éva Pállinger3, Judith Appel2, Teréz Szabó4, Pál Magyar2, András Falus1,3 and Csaba Szalai3,4

1 Department of Genetics, Cell and Immunobiology, Semmelweis University Medical School, Budapest 1445, Hungary 2 Department of Pulmonology, Semmelweis University Budapest, Diosarok u 1/c, Hungary 3 Molecular Immunology Research Group, Hungarian Academy of Sciences Semmelweis University, Budapest 1089, Hungary 4 Heim Pál Pediatric Hospital Budapest, Budapest 1958, Hungary

Correspondence to: A. Falus, Department of Genetics, Cell and Immunobiology, Semmelweis University Medical School, PO Box 370, Nagyvárad tér 4, 1445 Budapest, Hungary. E-mail: faland{at}dgci.sote.hu
Transmitting editor: W. Knapp

Histamine is an important mediator released from activated mast cells provoked by allergen and has a substantial role in the pathophysiology of asthma. However, several lines of evidence indicate that histamine could also have important functions in the regulation of basic cell biological processes. We have used histidine decarboxylase gene-targeted (HDC-KO) mice, lacking histamine, to investigate the effect of histamine deficiency in an animal model of asthma. Our previous investigations revealed that HDC-KO mice had fewer mast cells with reduced granular content and defective degranulation characteristics. Ovalbumin (OVA)-sensitized and challenged HDC-KO mice had significantly reduced airway hyper-responsiveness, lung inflammation, bronchoalveolar lavage eosinophilia, and OVA-specific IgE compared with congenic wild-type littermates treated in the same way. Comparing the expression profiles of cytokines, the levels of IL-1{alpha}, IL-1ß, IL-4, IL-5, IL-6 and IFN-{gamma} were significantly lower in the HDC-KO mice in asthmatic late phase, indicating a significantly altered immune response to OVA provocation and challenge. Evaluation of chemokine gene expression revealed that OVA treatment caused elevation of both Th1- and Th2-type chemokines in wild-type mice, while the chemokine expression was polarized toward a Th1 response in HDC-KO mice. According to our results we can suggest that the possible causes of the reduced asthma symptoms in the HDC-KO mice may be the imperfect mast and eosinophil cell system, and an altered immune response to OVA provocation and challenge.

Keywords: chemokine, inflammation, knockout, mast cell, Th1/Th2 cell


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Int ImmunolHome page
G. Tolgyesi, V. Molnar, A. F. Semsei, P. Kiszel, I. Ungvari, P. Pocza, Z. Wiener, Z. I. Komlosi, L. Kunos, G. Galffy, et al.
Gene expression profiling of experimental asthma reveals a possible role of paraoxonase-1 in the disease
Int. Immunol., August 1, 2009; 21(8): 967 - 975.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. Koncz, M. Pasztoi, M. Mazan, F. Fazakas, E. Buzas, A. Falus, and G. Nagy
Nitric Oxide Mediates T Cell Cytokine Production and Signal Transduction in Histidine Decarboxylase Knockout Mice
J. Immunol., November 15, 2007; 179(10): 6613 - 6619.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
X. Xu, D. Zhang, H. Zhang, P. J. Wolters, N. P. Killeen, B. M. Sullivan, R. M. Locksley, C. A. Lowell, and G. H. Caughey
Neutrophil histamine contributes to inflammation in mycoplasma pneumonia
J. Exp. Med., December 25, 2006; 203(13): 2907 - 2917.
[Abstract] [Full Text] [PDF]

Home page
 J Biomol ScreenHome page
E. M. August, L. Patnaude, J. Hopkins, J. Studts, E. Gautschi, A. Shrutkowski, A. Kronkaitis, M. Brown, A. Kabcenell, and D. Rajotte
Development of a High-Throughput Assay to Measure Histidine Decarboxylase Activity
J Biomol Screen, October 1, 2006; 11(7): 816 - 821.
[Abstract] [PDF]

Home page
 J. Immunol.Home page
P. J. Dunford, N. O'Donnell, J. P. Riley, K. N. Williams, L. Karlsson, and R. L. Thurmond
The Histamine H4 Receptor Mediates Allergic Airway Inflammation by Regulating the Activation of CD4+ T Cells.
J. Immunol., June 1, 2006; 176(11): 7062 - 7070.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.