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Infection and Immunity, March 2003, p. 1281-1287, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1281-1287.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Analysis of the Role of Bphs/Hrh1 in the Genetic Control of Responsiveness to Pertussis Toxin

Jian Feng Gao,1 Stanford B. Call,1 Parley D. Fillmore,2 Takeshi Watanabe,3 Nathan D. Meeker,4 and Cory Teuscher1*

Department of Medicine, University of Vermont School of Medicine, Burlington, Vermont 05405,1 Department of Veterinary Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802,2 Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan,3 Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 191044

Received 18 September 2002/ Returned for modification 15 November 2002/ Accepted 4 December 2002

In vivo intoxication with Bordetella pertussis toxin (PTX) elicits a variety of physiological responses including a marked leukocytosis, disruption of glucose regulation, adjuvant activity, alterations in vascular function, hypersensitivity to vasoactive agents, and death. We recently identified Bphs, the locus controlling PTX-induced hypersensitivity to the vasoactive amine histamine, as the histamine H1 receptor (Hrh1). In this study Bphs congenic mice and mice with a disrupted Hrh1 gene were used to examine the role of Bphs/Hrh1 in the genetic control of susceptibility to a number of phenotypes elicited following in vivo intoxication. We report that the contribution of Bphs/Hrh1 to the overall genetic control of responsiveness to PTX is restricted to susceptibility to histamine hypersensitivity and enhancement of antigen-specific delayed-type hypersensitivity responses. Furthermore, the genetic contribution of Bphs/Hrh1 to vasoactive amine sensitization is specific for histamine, since hypersensitivity to serotonin was unaffected by Bphs/Hrh1. Bphs/Hrh1 also did not significantly influence susceptibility to the lethal effects, the leukocytosis response, disruption of glucose regulation, and histamine-independent increases in vascular permeability associated with in vivo intoxication. Nevertheless, significant interstrain differences in susceptibility to the lethal effects of PTX and leukocytosis response were observed. These results indicate that the phenotypic variation in responsiveness to PTX reflects the genetic control of distinct intermediate phenotypes rather than allelic variation in genes controlling overall susceptibility to intoxication.

* Corresponding author. Mailing address: C317 Given Medical Bldg., University of Vermont, Burlington, VT 05405. Phone: (802) 656-3270. Fax: (802) 656-3854. E-mail: cteusche{at}zoo.uvm.edu.

Editor: J. T. Barbieri

Infection and Immunity, March 2003, p. 1281-1287, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1281-1287.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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