ArticleInfection and immunity2003
Analysis of the role of Bphs/Hrh1 in the genetic control of responsiveness to pertussis toxin.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- A genetic locus complements resistance to Bordetella pertussis-induced histamine sensitization.Communications biology · 2023Article
- G proteins Gαi1/3 are critical targets for Bordetella pertussis toxin-induced vasoactive amine sensitization.Infection and immunity · 2014Article
- Endothelial histamine H1 receptor signaling reduces blood-brain barrier permeability and susceptibility to autoimmune encephalomyelitis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- von-Willebrand factor influences blood brain barrier permeability and brain inflammation in experimental allergic encephalomyelitis.The American journal of pathology · 2008Article
- Autoimmune disease-associated histamine receptor H1 alleles exhibit differential protein trafficking and cell surface expression.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Histamine receptor H1 is required for TCR-mediated p38 MAPK activation and optimal IFN-gamma production in mice.The Journal of clinical investigation · 2007Article
- Attenuation of Th1 effector cell responses and susceptibility to experimental allergic encephalomyelitis in histamine H2 receptor knockout mice is due to dysregulation of cytokine production by antigen-presenting cells.The American journal of pathology · 2004Article
- Temporal expression of pertussis toxin and Ptl secretion proteins by Bordetella pertussis.Journal of bacteriology · 2004Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
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 H(1) 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.
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