A genetic locus complements resistance to Bordetella pertussis-induced histamine sensitization. Commun Biol. 2023;6(1):244
Animals, Mice, Bordetella pertussis, Histamine, Pertussis Toxin, Signal Transduction, Complement System Proteins, Genetic Loci, Membrane Glycoproteins, Intracellular Signaling Peptides and Proteins, Ribonucleoproteins
Commun Biol. 2023;6(1):244
Anna Tyler and J. Matthew Mahoney were supported by a grant (R21 LM012615; ALT and JMM) from the National Library of Medicine and a grant (P20GM130454; JMM) from the National Institute of General Medical Sciences of the United States National Institutes of Health (NIH). Abbas Raza, Dimitry Krementsov, Elizabeth Blankenhorn, and Cory Teuscher were supported by grants from the NIH and the National Multiple Sclerosis Society (NMSS). Elissa Chesler, Vivek Philip and the Mouse Phenome Database are supported by R01 DA028420. Robyn Ball and Elissa Chesler are supported by U54 OD030187. Dimitry Krementsov was supported by NIH grants from the National Institute of Neurological Disease and Stroke (R01 NS097596), National Institute of Allergy and Infectious Disease (R21 AI145306), and the NMSS (RR-1602-07780). We would like to thank Keith Sheppard and Molly Bogue for their assistance with genomic imputation as well as the Mouse Phenome Database web resource (RRID:SCR_003212) and the JAX Cancer Center Support Grant.
Histamine plays pivotal role in normal physiology and dysregulated production of histamine or signaling through histamine receptors (HRH) can promote pathology. Previously, we showed that Bordetella pertussis or pertussis toxin can induce histamine sensitization in laboratory inbred mice and is genetically controlled by Hrh1/HRH1. HRH1 allotypes differ at three amino acid residues with P