| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of
* Cellular Pharmacology and
Dermatology, and
Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine, Sendai, Japan; and
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada
We prepared a model of experimental peritonitis by introducing Escherichia coli into the peritoneal cavity of the histamine-deficient mice generated by a disruption of the gene for histidine decarboxylase (HDC), the unique histamine-synthesizing enzyme. When we inoculated E. coli into the peritoneal cavities of the HDC-/- (histamine-deficient) mice, they eliminated E. coli more efficiently than did the wild-type mice. Histamine was released efficiently from the peritoneal cells after E. coli inoculation in HDC+/+ mice, although only trace amounts were detected in the peritoneal cells of HDC-/- mice. Two histamine agonists (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)hepatanecarboxamide (H1) and dimaprit (H2)) impaired the clearance of E. coli from the peritoneal cavity in HDC-/- mice, suggesting that the activation of both H1 and H2 receptors suppresses the clearance. In contrast, two kinds of H1 and H2 receptor antagonists, cimetidine and pyrilamine, promoted the clearance of E. coli in HDC+/+ mice. Phagocytosis appeared to be enhanced in HDC-/- mice, since the number of neutrophils in the peritoneal cavity of HDC-/- mice was markedly increased. This enhanced recruitment of neutrophils was suppressed in the presence of the histamine agonists, 6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)hepatanecarboxamide and dimaprit. In this report histamine was first shown to be an important mediator in an E. coli infectious peritonitis model, causing a delay in the elimination of bacteria. This also raised the possibility of the use of antihistamine drugs for bacterial infection.
This article has been cited by other articles:
|
|
 |
|
  I. Mulero, M. P. Sepulcre, J. Meseguer, A. Garcia-Ayala, and V. Mulero Histamine is stored in mast cells of most evolutionarily advanced fish and regulates the fish inflammatory response PNAS, December 4, 2007; 104(49): 19434 - 19439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Thakurdas, E. Melicoff, L. Sansores-Garcia, D. C. Moreira, Y. Petrova, R. L. Stevens, and R. Adachi The Mast Cell-restricted Tryptase mMCP-6 Has a Critical Immunoprotective Role in Bacterial Infections J. Biol. Chem., July 20, 2007; 282(29): 20809 - 20815. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. R. Hoffman and S. I. Miller The systems biology of infection in animal models bears fruit PNAS, June 20, 2006; 103(25): 9377 - 9378. [Full Text] [PDF]
|
|
|
|
|
|
S. A. Handley, P. H. Dube, and V. L. Miller From the Cover: Histamine signaling through the H2 receptor in the Peyer's patch is important for controlling Yersinia enterocolitica infection PNAS, June 13, 2006; 103(24): 9268 - 9273. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Musio, B. Gallo, S. Scabeni, M. Lapilla, P. L. Poliani, G. Matarese, H. Ohtsu, S. J. Galli, R. Mantegazza, L. Steinman, et al. A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-Deficient Mice J. Immunol., January 1, 2006; 176(1): 17 - 26. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. T. Kozma, G. Losonczy, M. Keszei, Z. Komlosi, E. Buzas, E. Pallinger, J. Appel, T. Szabo, P. Magyar, A. Falus, et al. Histamine deficiency in gene-targeted mice strongly reduces antigen-induced airway hyper-responsiveness, eosinophilia and allergen-specific IgE Int. Immunol., August 1, 2003; 15(8): 963 - 973. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
