Local histamine release after immunological and non-immunological mast cell degranulationin vivo

1984 ◽  
Vol 14 (3-4) ◽  
pp. 417-419 ◽  
Author(s):  
P. W. Ind ◽  
A. Miyatake ◽  
D. J. Heavey ◽  
C. T. Dollery
Keyword(s):  
2008 ◽  
Vol 84 (4) ◽  
pp. 1151-1158 ◽  
Author(s):  
Jacqueline M. Langdon ◽  
John T. Schroeder ◽  
Becky M. Vonakis ◽  
Anja P. Bieneman ◽  
Kristin Chichester ◽  
...  

2018 ◽  
Vol 45 (6) ◽  
pp. 885.e4
Author(s):  
Taylor Curley ◽  
Pedro Boscan ◽  
Douglas Thamm ◽  
Sam Johnson

1979 ◽  
Vol 59 (4) ◽  
pp. 403-407 ◽  
Author(s):  
Takeru Ishikawa ◽  
Tetsuo Shimada ◽  
Nobuko Kessoku ◽  
Masayoshi Kiyoi

1992 ◽  
Vol 73 (3) ◽  
pp. 1093-1101 ◽  
Author(s):  
J. Lucio ◽  
J. D'Brot ◽  
C. B. Guo ◽  
W. M. Abraham ◽  
L. M. Lichtenstein ◽  
...  

Heparin has been shown to act as a competitive inhibitor of inositol 1,4,5-triphosphate (InsP3) receptors in various cell types. Because InsP3 is one of the second messengers involved in stimulus-secretion coupling in mast cells, it is possible that heparin may inhibit mast cell-mediated reactions. Therefore, in allergic sheep, we tested this hypothesis in two mast cell-mediated reactions induced by immunologic and nonimmunologic stimuli: immediate cutaneous reaction (ICR) and acute bronchoconstrictor response (ABR). In 12 sheep allergic to Ascaris suum antigen, the surface area of the skin wheal was determined 20 min after intradermal injection (0.05 ml) of increasing concentrations of specific antigen, compound 48/80, and histamine, without and after pretreatment with heparin (100, 300, or 1,000 U/kg i.v.). Antigen, compound 48/80, and histamine produced concentration-dependent increases in ICR. Heparin “partially” inhibited the ICR to antigen and compound 48/80 in a dose-dependent manner without modifying the ICR to histamine. The heparin preservative benzyl alcohol was ineffective. In 11 additional sheep, specific lung resistance was measured before and after inhalation challenges with antigen, compound 48/80, and histamine without and with aerosol heparin pretreatment (1,000 U/kg). Heparin blocked the antigen- and compound 48/80-induced bronchoconstriction without modifying the airway effects of histamine. In isolated human uterine mast cells, heparin inhibited the anti-immunoglobulin E- but not the calcium ionophore- (A23187) induced histamine release. These data suggest that heparin inhibits the ICR and ABR induced by stimuli that produce immunologic and nonimmunologic mast cell degranulation without attenuating the effects of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)


Blood ◽  
1992 ◽  
Vol 79 (3) ◽  
pp. 708-712 ◽  
Author(s):  
CB Guo ◽  
A Kagey-Sobotka ◽  
LM Lichtenstein ◽  
BS Bochner

Abstract Human mast cells have been purified from uterine tissues, and their surface marker profile and function have been evaluated as part of ongoing studies of mast cell heterogeneity. Using a panel of antibodies, purified uterine mast cells (UMC; 81% +/- 7% purity, n = 10) were analyzed by immunofluorescence and flow cytometry for surface expression of various antigens. Consistent with previous analyses of mast cells from other tissues, UMC expressed HLA class I, IgE, c-kit receptor, CD9, CD33, CD43, CD45, and CD54, while CD11a, CD11b, CD14, CD16, CD23, and CD64 were not detected. Unlike other mast cells, UMC expressed CD11c/CD18 (p150,95) and CD32 (Fc gamma RII). Additional antigens not previously studied on mast cells included the selectin LECAM-1 (Leu-8) and several beta 1 and beta 3 integrins; expression of very late activation antigen-4 (VLA-4) (CD49d/CD29), VLA-5 (CD49e/CD29), and the vitronectin receptor (CD51/CD61) was seen. Functional studies showed that treatment of human umbilical vein endothelial cells with interleukin-1 (5 ng/mL for 4 hours) resulted in a twofold to threefold increase in adhesiveness for UMC. Purification procedures did not alter histamine release responses to anti-IgE or the calcium ionophore A23187, and treatment of UMC with an anti-CD32 monoclonal antibody (IV.3) did not induce histamine release or alter anti-IgE-induced release. These data suggest that UMC may possess unique phenotypic characteristics, and support the concept of mast cell heterogeneity.


1970 ◽  
Vol 46 (7Supplement) ◽  
pp. 831-836 ◽  
Author(s):  
Kenji TASAKA ◽  
Koiti ENDO ◽  
Hidemasa YAMASAKI

1986 ◽  
Vol 34 (3) ◽  
pp. 1333-1336 ◽  
Author(s):  
SHOGO INOSHIRI ◽  
MANAMI SASAKI ◽  
YUKO HIRAI ◽  
HIROSHI KOHDA ◽  
HIDEAKI OTSUKA ◽  
...  
Keyword(s):  

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