Control Mechanisms of Histamine Release from Human Basophils in vitro: The Role of Phospholipase A2 and of Lipoxygenase Metabolites

1981 ◽  
Vol 66 (1) ◽  
pp. 144-148 ◽  
Author(s):  
Gianni Marone ◽  
Anne Kagey-Sobotka ◽  
Lawrence M. Lichtenstein
Keyword(s):  
Histamine Release ◽  
Phospholipase A ◽  
Control Mechanisms ◽  
Human Basophils

Role of nitric oxide in histamine release from human basophils and rat peritoneal mast cells

2001 ◽  
Vol 425 (3) ◽  
pp. 229-238 ◽  
Author(s):  
Kheng H. Peh ◽  
Andrew Moulson ◽  
Beatrice Y.C. Wan ◽  
El-Sayed K. Assem ◽  
Frederick L. Pearce
Keyword(s):  
Nitric Oxide ◽  
Mast Cells ◽  
Histamine Release ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Human Basophils

scholarly journals The inhibitory effect of 3,3',4,5'-tetrahydroxystilbene, a constituent of Cassia garrettiana, on anti-IgE-induced histamine release from human basophils in vitro.

1991 ◽  
Vol 39 (3) ◽  
pp. 805-807 ◽  
Author(s):  
Yoshihiko INAMORI ◽  
Masafumi OGAWA ◽  
Hiroshi TSUJIBO ◽  
Kimiye BABA ◽  
Mitsugi KOZAWA ◽  
...  
Keyword(s):  
Histamine Release ◽  
Inhibitory Effect ◽  
Human Basophils

scholarly journals Mast cells are responsible for the lack of anti-inflammatory effects of morphine in CBA mice

2004 ◽  
Vol 13 (5-6) ◽  
pp. 365-368 ◽  
Author(s):  
Elzbieta Stankiewicz ◽  
Ewa Wypasek ◽  
Barbara Plytycz
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Swiss Mice ◽  
Cba Mice ◽  
Peritoneal Mast Cells ◽  
Anti Inflammatory ◽  
Zymosan Peritonitis

BACKGROUND and aim: Morphine co-injection has anti-inflammatory effects on zymosan-induced peritonitis in several strains of mice except that of CBA. As peritoneal mast cells (pMCs) are much more numerous in CBA mice than in SWISS mice, the role of pMCs in morphine-modulated zymosan peritonitis is compared in CBA and SWISS males.Methods: pMCs were treatedin vitrowith morphine or C48/80 for comparison of histamine release.In vivoaccumulation of leukocytes and histamine in peritoneal exudate were recorded after intraperitoneal injection with morphine, zymosan, or zymosan plus morphine.Results and conclusion: Morphine induces histamine release by pMCs from CBA mice but not SWISS mice.In vivomorphine-induced peritonitis is stronger in CBA mice than SWISS mice. Corollary, morphine anti-inflammatory effects on zymosan peritonitis are reversed in CBA mice by its pro-inflammatory action through CBA pMCs.

scholarly journals Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon.

1977 ◽  
Vol 145 (4) ◽  
pp. 892-906 ◽  
Author(s):  
S Ida ◽  
J J Hooks ◽  
R P Siraganian ◽  
A L Notkins
Keyword(s):  
Tissue Culture ◽  
Antiviral Activity ◽  
Histamine Release ◽  
Influenza A ◽  
Culture Fluid ◽  
Soluble Factor ◽  
Release Histamine ◽  
Ige Mediated ◽  
Human Basophils

Human leukocytes maintained in culture are induced to release histamine when exposed to ragweed antigen E or anti-IgE. Leukocyte cultures incubated with virus (i.e. HSV-1, Influenza A, and Adeno-1) but not exposed to ragweed antigen E or anti-IgE fail to release histamine. If, however, leukocyte cultures are first exposed to virus and then to ragweed antigen E or anti-IgE, significant enhancement of histamine release occurs. Both infectious and inactivated virus enhance histamine release and the degree of enhancement is related to the concentration of virus and the length of the incubation. Tissue culture fluid harvested 8 h after exposure of leukocytes to virus contains a soluble factor which is capable of enhancing histamine release when added to fresh leukocyte cultures. This factor has all the properties of interferon including species specificity and cannot be dissociated from the antiviral activity of interferon. Moreover, both known inducers of interferon (poly I:poly C) and standard preparations of interferon are capable of enhancing histamine release. The enhancement of histamine release by interferon represents a new biological role for interferon.

H(+)-K(+)-ATPase contributes to regulation of pHi in frog oxynticopeptic cells

1991 ◽  
Vol 261 (5) ◽  
pp. G781-G789 ◽  
Author(s):  
A. Yanaka ◽  
K. J. Carter ◽  
P. J. Goddard ◽  
M. C. Heissenberg ◽  
W. Silen
Keyword(s):  
Steady State ◽  
Gastric Mucosa ◽  
Histamine Release ◽  
Rana Catesbeiana ◽  
Intracellular Acidosis ◽  
Endogenous Histamine ◽  
Decreasing Ph ◽  
Oxynticopeptic Cells

The effect of intracellular acidosis on luminal H+ secretion and the role of H(+)-K(+)-ATPase in regulation of intracellular pH (pHi) in oxynticopeptic cells (OPC) (measured with a pH-sensitive fluorescent dye) were examined in intact sheets of in vitro frog (Rana catesbeiana) gastric mucosa. Intracellular acidosis of OPC induced by decreasing pH in the serosal solution (pHs) from 7.2 to 6.0 reversibly increased forskolin-stimulated H+ secretion without increasing endogenous histamine release. The observed increase in H+ secretion was unaffected by either 1 mM cimetidine or 1 mM histamine, but was accentuated by 1 mM amiloride, an effect abolished by 0.3 mM omeprazole. Steady-state pHi values in stimulated or resting OPC at pHs 7.2 were not significantly different. However, pHi in OPC was significantly higher in stimulated than in resting tissues at pHs 6.9, a difference accentuated by decreasing pHs to 6.4 or by 1 mM amiloride. Amiloride completely prevented recovery from intracellular acidosis induced by pHs 6.4 or 6.9 in omeprazole-treated tissues, but only partially mitigated recovery in cimetidine- or forskolin-treated tissues. At pHs 6.4, high luminal [K+] (100 mM) increased H+ secretion and hastened recovery of pHi in cimetidine-treated tissues in the presence of amiloride. These results suggest that, in intact sheets of in vitro frog gastric mucosa, 1) intracellular acidosis stimulates luminal H+ secretion via histamine-independent mechanisms and 2) H(+)-K(+)-ATPase contributes to the recovery of OPC from intracellular acidosis.

Histamine and cAMP as possible mediators of acetylcholine-induced acid secretion

1980 ◽  
Vol 239 (4) ◽  
pp. G255-G260
Author(s):  
E. B. Ekblad
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Histamine Release ◽  
Transient Increase ◽  
Cyclic Monophosphate ◽  
H2 Antagonist ◽  
Alkaline Secretion ◽  
Camp And Cgmp

Data are presented in support of the role of histamine and adenosine 3',5'-cyclic monophosphate (cAMP) as mediators of acetylcholine-induced acid secretion in frog gastric mucosa. These data also support the notion that acetylcholine-induced alkaline secretion is mediated by guanosine 3',5'-cyclic monophosphate (cGMP). Tissue cAMP and cGMP and rates of acid secretion and histamine release were measured in in vitro preparations of frog gastric mucosa that had been stimulated by acetylcholine. A transient increase in each variable was observed, the sequence of transient maxima being histamine release, cGMP, cAMP, and acid secretion. Atropine, an anticholnergic agent, eliminated all four transient increases, the variables remaining at resting levels. Metiamide, a H2-antagonist, modified the changes observed after acetylcholine stimulation. The acid secretion transience was abolished and the transient increase in tissue cAMP was greatly diminished, whereas the tissue of cGMP transience and histamine release transience remained unchanged. A model is proposed in which acetylcholine initiates two different processes, acid and alkaline secretions.

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