Histamine Enhanced the TNF-α-Induced Expression of E-Selectin and ICAM-1 on Vascular Endothelial Cells

Miki, Ichiro; Kusano, Akira; Ohta, Shuji; Hanai, Nobuo; Otoshi, Masanari; Masaki, Shigehiro; Sato, Soichiro; Ohmori, Kenji

doi:10.1006/cimm.1996.0205

Cited by 72 publications

(48 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In agreement with these findings, we observed that both H1 and H2 receptors are involved in histamine-induced DC activation. Finally, histamine increases TNF-␣-induced E-selectin, ICAM-1, and LFA-1 expression on endothelial cells through H1 receptors (13). Together, these data suggest an inflammatory activity of histamine that is mediated through both H1 and H2 receptors and an anti-inflammatory role for H1 receptor antagonists.…”

Section: ϫ4mentioning

confidence: 67%

Histamine Induces CD86 Expression and Chemokine Production by Human Immature Dendritic Cells

Caron

Delneste

Roelandts³

et al. 2001

The Journal of Immunology

149

132

View full text Add to dashboard Cite

Mast cells and immature dendritic cells (DC) are in close contact in peripheral tissues. Upon activation, mast cells release histamine, a mediator involved in the immediate hypersensitivity reaction. We therefore tested whether histamine could affect human DC activation and maturation. Histamine induces CD86 expression on immature DC in a dose-dependent (significant at 10−7 M) and transient manner (maximal after 24-h stimulation). Histamine also transiently up-regulates the expression of the costimulatory and accessory molecules, CD40, CD49d, CD54, CD80, and MHC class II. As a consequence, immature DC exposed for 24 h to histamine stimulate memory T cells more efficiently than untreated DC. In addition, histamine induces a potent production of IL-6, IL-8, monocyte chemoattractant protein 1, and macrophage-inflammatory protein 1α by immature DC and also up-regulates IL-1β, RANTES, and macrophage-inflammatory protein 1β but not TNF-α and IL-12 mRNA expression. Histamine activates immature DC through both the H1 and H2 receptors. However, histamine-treated DC do not have a phenotype of fully mature cells, as they do neither show significant changes in the expression of the chemokine receptors, CCR5, CCR7 and CXC chemokine receptor 4, nor expression of CD83 de novo. These data demonstrate that histamine activates immature DC and induces chemokine production, thereby suggesting that histamine, via stimulation of resident DC, may participate locally in T cell stimulation and in the late inflammatory reaction associated with allergic disorders.

show abstract

Section: ϫ4mentioning

confidence: 67%

Histamine Induces CD86 Expression and Chemokine Production by Human Immature Dendritic Cells

Caron

Delneste

Roelandts³

et al. 2001

The Journal of Immunology

149

132

View full text Add to dashboard Cite

show abstract

“…In addition, these IC 50 values by olopatadine are almost equal to IC 50 values by this drug for histamine-induced cytokine or adhesion molecule expression in the other types of cells [5, 11, 12]. …”

Section: Discussionmentioning

confidence: 96%

“…Binding of histamine to H 1 R increases in intracellular calcium ion, which triggers the symptoms of acute allergic responses, such as smooth muscle contraction and vascular permeability [1, 3]. It has recently become apparent that H 1 R participates in the up-regulation of expression of cytokines, chemokines and adhesion molecules, suggesting that H 1 R is involved in inflammation followed by acute allergic responses [5,6,7,8,9,10,11,12]. …”

Section: Introductionmentioning

confidence: 99%

Histamine H<sub>1</sub> Receptor-Stimulated Interleukin 8 and Granulocyte Macrophage Colony-Stimulating Factor Production by Bronchial Epithelial Cells Requires Extracellular Signal-Regulated Kinase Signaling via Protein Kinase C

Matsubara¹,

Ohmori

Hasegawa³

2006

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

Background: Histamine stimulates the release of several cytokines, such as interleukin (IL)-8 and granulocyte macrophage colony-stimulating factor, from bronchial epithelial cells. However, the functional individual histamine receptor subtype and intracellular signaling in bronchial epithelial cells are poorly defined. Methods: Using human primary epithelial cells and the NCI-H292 cell line, we examined the expression of histamine receptor subtypes and histamine-induced second messenger. We also evaluated the involvements of mitogen-activated protein kinase, protein kinase C (PKC) and epidermal growth factor receptor in cytokine expression caused by histamine. Results: Histamine H₁ receptor (H₁R) was the only subtype expressed in both types of cells. Histamine elevated intracellular calcium ion without affecting cAMP levels. Histamine induced the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Histamine also phosphorylated PKC and myristoylated alanine-rich C kinase substrate. Ro-31-8220, a PKC inhibitor, and PD98059, a mitogen-activated protein/ERK kinase inhibitor, suppressed the histamine-induced ERK activation and the production of granulocyte macrophage colony-stimulating factor and IL-8. On the contrary, histamine had no effect on the phosphorylation of epidermal growth factor receptor, and its specific inhibitor AG1478 failed to inhibit the histamine-induced ERK activation. Olopatadine, an H₁ antagonist, completely blocked the histamine-related responses, whereas H₂ and H₃ antagonists did not. Histamine also augmented the IL-8 production caused by IL-4 or tumor necrosis factor-α. Conclusions: The H₁R-PKC-ERK pathway may play crucial roles in eliciting cytokine production from bronchial epithelial cells stimulated by histamine, leading to airway inflammation.

show abstract

“…Expression of intercellular adhesion molecule-1 (ICAM-1, CD54), vascular cell adhesion molecule-1 (VCAM-1, CD106), P-selectin (CD62P) and E-selectin (CD62E) was induced on endothelial cells by proinflammatory cytokines such as tumor necrosis factor-a (TNF-a ) and interleukin (IL)-1 (22). Miki et al showed that histamine by itself did not induce expression of ICAM-1 and Eselectin, whereas histamine enhanced the TNF-a -induced expression of ICAM-1 and E-selectin on human umbilical vein endothelial cells through histamine H 1 receptors (23). Olopatadine inhibited the histamine-enhanced expression of ICAM-1 and E-selectin with IC50 values of 2.3 and 4.4 nmol / L, respectively (23).…”

Section: -2 Mode Of Action 2-2-1 Histamine H1-receptor Antagonistimentioning

confidence: 99%

“…Miki et al showed that histamine by itself did not induce expression of ICAM-1 and Eselectin, whereas histamine enhanced the TNF-a -induced expression of ICAM-1 and E-selectin on human umbilical vein endothelial cells through histamine H 1 receptors (23). Olopatadine inhibited the histamine-enhanced expression of ICAM-1 and E-selectin with IC50 values of 2.3 and 4.4 nmol / L, respectively (23). In addition, it is reported that histamine caused a dose-dependent stimulation of IL-6 and IL-8 release by normal and transformed human bronchial epithelial cells that appeared to occur via histamine H 1 -receptor activation (24).…”

Section: -2 Mode Of Action 2-2-1 Histamine H1-receptor Antagonistimentioning

confidence: 99%

Pharmacological, Pharmacokinetic and Clinical Properties of Olopatadine Hydrochloride, a New Antiallergic Drug

Ohmori

Hayashi

Kaise

et al. 2002

Japanese Journal of Pharmacology

Self Cite

View full text Add to dashboard Cite

ABSTRACT-Olopatadine hydrochloride (olopatadine, 11-[(Z)-3-(dimethylamino)propylidene]-6,11-dihydrodibenz [b,e]oxepin-2-acetic acid monohydrochloride) is a novel antiallergic/ histamine H 1 -receptor antagonistic drug that was synthesized and evaluated in our laboratories. Oral administration of olopatadine at doses of 0.03 mg/ kg or higher inhibited the symptoms of experimental allergic skin responses, rhinoconjunctivitis and bronchial asthma in sensitized guinea pigs and rats. Olopatadine is a selective histamine H 1 -receptor antagonist possessing inhibitory effects on the release of inflammatory lipid mediators such as leukotriene and thromboxane from human polymorphonuclear leukocytes and eosinophils. Olopatadine also inhibited the tachykininergic contraction in the guinea pig bronchi by prejunctional inhibition of peripheral sensory nerves. Olopatadine exerted no significant effects on action potential duration in isolated guinea pig ventricular myocytes, myocardium and human ether-a-go-go-related gene channel. Olopatadine was highly and rapidly absorbed in healthy human volunteers. The urinary excretion of olopatadine accounted for not less than 58% and the contribution of metabolism was considerably low in the clearance of olopatadine in humans. Olopatadine is one of the few renal clearance drugs in antiallergic drugs. Olopatadine was shown to be useful for the treatment of allergic rhinitis and chronic urticaria in double-blind clinical trials. Olopatadine was approved in Japan for the treatment of allergic rhinitis, chronic urticaria, eczema dermatitis, prurigo, pruritis cutaneous, psoriasis vulgaris and erythema exsudativum multiforme in December, 2000. Ophthalmic solution of olopatadine was also approved in the United States for the treatment of seasonal allergic conjunctivitis in December, 1996 (Appendix: also in the European Union, it was approved in February 2002).

show abstract

Histamine Enhanced the TNF-α-Induced Expression of E-Selectin and ICAM-1 on Vascular Endothelial Cells

Cited by 72 publications

References 0 publications

Histamine Induces CD86 Expression and Chemokine Production by Human Immature Dendritic Cells

Histamine Induces CD86 Expression and Chemokine Production by Human Immature Dendritic Cells

Histamine H<sub>1</sub> Receptor-Stimulated Interleukin 8 and Granulocyte Macrophage Colony-Stimulating Factor Production by Bronchial Epithelial Cells Requires Extracellular Signal-Regulated Kinase Signaling via Protein Kinase C

Pharmacological, Pharmacokinetic and Clinical Properties of Olopatadine Hydrochloride, a New Antiallergic Drug

Contact Info

Product

Resources

About