Role of H1 receptors and P-selectin in histamine-induced leukocyte rolling and adhesion in postcapillary venules.

Asako, Hiroshi; Kurose, Iwao; Wolf, Robert; DeFrees, Shawn; Zheng, Zhong-Li; Phillips, M. L.; Paulson, James C.; Granger, D. Neil

doi:10.1172/jci117129

Cited by 144 publications

(101 citation statements)

References 39 publications

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“…As suggested in animal (33)(34)(35) and human studies, allergen challenge induces strong leukocyte recruitment, as has been detected in tissue biopsies, (36 -38) although histamine alone cannot induce any extravasation (30,36,39). Previous results are in line with our data that histamine is sufficient to induce leukocyte rolling, but endogenous mediators other than histamine are likely to participate in the reduction in velocity of the rolling leukocytes and in the actual extravasation during the generation of acute allergen-induced inflammation (7).…”

Section: Discussionmentioning

confidence: 84%

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

Helintö

Renkonen

Tervo³

et al. 2004

The Journal of Immunology

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Immediate allergic reactions are initiated by allergen-induced, specific IgE-mediated mast cell degranulation and involve leukocyte recruitment into the inflamed site. We compared conjunctival signs, symptoms, and in vivo leukocyte rolling and extravasation into sites of inflammation in five patients allergic to birch pollen and in 10 nonallergic controls who received a challenge to birch allergen or histamine. Both the specific allergen in allergic patients and histamine, both in patients and in healthy controls, induced symptoms and signs of an immediate allergic reaction together with leukocyte rolling within the conjunctival blood vessels. However, only allergen, not histamine, caused leukocyte extravasation into the site of inflammation in the allergic patients. Allergen also increased expression of endothelial P-selectin in conjunctival vessels and slowed the rolling of leukocytes which is required for their extravasation from blood circulation into the target tissue. Finally, i.v. heparin strongly reduced the number of slowly rolling cells during allergen- or histamine-induced reactions and this can probably hinder the leukocyte extravasation after allergen exposure. These findings suggest that slow rolling is required for leukocyte extravasation in acute allergic reactions, and it can be inhibited by heparin in vivo in therapeutically relevant conditions.

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Section: Discussionmentioning

confidence: 84%

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

Helintö

Renkonen

Tervo³

et al. 2004

The Journal of Immunology

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“…Mast cell-derived histamine may critically affect leukocyteendothelial interactions by increasing endothelial P-selectin expression and by facilitating recruitment of rolling leukocytes [222]. Tryptase, the most abundant protease found in mast cell granules stimulates granulocyte recruitment [223], and upregulates cytokine and chemokine synthesis [224], [225].…”

Section: The Mast Cellsmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

572

499

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Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

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“…Histamine receptors, through which histamine exerts its functions, are expressed in intimal atherosclerotic lesions (5). Histamine induces endothelial cells to produce proinflammatory cytokines such as interleukin 6 (IL6) and interleukin 8 (IL8) (6 -8); adherent molecules such as p-selectin (9), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) (10), and tissue factor (11), a prominent initiator of blood coagulation. Histamine also induces tissue factor expression in smooth muscle cells (11), and smooth muscle cell proliferation (12,13).…”

mentioning

confidence: 99%

Histamine Induces Egr-1 Expression in Human Aortic Endothelial Cells via the H1 Receptor-mediated Protein Kinase Cδ-dependent ERK Activation Pathway

Feng

Tan

et al. 2008

Journal of Biological Chemistry

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Histamine, a potent inflammatory mediator, has multiple effects on the pathogenesis of atherosclerosis. This study investigates the effect of histamine on the expression of early growth response factor 1 (Egr-1), a master transcription factor that regulates the expression of an array of atherogenic genes in atherosclerotic lesions. Histamine markedly and rapidly induces Egr-1 mRNA and protein expression in primary human aortic endothelial cells (HAECs). Histamine-induced Egr-1 expression is dependent on the activation of the H1 receptor. Histamine also rapidly and transiently activates protein kinase C-␦ (PKC␦), extracellular signal-regulated kinase (ERK)1/2, p38 kinase, and c-Jun N-terminal kinase (JNK) prior to Egr-1 induction. Using specific pharmacological inhibitors and small interfering RNA technology, we determined that PKC␦ and ERK, but not p38 and JNK, mediate histamine-induced Egr-1 expression. Our data provide the first evidence that histamine regulates expression of Egr-1 in mammalian cells and demonstrate a novel role of PKC␦ in up-regulation of Egr-1 expression. The present study reveals the following regulatory mechanism: histamine up-regulates Egr-1 expression in primary HAECs via the H1 receptor and the PKC␦-dependent ERK activation pathway. Our data also imply that CREB, a downstream component of the ERK pathway, regulates Egr-1 expression in HAECs. Importantly, these results suggest a central role of Egr-1 in histamine-induced gene expression and in histamine-induced vascular disease.

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Role of H1 receptors and P-selectin in histamine-induced leukocyte rolling and adhesion in postcapillary venules.

Cited by 144 publications

References 39 publications

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

The immune system and cardiac repair

Histamine Induces Egr-1 Expression in Human Aortic Endothelial Cells via the H1 Receptor-mediated Protein Kinase Cδ-dependent ERK Activation Pathway

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