Hemin and Carbon Monoxide  Modulate the Immunological Response of Human Basophils

Mirabella, C.; Baronti, Roberto; Berni, L.A.; Gai, P.; Ndisang, Joseph Fomusi; Masini, Emanuela; Mannaioni, P. F.

doi:10.1159/000024092

Cited by 12 publications

(4 citation statements)

References 5 publications

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“…Hemin did not, at concentrations up to 10 −5 M, alter the viability of the studied cells. Earlier studies have shown that hemin induces HO‐1 in various cells, and that an incubation period of 4 h seems to be optimal for the present experiments (20–22). Following 4 h of incubation, 15 ml of a mixture containing two parts Macrodex ® (Dextran 70, 60 g/1000 ml 9% NaCl; Pharmalink Basläkemedel AB, Spånga, Sweden) and one part sodium metrizoate 32,8% (Nycomed Pharma AS, Oslo, Norway) was added to the heparinized blood.…”

Section: Methodsmentioning

confidence: 81%

Hemin, a heme oxygenase substrate analog, inhibits the cell surface expression of CD11b and CD66b on human neutrophils

Andersson

Egesten

Cardell

2002

Allergy

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Section: Methodsmentioning

confidence: 81%

Hemin, a heme oxygenase substrate analog, inhibits the cell surface expression of CD11b and CD66b on human neutrophils

Andersson

Egesten

Cardell

2002

Allergy

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“…Therefore, novel therapeutic strategies that concomitantly ablate inflammation and insulin resistanc, but enhance adiponectin are needed. Interestingly, the HO system has been shown to modulate both the metabolic and inflammatory systems suppressing insulin resistance and inflammation while enhancing adiponectin levels [40–44, 47, 48, 51, 55, 56, 82, 103–113]. Therefore the inflammatory and metabolic effects of HO may be highly integrated and the proper function of each may depend on the other [37].…”

Section: The Role Of Ho System In Inflammation and Insulin Resistancementioning

confidence: 99%

Role of Heme Oxygenase in Inflammation, Insulin-Signalling, Diabetes and Obesity

Ndisang

2010

Mediators of Inflammation

144

151

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Diabetes and obesity are chronic conditions associated with elevated oxidative/inflammatory activities with a continuum of tissue insults leading to more severe cardiometabolic and renal complications including myocardial infarction and end-stage-renal damage. A common denominator of these chronic conditions is the enhanced the levels of cytokines like tumour necrosis factor-alpha (TNF-α), interleukin (IL-6), IL-1β and resistin, which in turn activates the c-Jun-N-terminal kinase (JNK) and NF-κB pathways, creating a vicious cycle that exacerbates insulin resistance, type-2 diabetes and related complications. Emerging evidence indicates that heme oxygenase (HO) inducers are endowed with potent anti-diabetic and insulin sensitizing effects besides their ability to suppress immune/inflammatory response. Importantly, the HO system abates inflammation through several mechanisms including the suppression of macrophage-infiltration and abrogation of oxidative/inflammatory transcription factors like NF-κB, JNK and activating protein-1. This review highlights the mechanisms by which the HO system potentiates insulin signalling, with particular emphasis on HO-mediated suppression of oxidative and inflammatory insults. The HO system could be explored in the search for novel remedies against cardiometabolic diseases and their complications.

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“…Concerning allergic reactions, it is noteworthy that mast cells and basophils are capable of generating CO, which exerts a negative feedback on allergen-induced histamine release [31,32]. Moreover, the heart can express HO-1 and is a site for basal HO-1 activity, because bilirubin, the stable co-product of enzymatic heme degradation, can be measured in normal heart tissue [33].…”

Section: Carbon Monoxide and Cardiac Anaphylaxismentioning

confidence: 99%

Cardiac anaphylaxis: Pathophysiology and therapeutic perspectives

Bani

Nistri²,

Mannaioni³

et al. 2006

Curr Allergy Asthma Rep

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Cardiac anaphylaxis refers to the functional and metabolic changes in the heart caused by the anaphylactic release of histamine and vasoactive products of arachidonic acid cascade by mast cells and basophils. As in most type I hypersensitivity-based diseases, histamine plays a key role in the pathophysiology of cardiac anaphylaxis. In the heart, mast cell activation and histamine release are controlled by multiple endogenous mechanisms, including adrenergic neural control, histamine-dependent negative feedback operated through H2 receptors, and the endogenous generation of nitric oxide (NO) and carbon monoxide (CO). All these mechanisms can be targeted by substances that have revealed a clear-cut effect in blunting cardiac anaphylaxis in experimental animal models, and could be developed as potential, novel anti-anaphylactic drugs. In this article, we discuss new findings and significant trends related to this topic.

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Hemin and Carbon Monoxide Modulate the Immunological Response of Human Basophils

Cited by 12 publications

References 5 publications

Hemin, a heme oxygenase substrate analog, inhibits the cell surface expression of CD11b and CD66b on human neutrophils

Hemin, a heme oxygenase substrate analog, inhibits the cell surface expression of CD11b and CD66b on human neutrophils

Role of Heme Oxygenase in Inflammation, Insulin-Signalling, Diabetes and Obesity

Cardiac anaphylaxis: Pathophysiology and therapeutic perspectives

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