CO

[michael edward badolato jr]

The following hints may lend support that many MCS people just start overproducing CO as part of the hyper neuro-immune inflammatory response.

Allergy. 2002 Aug;57(8):718-22.

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

Andersson JA¹, Egesten A, Cardell LO.

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Abstract

BACKGROUND:

Neutrophils are signaled to sites of infection and inflammation by different chemotactic stimuli. In order to reach the airways they have to adhere to, and then migrate through, the endothelium of pulmonary vessels. Carbon monoxide (CO) is a gaseous mediator, endogenously produced in the human airways. Increased CO production has been demonstrated during airway inflammation and CO as well as hemin, a substrate for CO producing enzymes, has been shown to affect neutrophil migration. Our objective was to investigate if the neutrophil cell surface expression of CD11b, CD66b and CD63 was changed during intermittent allergic rhinitis and to establish whether CO could affect the expression of these markers of cellular activation.

METHODS:

Blood from 10 healthy volunteers was drawn and incubated with different concentrations of hemin. Blood from 12 other healthy volunteers and from 12 patients with intermittent allergic rhinitis was also drawn during grass pollen season. Neutrophils were then isolated from all these three sets, and their expression of CD antigens measured using flow cytometry.

RESULTS:

Patients with symptomatic intermittent allergic rhinitis exhibited lower levels of CD11b and CD66b on the neutrophil cell surface. Incubation with hemin decreased the expression of CD11b and CD66b. CD63 was generally weakly expressed and not significantly affected by hemin incubation.

CONCLUSION:

Our results demonstrate that expressions of neutrophil cell surface glycoproteins are changed during the season in patents with intermittent allergic rhinitis and that hemin, a substrate for CO production, may act as an inhibitor of neutrophil activation. This indicates a possible role for CO in the immune defense system.

PMID:

12121191

[PubMed - indexed for MEDLINE]

FASEB J. 2008 Sep;22(9):3380-8. doi: 10.1096/fj.08-107110. Epub 2008 Jun 12.

A carbon monoxide-releasing molecule (CORM-3) abrogates polymorphonuclear granulocyte-induced activation of endothelial cells and mast cells.

Masini E¹, Vannacci A, Failli P, Mastroianni R, Giannini L, Vinci MC, Uliva C, Motterlini R, Mannaioni PF.

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Abstract

We hypothesized that circulating polymorphonuclear granulocytes (PMNs), vascular endothelial cells (ECs), and perivascular mast cells (MCs) may initiate and sustain the inflammatory response through the generation of the superoxide anion (O(2)(*-)) by PMNs primed by inflammatory stimuli, which in turn evoked the overexpression of adhesion molecules from ECs and release of histamine by MCs. To pin-point the role of carbon monoxide (CO) in curbing vascular inflammation, we studied the effect of a water-soluble CO-releasing molecule [tricarbonylchloro-glycinate-ruthenium (II); CORM-3] on an experimental model of vascular inflammation. The model consists of coincubating formyl-methionyl peptide (fMLP) -primed human PMNs with rat ECs or with rat MCs. The effects of CORM-3 were evaluated by measuring the generation of O(2)(*-) and the expression of CD11b in fMLP-primed PMNs; the expression of ICAM-1 and CD203c in ECs and MCs, respectively; and the release of histamine from MCs. Our results show that the chemotactic peptide fMLP primes PMNs to generate O(2)(*-) and overexpress CD11b, both events being central to the inflammatory process, while CORM-3 significantly decreases these events (IC(50)=1.66 microM for O(2)(*-) production; 1.20 microM for CD11b expression in human PMNs). The experiments also show that fMLP-primed PMNs increase the CD54 expression by coincubated ECs, and the expression of CD203c and the release of histamine by coincubated MCs. Once again, CORM-3 abolishes these events (IC(50)=6.78 microM for CD54 expression in ECs; 1.18 microM for CD203 expression; 1.15 microM for histamine release in MCs). Thus, CORM-3 exerts a powerful anti-inflammatory action by down-regulating the oxidative burst in PMNs, the overexpression of adhesion molecules in PMNs and ECs, the release of histamine, and the overexpression of an activation marker by MCs.

 

Hypoxia and carbon monoxide in the vasculature.

Kourembanas S¹.

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Abstract

Hypoxia is sensed by all mammalian cells and elicits a variety of adaptive and pathophysiological responses at the molecular and cellular level. For the pulmonary vasculature, hypoxia causes increased vasoconstriction and vessel-wall remodeling. These responses are mediated by complex intracellular cascades leading to altered gene expression and cell-cell interaction. Hypoxia transiently increases the transcriptional rate of the heme oxygenase-1 (HO-1) gene, resulting in increased production of carbon monoxide (CO) and bilirubin. CO has vasodilatory and antiinflammatory properties in the vasculature, whereas bilirubin is an antioxidant. Both enzymatic products could thus modulate the hypoxic cellular response. Accumulating data suggest that CO inhibits the hypoxic induction of genes encoding vasoconstrictors and smooth muscle cell mitogens in the early hypoxic phase. During chronic hypoxia, low CO levels tilt the balance toward increased production of growth factors and vasoconstrictors that promote vessel-wall remodeling. Mice null in the HO-1 gene manifest decreased tolerance to hypoxia with right ventricular dilatation and infarction, whereas targeted lung overexpression of HO-1 prevents hypoxia-induced inflammatory responses and protects against the development of pulmonary hypertension. Such observations point to CO as a critical modulator of the body's adaptive responses to hypoxia.

Article

Mast cells, hypoxia and structure of the vascular bed.

• 
  Hana Maxová
  • Hana Maxová

    Charles University in Prague

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• 
  Martin Vízek
  • Martin Vízek

    Charles University in Prague

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Institute of Pathological Physiology of the Second Faculty of Medicine, Charles University in Prague, and Centre for Cardiovascular Research, Czech Republic.

Prague medical report 02/2005; 106(4):359-66.

Source: PubMed

ABSTRACT Mast cells represent a heterogeneous and multifunctional cells population distributed throughout tissues. Their participation in the response to chronic hypoxia is discussed in consideration to their role in the angiogenesis and

Mast cells, hypoxia and structure of the vascular bed. (PDF Download Available). Available from: http://www.researchgate.net/publication/7206363_Mast_cells_hypoxia_... [accessed Jul 5, 2015].