A regulatory role for carbon monoxide in mast cell function

Bello, M. G. Di; Berni, L.A.; Gai, P.; Mirabella, C.; Ndisang, Joseph Fomusi; Masini, Emanuela; Sacchi, T. Banni; Mannaioni, P. F.

doi:10.1007/s000110050238

Cited by 18 publications

(9 citation statements)

References 7 publications

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“…Because histamine regulation can be part of the anti-inflammatory mechanisms of HO-1 (Di Bello et al, 1998;Takamiya et al, 2002) and NO has been proposed as a secondary mediator in histamine-induced allergic responses (Meijer et al, 1996), we have examined the possible participation of histamine in the inflammatory response to zymosan. Nevertheless, we have not detected histamine levels in exudates from zymosan-injected air pouches, and thus our results do not support a role for this mediator in our inflammatory model.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Heme Oxygenase-1 Up-Regulation in the Development of Experimental Inflammation Induced by Zymosan

Vicente¹,

Guillén²,

Habib³

et al. 2003

J Pharmacol Exp Ther

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Heme oxygenase-1 (HO-1) is part of the integrated response to oxidative stress. This enzyme may exert anti-inflammatory effects in some animal models, although the precise mechanisms are not fully understood. We have examined the role of HO-1 in the inflammatory response induced by zymosan in the mouse air pouch. Zymosan administration induced HO-1 protein expression in leukocytes migrating to exudates, with maximal levels in the late phase of this response (24 -48 h). This was accompanied by ferritin induction and bilirubin accumulation, indicating that this enzyme is active in our model. HO-1 expression by zymosan treatment was partly reduced by aminoguanidine, suggesting the participation of endogenous nitric oxide in the mechanisms leading to HO-1 synthesis in the zymosaninjected mouse air pouch. Up-regulation of HO-1 by hemin administration resulted in inhibition of nitric-oxide synthase-2 activity, cellular infiltration into the air pouch exudate, and plasmatic exudation. Leukotriene B 4 levels in exudates were significantly decreased in the early phase of this response (4 h), whereas interleukin-1␤ and tumor necrosis factor-␣ were inhibited at all time points. Inhibition of HO-1 activity by zinc protoporphyrin IX prevented most of the effects caused by hemin administration. Our results indicate that HO-1 exerts anti-inflammatory effects on the response to zymosan in the mouse air pouch and support a role for this enzyme in the modulation of inflammatory processes.

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Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Heme Oxygenase-1 Up-Regulation in the Development of Experimental Inflammation Induced by Zymosan

Vicente¹,

Guillén²,

Habib³

et al. 2003

J Pharmacol Exp Ther

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“…The initial observation that exposure to CO (100 %; 30 min) signifi cantly reduced the release of histamine and the sequential exocytosis induced by compound 48/80 in isolated purifi ed rat serosal mast cells [92], prompted an extension of the experiments on the modulation afforded by the HO/CO system on the allergic response of immunological cells and of sensitized tissue in vitro.…”

Section: Studies On Mast Cellsmentioning

confidence: 99%

Carbon monoxide: the bad and the good side of the coin, from neuronal death to anti-inflammatory activity

2006

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The double origin of carbon monoxide (CO) as an atmospheric pollutant or as an endogenous gaseous modulator of many pathophysiological processes prompted us to review some aspects of the bad side and of the good side of coin among the pleiotropic effects of CO. On the bad side of the coin, we focus on the interval form in acute CO poisoning, discussing experimental evidence suggesting that the delayed neuropathology after CO poisoning is a free radical-driven event. In this context, we challenge the mandatory place of hyperbaric oxygen therapy (HBO) in CO poisoning as a possible summation of oxy-radicals generated by HBO and the free radical cascade set in motion during the reoxygenation phase of acute CO-poisoning. We also discuss an opposing view, which provides evidence suggesting that HBO therapy actually decreases the load of free radicals in acute CO-poisoning and may be beneficial in preventing delayed neuropsychiatric sequelae.On the good side of the coin, we briefly outline the endogenous generation of CO and the leading role of heme-oxygenases (HO) in relation to the place of CO in biology and medicine. The main focus of this section is on the growing literature on CO and inflammation. Here we report on in-vitro and in-vivo studies on the modulation afforded by exogenously administered/endogenously produced CO in a variety of experimental and clinical settings of inflammation. Our recent studies on experimental models of allergic inflammation are also discussed, and the CO-releasing molecules envisaged as potential anti-inflammatory drugs suitable for clinical use.

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“…These protective mechanisms could involve the removal of the pro-oxidant heme (2,3), the removal of hydrogen superoxide during the degradation of heme (39), the induction of ferritin synthesis that sequesters redox-active iron (38 -40), and the regulation of superoxide anion production (41). Other possible mechanisms could involve the multiple ways by which CO modulates inflammatory processes, such as the reduction of neutrophil adhesion and extravasation (42), the reduction of histamine release from mast cells and human basophils (43,44), inhibition of the expression of proinflammatory cytokines such as tumor necrosis factor-␣ and IL-1␤, and an increase of anti-inflammatory cytokine IL-10 (45).…”

Section: Heme Oxygenase and Oxidative Stressmentioning

confidence: 99%

Role of Heme Oxygenase and Bilirubin in Oxidative Stress in Preterm Infants

et al. 2004

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In a previous study, it was found that the decrease in the total plasma bilirubin level (Btot) in preterm infants was associated with the decrease in oxidative stress. We hypothesized that this occurs as a result of a pro-oxidant effect of heme oxygenase (HO), which outcompetes with the antioxidant properties of bilirubin. In this study we studied 12 preterm infants in whom the plasma levels of Btot, total hydroperoxide (TH), protein SH groups, HO activity, non-transferrin-bound iron (NTBI), and erythrocyte CuZn superoxide dismutase (CuZn SOD) activity were concurrently measured when the Btot was Ͼ220 M and after a Btot drop of Ͼ34 M. The Btot decrease was concurrent with the TH decrease, protein SH groups increase, and the HO and CuZn SOD activity increase and was not associated with an NTBI increase. We concluded that 1) Btot does not exert a meaningful antioxidant effect in vivo; 2) HO does not exert a pro-oxidant effect involving an NTBI increase and that, on the contrary, it could exert an antioxidant effect; and 3) the concurrent HO and CuZn SOD activity increase could indicate a synergic antioxidant effect of the two enzymes. Many illnesses in preterm infants, including chronic lung disease, necrotizing enterocolitis, retinopathy of prematurity, and intracranial hemorrhage, are thought to be related to the action of reactive oxygen species. This presumably occurs because the antioxidant system of preterm infants is at the same time highly stressed and incompletely developed (1). Moreover, it is well known that during the first days of life, the catabolism of fetal Hb results in a tissue burden of heme that is a potentially pro-oxidant damaging molecule that not only provides a lipophilic form of iron but can itself directly attack the lipid bilayer, the cytoskeleton, and DNA (2,3). Several reports have emphasized the antioxidant role of bilirubin, which in human neonatal plasma seems to have a greater antioxidant potency than urates, ␣-tocopherol, or ascorbates (4). Nevertheless, although the antioxidant effect of bilirubin as a scavenger of reactive oxygen species is well documented in vitro (5-8) as well as in animal studies (9), its role in vivo has not been definitively clarified in preterm infants (10 -13). Even less is known about the role of heme oxygenase (HO) in oxidative stress of the newborn infant. Heme oxygenase is the enzyme responsible for physiologic heme degradation into equimolar amounts of CO and biliverdin and the release of free iron (14). It has been suggested that its inducible form, HO-1, might represent a generalized response to oxidative stress (15)(16)(17) and that HO-1 could confer cellular protection against oxidant stress (14,18 -20). However, recent studies suggest that HO-1 induction might not always be beneficial and that the release of redox-active iron from heme might induce enhance oxidative stress (21,22).In a previous study, we found that in jaundiced preterm infants, a decrease of bilirubin plasma level (Btot) was asso-

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A regulatory role for carbon monoxide in mast cell function

Cited by 18 publications

References 7 publications

Beneficial Effects of Heme Oxygenase-1 Up-Regulation in the Development of Experimental Inflammation Induced by Zymosan

Beneficial Effects of Heme Oxygenase-1 Up-Regulation in the Development of Experimental Inflammation Induced by Zymosan

Carbon monoxide: the bad and the good side of the coin, from neuronal death to anti-inflammatory activity

Role of Heme Oxygenase and Bilirubin in Oxidative Stress in Preterm Infants

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