Transfer of Heme Oxygenase 1 cDNA by a Replication-Deficient Adenovirus Enhances Interleukin 10 Production from Alveolar Macrophages That Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Mice

Inoue, Satoshi; Suzuki, Motoyoshi; Nagashima, Yoji; Suzuki, Shunsuke; Hashiba, Takafumi; Tsuburai, Takahiro; Ikehara, Kunihiko; Matsuse, Takeshi; Ishigatsubo, Yoshiaki

doi:10.1089/104303401750195926

Cited by 124 publications

(87 citation statements)

References 51 publications

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“…31,32 It has also been demonstrated that overexpression of exogenously inserted HO-1 cDNA in gene transfer vectors confer therapeutic benefit on a murine model of hyperoxia 33 or LPS induced lung injury. 34 These experimental results demonstrated by using relatively simple proinflammatory stimuli (LPS, hyperoxia, hydrogen peroxide, TNF-␣) are consistent with the concept that HO-1 overexpression has the ability to attenuate lung injury induced by a variety of airborne pathogens by modulating cytokines expression profiles via a change in the p38MAPK activity, by decreasing inflammatory cell migrations into the lung, or by suppressing apoptotic deaths of respiratory epithelial cells induced by reactive oxygen species.…”

Section: Introductionsupporting

confidence: 82%

“…Consistent with this observation, neutrophil migration into the lung following an intratracheal challenge of LPS was attenuated when animals breathed air containing CO, but that was not attenuated in animals lacking p38 MAPK. 28,30 Inoue et al 34 have also demonstrated that neutrophil migration to the lung following LPS inhalation was markedly attenuated by pre-administration of an endogenous HO-1 inducer, hemin, or an Ad expressing HO-1 in mice, and further demonstrated that IL-10 overproduction by macrophages was essential for suppressed neutrophilic inflammation. Together, these data suggest that overexpression of HO-1 results in CO production, which modifies cytokine profiles within both inflammatory and respiratory epithelial cells, thus suppressing neutrophil migration into the lung in response to LPS.…”

Section: Discussionmentioning

confidence: 95%

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Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

et al. 2001

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Section: Introductionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 95%

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

et al. 2001

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“…For example, carbon monoxide has been shown to mediate the antiinflammatory effects of IL-10 in a mouse model of septic shock (35). In addition, exogenous administration of HO-1 increases IL-10 production in macrophages, which leads to the resolution of neutrophilic migration in the lung after lipopolysaccharide administration (36). In contrast, HO-1 does not seem to play a significant role in the antiinflammatory activity of IL-10 in human monocytes or macrophages (37,38), and an autoregulatory feedback loop is present in lipopolysaccharide-stimulated human monocytes, involving proinflammatory cytokines and IL-10 (39), with a likely predominant role of TNF␣ (40).…”

Section: Discussionmentioning

confidence: 99%

“…HO-1 overexpression has shown antiinflammatory or immunomodulatory effects in models of acute disease (10,16,36,(45)(46)(47). Less is known about the possible role of this enzyme in chronic inflammatory diseases, which involve complex interactions between different cell populations and a wide range of mediators.…”

Section: Discussionmentioning

confidence: 99%

Influence of heme oxygenase 1 modulation on the progression of murine collagen‐induced arthritis

Devesa¹,

Ferrándiz²,

Terencio³

et al. 2005

Arthritis & Rheumatism

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Objective. Heme oxygenase 1 (HO-1) can be induced by inflammatory mediators as an adaptive response. The objective of the present study was to determine the consequences of HO-1 modulation in the murine collagen-induced arthritis (CIA) model.Methods. DBA/1J mice were treated with an inhibitor of HO-1, tin protoporphyrin IX (SnPP), or with an inducer of HO-1, cobalt protoporphyrin IX (CoPP), from day 22 to day 29 after CIA induction. The clinical evolution of disease was monitored visually. At the end of the experiment, joints were examined for histopathologic changes. Cytokine levels in paws were measured by enzyme-linked immunosorbent assay. Levels of HO-1, cyclooxygenase 2 (COX-2), and prostaglandin E 2 (PGE 2 ) were determined. Effects of treatments on the early phase of disease and after prophylactic administration were also assessed.Results. CoPP strongly induced HO-1, resulting in the inhibition of cartilage erosion accompanied by extensive fibrosis in the joint. Levels of tumor necrosis factor ␣ (TNF␣), interleukin-2 (IL-2), and IL-10 were inhibited by CoPP, whereas levels of vascular endothelial growth factor were increased. Treatment with SnPP significantly reduced the severity of CIA, with inhibition of joint inflammation and cartilage destruction. The levels of PGE 2 , IL-1␤, and TNF␣ were also significantly reduced by SnPP treatment, which did not modify COX-2 protein expression. SnPP was more effective than CoPP in preventing the development of CIA (prophylactic administration).Conclusion. HO-1 is induced during CIA. Although overexpression of this protein causes some beneficial effects, strategies aimed at HO-1 overexpression cannot slow the progression of the chronic inflammatory disease, whereas treatment with SnPP, which inhibits HO-1, exerts prophylactic and therapeutic effects.

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“…NIH-PA Author Manuscript NIH-PA Author Manuscript that cause oxidative stress and/or in response to environmental stress [5][6][7][8]. For example, increased HO-1 expression has recently been found in the alveolar spaces in the resident macrophages of smokers [9].…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

HNE increases HO-1 through activation of the ERK pathway in pulmonary epithelial cells

Iles

Dickinson

Wigley

et al. 2005

Free Radical Biology and Medicine

101

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Heme oxygenase-1 (HO-1) is a key cytoprotective enzyme and an established marker of oxidative stress. Increased HO-1 expression has been found in the resident macrophages in the alveolar spaces of smokers. The lipid peroxidation product 4-hydroxynonenal (HNE) is also increased in the bronchial and alveolar epithelium in response to cigarette smoke. This suggests a link between a chronic environmental stress, HNE formation, and HO-1 induction. HNE is both an agent of oxidative stress in vivo and a potent cell signaling molecule. We hypothesize that HNE acts as an endogenously produced pulmonary signaling molecule that elicits an adaptive response culminating in the induction of HO-1. Here we demonstrate that HNE increases HO-1 mRNA, protein, and activity in pulmonary epithelial cells and identify ERK as a key pathway involved. Treatment with HNE increased ERK phosphorylation, c-Fos protein, JNK phosphorylation, c-Jun phosphorylation, and AP-1 binding. Whereas inhibiting the ERK pathway with the MEK inhibitor PD98059 significantly decreased HNEmediated ERK phosphorylation, c-Fos protein induction, AP-1 binding, and HO-1 protein induction, inhibition of the ERK pathway had no effect on HNE-induced HO-1 mRNA. This suggests that ERK is involved in the increase in HO-1 through regulation of translation rather than transcription. Keywords 4-Hydroxynonenal; Oxidative stress; HO-1; MAPK signaling; Free radicals Heme oxygenase-1 (HO-1) is an important cytoprotective enzyme and widely accepted marker of oxidative stress. HO-1 catalyzes the first and rate-limiting step in the catabolism of heme, which generates equimolar amounts of biliverdin, ferrous iron, and carbon monoxide [1][2][3]. Although heme is the major substrate of HO-1, a variety of non-heme-containing agents are also strong inducers of HO-1. HO-1 has been shown to respond to a number of proinflammatory cytokines, including TNF-α, . HO-1 is also induced by a variety of agents NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript that cause oxidative stress and/or in response to environmental stress [5][6][7][8]. For example, increased HO-1 expression has recently been found in the alveolar spaces in the resident macrophages of smokers [9]. Once induced, HO-1 provides protection against multiple types of tissue injury [10][11][12][13]; specific to the lung, overexpression of HO-1 in pulmonary epithelial cells has been shown to protect against oxygen toxicity [14]. In contrast, HO-1 deficiency in mice (HO-1 −/− ) increases susceptibility to inflammatory lung injury [15], as does HO-1 deficiency in humans [16]. Although the precise mechanisms by which HO-1 exerts its cytoprotective effects are not known, there is mounting evidence that carbon monoxide plays a key role in this process. For thorough reviews of the recent literature see [17,18].Another characteristic of oxidative stress is the formation of the lipid peroxidation product 4-hydroxy-2-nonenal (HNE). HNE has been shown to increase HO-1 in the cell [19,20], but the mechanism(s...

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Transfer of Heme Oxygenase 1 cDNA by a Replication-Deficient Adenovirus Enhances Interleukin 10 Production from Alveolar Macrophages That Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Mice

Cited by 124 publications

References 51 publications

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

Adenovirus-mediated transfer of heme oxygenase-1 cDNA attenuates severe lung injury induced by the influenza virus in mice

Influence of heme oxygenase 1 modulation on the progression of murine collagen‐induced arthritis

HNE increases HO-1 through activation of the ERK pathway in pulmonary epithelial cells

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