Effect of Inhaled N G -Nitro-L-Arginine Methyl Ester on Candida-Induced Acute Lung Injury

Nagata, Kazuhiro; Iwasaki, Yoshinobu; Takemura, Yoshizumi; Harada, Hidehiko; Yokomura, Ichiro; Fushiki, Shinji; Nakagawa, Masao

doi:10.1378/chest.124.6.2293

Cited by 10 publications

(6 citation statements)

References 31 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the results of our study are generally consistent with those of other reports, in which neutrophil accumulation and cytokine expression were reduced in iNOS )/) mice as compared with wild-type mice in a zymosan-induced acute lung inflammation model 46,47 and the inhibition of NO in the alveolar space reduced CXC chemokine and neutrophil migration to the lungs in a Candida-induced acute lung injury model. 48 Further studies will be required to address the mechanism underlying the capacity of NO to augment the expression of CXC chemokines.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide plays a key role in the platelet‐activating factor‐induced enhancement of resistance against systemic candidiasis

Kim

et al. 2008

Immunology

View full text Add to dashboard Cite

SummaryPlatelet-activating factor (PAF) has been demonstrated to augment resistance against Candida albicans infection. In this study, the role of nitric oxide (NO) in PAF-induced resistance in the kidneys was investigated. Pretreatment of the C. albicans-infected mice with PAF resulted in strong expression of messenger RNA (mRNA) and the protein synthesis of inducible nitric oxide synthase (iNOS). These PAF effects were inhibited to a significant degree by pretreatment with the nuclear factor-jB inhibitor, pyrrolidinedithiocarbamate. Pretreatment with PAF protected the mice from death caused by C. albicans infection and reduced the growth of fungus in the kidneys. The protective activity of PAF was abrogated by pretreatment with the iNOS inhibitor, aminoguanidine, and in the iNOS )/) mice. The PAF markedly increased the infiltration of neutrophils, but not macrophages, and also enhanced the mRNA expression levels of the CXC chemokine, keratinocyte-derived chemokine, in C. albicansinfected kidneys. These effects of PAF were attenuated in the aminoguanidine-treated mice and the iNOS )/) mice. These data show that NO plays an important role in PAF-induced protection against C. albicans.

show abstract

Section: Discussionmentioning

confidence: 99%

Nitric oxide plays a key role in the platelet‐activating factor‐induced enhancement of resistance against systemic candidiasis

Kim

et al. 2008

Immunology

View full text Add to dashboard Cite

show abstract

“…Numerous experimental studies of acute lung injury (Kao et al, 2003;Nagata et al, 2003;Wang et al, 1999) have reported an increased content of NO, presence of inducible NOS (iNOS) and nitrotyrosine, markers of peroxynitrite tissue damag, in alveolar spaces, which implied that NO produced via NOS may play a significant role in the pathogenesis of acute pulmonary damage. It has been shown that NO generated by iNOS interacts with ROS derived from neutrophils and macrophages and forms peroxynitrite (Lang et al, 2002), a potent oxidant that induces extensive tyrosine nitration and subsequent production of nitrotyrosine (Squadrito and Pryor, 1998).…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress in blast-induced acute lung injury is independent of enzymatic nitric oxide production

Kotur-Stevuljevic¹,

Savic²,

Prokić³

et al. 2005

Acta vet. (Beogr.)

View full text Add to dashboard Cite

Lung trauma has been considered to be one of the vital injuries induced by explosion-generated blast overpressure. Conflicting evidence exists as to whether nitric oxide plays a crucial role in acute lung injury induced by blast. Data presented in this study demonstrate that local exposure of midthoracic region to moderate-level blast overpressure significantly enhanced lipid peroxidation product malondialdehyde and superoxide anion generation in rabbit's lungs 30 minutes after exposure, whereas the activities of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) activity showed parallel increase. NG-nitro-L-arginine methyl ester, a non-specific inhibitor of nitric oxide synthase (NOS), had no effects on the measured parameters suggesting that oxidative stress induced by blast exposure might be independent from NOS

show abstract

“…However, the involved mechanisms remain unclear. We also reported that nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) played a crucial role in Candida-induced ALI and demonstrated that the iNOS inhibitor L-NAME had a beneficial effect on Candida-induced ALI (17). Furthermore, we showed that a novel iNOS inhibitor, ONO-1714, a novel selective iNOS inhibitor (1S,5S,6R,7R)-7-chloro-3-imino-5-methyl-2-azabicyclo[4.1.0]heptane hydrochloride), reduced Candida-induced ALI (20).…”

Section: Bronchoalveolar Lavage (Bal)mentioning

confidence: 99%

“…Several studies have reported high mortality rates due to candidemia (4,18,19). We previously showed that Candida-induced ALI was characterized by cellular aggregates surrounding yeast within blood vessels, extravasated erythrocytes in the perivascular interstitium of arterioles, alveolar hemorrhage, and fibrin deposition in a mouse model of Candida-induced ALI (17,26,30). Alveolar epithelia play an important role in preventing alveolar flooding in ALI.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Effect of inducible nitric oxide synthase on apoptosis in Candida-induced acute lung injury

et al. 2008

Self Cite

View full text Add to dashboard Cite

Excessive nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) aggravates acute lung injury (ALI) by producing peroxinitrite. We previously showed that the expression of iNOS and lung injury were suppressed by inhalation of a novel iNOS inhibitor, ONO-1714, in mice with Candida-induced ALI, and that nitric oxide produced by iNOS and apoptosis of epithelial cells were found to have a crucial role in Candida-induced ALI. In the present study, we investigated the effect of NO on the apoptosis of alveolar epithelial cells in Candida-induced ALI. Mice were pretreated by inhalation of ONO-1714 or saline (vehicle control of ONO-1714), and were given an intravenous injection of Candida albicans to induce ALI. After 24 h from injection of Candida albicans, we performed bronchoalveolar lavage and removed lung tissues. We assessed apoptosis on the basis of TUNEL staining and caspase 3 activity. Our results showed that apoptosis was suppressed by inhibition of iNOS-derived NO production by ONO-1714 inhalation. The augmented production of NO increased FasL, TNF-α, and mRNA production of Bax of lung that induced apoptosis of alveolar epithelial cells. Inhibition of iNOS-derived NO production by ONO-1714 inhalation ameliorated Candida-induced ALI and improved survival by suppressing apoptosis of alveolar epithelial cells.

show abstract

Effect of Inhaled N G -Nitro-L-Arginine Methyl Ester on Candida-Induced Acute Lung Injury

Cited by 10 publications

References 31 publications

Nitric oxide plays a key role in the platelet‐activating factor‐induced enhancement of resistance against systemic candidiasis

Nitric oxide plays a key role in the platelet‐activating factor‐induced enhancement of resistance against systemic candidiasis

Oxidative stress in blast-induced acute lung injury is independent of enzymatic nitric oxide production

Effect of inducible nitric oxide synthase on apoptosis in Candida-induced acute lung injury

Contact Info

Product

Resources

About