Cyclooxygenase-2 Suppresses Polymorphonuclear Neutrophil Apoptosis After Acute Lung Injury

Zhang, Jinzhou; He, Tao; Chen, Wensheng; Wang, Wen; Liu, Jincheng; Cui, Qin; Zhu, Hu; Liu, Weiyong

doi:10.1097/ta.0b013e318047c07c

Cited by 7 publications

(10 citation statements)

References 17 publications

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“…A higher number of apoptotic neutrophils in COX-2 deficient mice than COX-1 deficient mice suggested an anti-apoptotic role for COX-2 (37). Jinzhou et al demonstrated that up-regulation of intrapulmonary COX-2 expression contributed to the suppression of polymorphonuclear neutrophil (PMN) apoptosis after acute lung injury (38). Moreover, overexpression of COX-2 was thought to be linked to down regulation of apoptosis in many cell types (39) and played an anti-apoptotic role in human bronchial epithelial cells (40).…”

Section: Discussionmentioning

confidence: 99%

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

et al. 2017

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Background: Apoptosis has been demonstrated to be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cyclooxygenase-2 (COX-2) seems to be biologically relevant in COPD. However, the role of COX-2 in the apoptosis in vascular endothelial cells induced by cigarette smoke extract (CSE) remains to be elucidated. Our recent study found that the prostacyclin, one of the COX products in the microvascular endothelium, inhibited apoptosis in the emphysematous lungs of rats induced by CSE. In order to clarify the role of COX-2 in the apoptosis of vascular endothelial cells induced by CSE, we performed the present experiment to elucidate it. Methods: Twenty surgical lung specimens were obtained from 6 patients with COPD, 7 smoking controls and seven nonsmoking controls. The apoptotic index (AI) and COX-2 protein expression were detected in lung tissues. To further investigate the effects of CSE on the apoptosis and COX-2 expression in a human vascular endothelial cell line, the apoptosis rate and COX-2 expression were examined in human umbilical vein endothelial cells (ECV304) under exposure to varied concentrations of CSE as well as under exposure to 5.0% CSE for varied durations. Repeatedly, the apoptosis rate and COX-2 expression in ECV304 cells under 5.0% CSE were examined after exposing to varied concentrations of celecoxib, a highly selective COX-2 inhibitor. Results: Significantly increased AI and expression of COX-2 were found both in the lungs of patients with COPD and smoking controls compared with nonsmoking controls. The CSE induced apoptosis in ECV304 cells in means of both dose-dependent and time-dependent manners. The COX-2 was slightly expressed in the cells after exposing to 5% CSE for 3 and 6 h, and markedly expressed after the exposure time for 9 and 12 h, but vanished after 24 h of the exposure. Of interest, with the completely block of the COX-2 expression by celecoxib at 50.0 μmol/L, the apoptosis rate was markedly increased again in ECV304 cells under exposure to 5.0% CSE. Conclusions: Endothelial cell apoptosis and the expression of COX-2 protein were increased in both COPD patients and CSE-induced vascular endothelial cells. Of interest, it seems that the COX-2 probably had a protective role against the apoptosis in the vascular endothelial cells induced by cigarette smoking.

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Section: Discussionmentioning

confidence: 99%

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

et al. 2017

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“…Previous studies have reported that iNOS and COX-2 play a critical role in acute lung injury and suppression of iNOS and COX-2 expression protects against sepsis (Speyer et al 2003;Fukunaga et al 2005;Peng et al 2005;Jinzhou et al 2008;Kung et al 2011). To investigate the possible mechanism underlying the protective effect of acacetin in sepsis mice in vivo, we measured the effect of acacetin on iNOS and COX-2 expression in the different treatment groups.…”

Section: The Effect Of Acacetin On Sepsis-induced Inos and Cox-2 Expression In Lung Tissue Of Sepsis Micementioning

confidence: 99%

Protective effect of acacetin on sepsis-induced acute lung injury via its anti-inflammatory and antioxidative activity

Sun

Guo

et al. 2017

Arch. Pharm. Res.

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Sepsis is a clinical syndrome with no effective protective or therapeutic treatments. Acacetin, a natural flavonoid compound, has anti-oxidative and anti-inflammatory effects which can potentially work to reduce sepsis. We investigated the potential protective effect of acacetin on sepsis-induced acute lung injury (ALI) ALI and dissect out the underlying mechanisms. Mice were divided into five groups: a sham group, a sepsis-induced ALI group, and three sepsis groups pre-treated with 20, 40, and 80 mg/kg body weight of acacetin. We found that acacetin significantly attenuated sepsis-induced ALI, in histological examinations and lung edema. Additionally, acacetin treatment decreased protein and inflammatory cytokine concentration and the number of infiltrated inflammatory cells in BALF compared with that in the non-treated sepsis mice. Pulmonary myeloperoxidase (MPO) activity was lower in the acacetin-pre-treated sepsis groups than in the sepsis group. The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.

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“…For example, B. bifidum increases the expression of cyclooxygenase-2 (COX-2) (Khailova et al 2010). COX-2 is involved in apoptosis regulation and suppresses neutrophil apoptosis (Jinzhou et al 2008). On the other hand, Lactobacillus significantly increased COX-2 expression in intestinal cells (Otte et al 2008) and this can lead to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effect of probiotics on the viability of porcine and human neutrophils in vitro

Sustrova¹,

Ondráčková²,

Levá³

et al. 2017

Vet. Med. - Czech

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Lactobacillus, Bifidobacterium and Enterococcus cultures are increasingly used as probiotics for humans and pigs. The aim of this study was to investigate if co-cultivation of porcine and human neutrophils with probiotics can lead to increased apoptosis in vitro. Ten adult Large white pigs and 10 healthy human donors were used in this study. Neutrophils were isolated by dextran sedimentation and cultivated with and without the lactic acid bacteria Bifidobacterium bifidum, Lactobacillus rhamnosus, and Enterococcus faecium for 2, 4, 24 and 48 h. Early and late apoptosis was measured using flow cytometry, and cell lysis was detected based on lactate dehydrogenase activity (LDH). A significant (P < 0.05; P < 0.01) increase in apoptotic neutrophils and LDH was observed at 24 h and 48 h in vitro. All probiotics exerted their greatest effects on the early apoptosis of porcine neutrophils, while the effects of L. rhamnosus were most pronounced on late apoptosis and those of B. bifidum on LDH release of human neutrophils. The increased neutrophil apoptosis caused by probiotic bacteria can be beneficial for more efficient efferocytosis and faster resolution of inflammation and tissue regeneration. In conclusion, we have demonstrated that the interaction of B. bifidum, L. rhamnosus, and E. faecium with human and porcine neutrophils leads to their apoptosis.

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Cyclooxygenase-2 Suppresses Polymorphonuclear Neutrophil Apoptosis After Acute Lung Injury

Abstract: Up-regulation of intrapulmonary COX-2 expression contributes to the suppression of PMN apoptosis after ALI.

Cited by 7 publications

References 17 publications

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking

Protective effect of acacetin on sepsis-induced acute lung injury via its anti-inflammatory and antioxidative activity

Effect of probiotics on the viability of porcine and human neutrophils in vitro

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