Polymorphonuclear leucocyte (PMN)-derived inflammatory cytokines—regulation by oxygen tension and extracellular matrix

Derevianko, A.; D’Amico, Ronald; Simms, Henry S.

doi:10.1046/j.1365-2249.1996.d01-871.x

Cited by 24 publications

(14 citation statements)

References 21 publications

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“…Moreover, mechanical stress such as that induced by adherence and transendothelial migration can also contribute to PMN activation. For example, we and others have shown that cytokine production by PMN is dependent on integrin-extracellular matrix interactions (Derevianko et al, 1996;Gaudry et al, 1997).…”

Section: Grenier Et Almentioning

confidence: 84%

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Grenier

Combaux

Chastre

et al. 2001

Laboratory Investigation

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SUMMARY:Polymorphonuclear neutrophils (PMN) are involved in the pathogenesis of acute lung injury (ALI), secreting numerous mediators such as proteases, reactive oxygen species, and cytokines. Because we had recently observed the ability of normal human PMN to degranulate and synthesize oncostatin M (OSM), an IL-6 -family cytokine, we quantified OSM production ex vivo by highly purified blood and alveolar PMN from 24 ventilated patients with ALI, including some patients with severe pneumonia. Most of the patients had no detectable OSM in plasma, and OSM production by cultured blood PMN was similar to that of healthy controls. However, OSM was present in bronchoalveolar lavage (BAL) fluid supernatant, with significantly higher levels during pneumonia. In addition, alveolar OSM levels correlated with the number of PMN obtained by BAL, suggesting that PMN are an important source of OSM within the alveoli. Indeed, purified alveolar PMN from all of the patients, especially those with pneumonia, strongly produced OSM. Interestingly, in the latter patients, alveolar PMN always produced more OSM than autologous blood PMN. These results document the functional duality of PMN in ALI by showing the participation of PMN in the modulation of lung inflammation. (Lab Invest 2001, 81:133-141).

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Section: Grenier Et Almentioning

confidence: 84%

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Grenier

Combaux

Chastre

et al. 2001

Laboratory Investigation

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“…It is plausible that reduced oxygen tension may limit oxidative stress by generating less ROS. In addition, lower oxygen tension affects neutrophil response to stimulation by cytokines (33). The minimal oxidative injury caused by intra-amniotic endotoxin in the fetus may be reflective of the modulatory effects of the lower oxygen in the intrauterine environment.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress in Fetal Lambs Exposed to Intra-amniotic Endotoxin in a Chorioamnionitis Model

et al. 2008

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Chorioamnionitis is a risk factor for the development of bronchopulmonary dysplasia. Endotoxin-induced oxidative stress to the fetus in the uniquely hypoxic intrauterine environment has not been reported. Using a model of chorioamnionitis, we measured markers of pulmonary and systemic oxidant exposures in fetal lambs at 124 d gestation (term ϭ 150 d) exposed to 10 mg intra-amniotic endotoxin 2 d (n ϭ 6) or 7 d (n ϭ 6) before delivery, or saline as controls (n ϭ 9). The 7 d endotoxin-exposed animals had 3-fold higher protein carbonyls (0.66 Ϯ 0.46 versus 0.23 Ϯ 0.14 nmol/mg protein) and 10-fold greater myeloperoxidase activity (2.38 Ϯ 1.87 versus 0.27 Ϯ 0.18 nM) in the bronchoalveolar lavage fluid (BALF), suggestive of neutrophil-derived oxidant activity. However, in the lung tissue, protein carbonyls, superoxide dismutase, and peroxiredoxin 1 were not different between groups. The expression of peroxiredoxin 1 was prominent, primarily in the peri-bronchiolar epithelium. Notably, evidence of oxidant exposure was minimal at 2 d when BALF inflammatory cells, lung IL-1␤, and IL-8 were highest. Intra-amniotic endotoxin induced systemic oxidative stress as plasma protein carbonyl was elevated at 7 d (0.14 Ϯ 0.04 nmol/mg protein; p ϭ 0.005). Surfactant protein A and B mRNAs were highest at 2 d, suggesting that oxidative stress did not contribute to the lung maturation response. A modest lung oxidative stress in chorioamnionitis could contribute to bronchopulmonary dysplasia. (Pediatr Res 63: 274-279, 2008)

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“…Neutrophils recruited to the subtunical venules may secrete inflammatory cytokines such as TNF␣, IL-1␤, and IL-8 [30]. These aid in the recruitment of other leukocytes and enhance expression of the endothelial cell adhesion molecules, E-selectin and in- tercellular adhesion molecule (ICAM)-1 [31].…”

Section: Discussionmentioning

confidence: 99%

Essential Role of Neutrophils in Germ Cell-Specific Apoptosis Following Ischemia/Reperfusion Injury of the Mouse Testis1

Lysiak

Turner

Nguyen

et al. 2001

Biology of Reproduction

156

179

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This study investigates the role of neutrophils in ischemia-induced aspermatogenesis in the mouse. Previous studies in the rat have demonstrated that ischemia-inducing testicular torsion followed by torsion repair and reperfusion resulted in germ cell-specific apoptosis. This was correlated with an increase in neutrophil adhesion to subtunical venules, an increase in reactive oxygen species, and increased expression of several apoptosis-associated molecules. In the present investigation, wild-type C57BL/6 mice were subjected to various degrees and duration of testicular torsion. A torsion of 720 degrees for 2 h caused disruption of the seminiferous epithelium and significantly reduced testis weight and daily sperm production. An immunohistochemical method specific for apoptotic nuclei indicated that these effects were due to germ cell-specific apoptosis. An increase in myeloperoxidase (MPO) activity and an increase in the number of neutrophils adhering to testicular subtunical venules after torsion repair/reperfusion demonstrated an increase in neutrophil recruitment to the testis. In contrast, E-selectin knockout mice and wild-type mice rendered neutropenic showed a significant decrease in neutrophil recruitment as evidenced by MPO activity and microscopic examination of subtunical venules. Importantly, germ cell-specific apoptosis was also reduced. Thus, germ cell-specific apoptosis is observed after ischemia/reperfusion of the murine testis, and this apoptosis is directly linked to the recruitment of neutrophils to subtunical venules. Endothelial cell adhesion molecules, particularly E-selectin, play an important role in mediating this pathology.

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Polymorphonuclear leucocyte (PMN)-derived inflammatory cytokines—regulation by oxygen tension and extracellular matrix

Cited by 24 publications

References 21 publications

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Oxidative Stress in Fetal Lambs Exposed to Intra-amniotic Endotoxin in a Chorioamnionitis Model

Essential Role of Neutrophils in Germ Cell-Specific Apoptosis Following Ischemia/Reperfusion Injury of the Mouse Testis1

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