Role of tumor necrosis factor in oxygen toxicity

Jensen, J C; Pogrebniak, Helen W.; Pass, H. I.; Buresh, C M; Merino, María J.; Kauffman, Dorothy; Venzon, D.; Langstein, Howard N.; Norton, Jeffrey A.

doi:10.1152/jappl.1992.72.5.1902

Cited by 74 publications

(45 citation statements)

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“…In the majority of these studies, the cytokine ligand is induced and is presumed to mediate its effects by binding to its unaltered receptor (14,(25)(26)(27)(28)(29)31). Interestingly, our studies of IL-13 highlight a different paradigm with 100% O 2 stimulating the expression of both the IL-4R␣ and IL-13R␣1 subunits of the IL-13R without altering the expression of IL-13.…”

Section: Discussionmentioning

confidence: 92%

“…A variety of lines of evidence suggests that the consequences of hyperoxia are mediated and regulated, at least in part, by the ability of 100% O 2 to induce a variety of cytokine-receptor pathways (14,(25)(26)(27)(28)(29)(30)(31). In the majority of these studies, the cytokine ligand is induced and is presumed to mediate its effects by binding to its unaltered receptor (14,(25)(26)(27)(28)(29)31).…”

Section: Discussionmentioning

confidence: 99%

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Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Bhandari

Choo-Wing

Homer

et al. 2007

The Journal of Immunology

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IL-13 is a critical effector at sites of Th2 inflammation and remodeling. As a result, anti-IL-13-based therapies are being actively developed to treat a variety of diseases and disorders. However, the beneficial effects of endogenous IL-13 in the normal and diseased lung have not been adequately defined. We hypothesized that endogenous IL-13 is an important regulator of oxidant-induced lung injury and inflammation. To test this hypothesis, we compared the effects of 100% O2 in mice with wild-type and null IL-13 loci. In this study, we demonstrate that hyperoxia significantly augments the expression of the components of the IL-13R, IL-13Rα1, and IL-4Rα. We also demonstrate that, in the absence of IL-13, hyperoxia-induced tissue inflammation is decreased. In contrast, in the IL-13 null mice, DNA injury, cell death, caspase expression, and activation and mortality are augmented. Interestingly, the levels of the cytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in the bronchoalveolar lavage fluid. These studies demonstrate that the expression of the IL-13R is augmented and that the endogenous IL-13-IL-13R pathway contributes to the induction of inflammation and the inhibition of injury in hyperoxic acute lung injury.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Bhandari

Choo-Wing

Homer

et al. 2007

The Journal of Immunology

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“…Furthermore, Yang et al [58] also demonstrated the inhibition of TNF- production in a rat model of intestinal injury treated with HBOT. However, significant increases in the expression of IL-6, IL-1 and TNF- have been also reported [1,25,26,41,49].…”

Section: Discussionmentioning

confidence: 97%

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

et al. 2012

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Adipose tissue often becomes poorly oxygenated in obese subjects. This feature may provide cellular mechanisms involving chronic inflammation processes such as the release of proinflammatory cytokines and macrophage infiltration. In this context, the purpose of the present study was to determine whether a hyperoxia exposure on mature adipocytes may influence the expression of some adipokines and involve favorable changes in specific metabolic variables. 3T3-L1 adipocytes (14 days differentiated) were treated with 95% oxygen for 24 h. Cell viability, intra and extracellular reactive oxygen especies (ROS) content, glucose uptake and lactate and glycerol concentrations were measured in the culture media. Also, mRNA levels of HIF-1, leptin, IL-6, MCP-1, PPAR-, adiponectin, and ANGPTL-4 were analyzed.Hyperoxia treatment increased intra and extracellular ROS content, reduced glucose uptake and lactate release and increased glucose release. It also led to an upregulation of the expression of IL-6, MCP-1 and PPAR-, while ANGPTL4 was downregulated in the hyperoxia group with respect to control. The present data shows that hyperoxia treatment seems to provoke an inflammatory response due to the release of ROS and the upregulation of pro-inflammatory adipokines, such as IL-6 and MCP-1. On the other hand, hyperoxia may have an indirect effect on the improvement of insulin sensitivity, due to the upregulation of PPAR- gene expression as well as a possible modulation of both glucose and lipid metabolic markers. To our knownledge, this is the first study analyzing the effect of hyperoxia in 3T3-L1 adipocytes.

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“…The precise role of TNF-a in the development of hyperoxic lung damage has not yet been established. In most previous studies, exogenous TNF-a was used to explore its effects on the development of pulmonary oxygen toxicity [11][12][13][14]. We studied the effect of a single exposure to HBO on the endogenous secretion of TNF-a by blood monocytes, by macrophages from the lungs (as the main target of the oxidative insult) and by macrophages of the spleen (as a major immunoregulatory organ).…”

Section: Introductionmentioning

confidence: 99%

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-α) secretion from rat macrophages

Lahat

Bitterman

Yaniv

et al. 1995

Clinical and Experimental Immunology

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SUMMARYWe investigated the secretion of TNF-a by monocytes and macrophages derived from the peripheral blood, spleen, and lungs after a single exposure to a therapeutic profile of hyperbaric oxygen (HBO). Rats were exposed for 90 min to either 100% oxygen at 0 28 MPa (2-8 atmospheres absolute) or air. Immediately after exposure, mononuclear cells were isolated from blood, spleen, and lungs and cultured for 18h. The secretion of TNF-a from the cultured monocytes/macrophages was determined with and without stimulation with lipopolysaccharide (LPS). Exposure to hyperbaric oxygen induced a significant increase in the spontaneous ex vivo secretion of TNF-a (without LPS) by mononuclear cells from the blood, spleen, and lung (P < 0 05 from air controls). Stimulation with LPS after exposure to HBO induced a significant increase in TNF-a secretion by lung and spleen macrophages compared with air controls (P<005). However, absolute TNF-a levels were not significantly higher than those achieved 'spontaneously' in macrophages exposed to HBO without LPS. Stimulation with LPS induced a marked increase in secretion of TNF-a from blood monocytes after exposure to air, but not after exposure to HBO. These results provide evidence in support of a role played by TNF-a in mediating HBO effects on different tissues and their immune responses.

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Role of tumor necrosis factor in oxygen toxicity

Cited by 74 publications

References 0 publications

Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

Exposure to hyperbaric oxygen induces tumour necrosis factor-alpha (TNF-α) secretion from rat macrophages

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