Serial Review: Redox signaling in immune function and cellular responses in lung injury and diseases Serial Review Editors: Victor Darley–Usmar, Lin MantellCytokines in tolerance to hyperoxia-induced injury in the developing and adult lung
Section snippets
Mechanism(s) of tissue injury/cell death in HALI
At sites of tissue injury, cells can die via necrosis or apoptosis. Traditionally, these processes have been considered operationally and mechanistically distinct cell-death responses [27], [28]. This distinction may not be as clear-cut as previously thought [29]. Studies have shown that apoptosis-like deoxyribonucleic acid (DNA) laddering and positive terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling (TUNEL) staining can be seen in cells undergoing necrosis. Known inducers of
Cytokines (and select growth factors) involved in tolerance toward HALI
In this review, we will focus on cytokines (and select growth factors) that have been shown to be involved in tolerance toward HALI in animal models.
Conclusions
It is quite apparent that cytokines (and growth factors) have a significant role to play in tolerance to hyperoxic lung injury. Increased cytokine expression and release have a cascade effect. IL-1 precedes the increase in IL-6 and IL-8 and this seems to precede the influx of inflammatory cells. It is possible that resident cells in the lung initiate the inflammatory response to hyperoxia by the release of various cytokines, which, in turn, attract inflammatory cells to the alveolar space and
Acknowledgments
This work was supported in part by Grants HL-74195 (V.B.), HL-64242, HL-61904, and HL-56389 (J.A.E.) from the NHLBI of the National Institutes of Health, USA.
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