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Effect of hyperoxia on human macrophage cytokine response
P Desmarquest1, K Chadelat, S Corroyer
1Department of Pediatric Pulmonology-INSERUM U142, Trousseau Hospital, St. Antoine Medical School, University of Paris, France.
Abstract:
In the development of lung damage induced by oxidative stress, it has been proposed that changes in alveolar macrophages (AM) function with modifications in cytokine production may contribute to altered repair processes. To characterize the changes in profiles of cytokine production by macrophages exposed to oxidants, the effects of hyperoxia (95% O2) on interleukin (IL)-1 beta, IL-6, IL-8, and tumour necrosis factor-alpha (TNF-alpha) expression were studied. Experiments were first performed using AM obtained from control subjects and children with interstitial lung disease. Results showed that a 48 h O2 exposure was associated with two distinct patterns of response: a decrease in TNF-alpha, IL-1 beta and IL-6 expression, and an increase in IL-8. To complete these observations we used U937 cells that were exposed for various durations to hyperoxia. We confirmed that a 48 h O2 exposure led to similar changes with a decrease in TNF-alpha, IL-1 beta and IL-6 production and an increase in IL-8. Interestingly, this cytokine response was preceded during the first hours of O2 treatment by induction of TNF-alpha, IL-1 beta and IL-6. These data indicate that hyperoxia induces changes in the expression of macrophages inflammatory cytokines, and that these modifications appear to be influenced by the duration of O2 exposure.
Insights
Oxidative stress from hyperoxia alters macrophage cytokine production in lung injury. Long-term oxygen exposure decreases TNF-alpha, IL-1 beta, and IL-6 while increasing IL-8, impacting lung repair.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cell Biology
Background:
- Oxidative stress contributes to lung damage.
- Alveolar macrophages (AM) play a role in lung repair through cytokine production.
- Dysregulated cytokine profiles in AM may impair lung repair processes.
Purpose of the Study:
- To investigate the impact of hyperoxia on macrophage cytokine production.
- To characterize changes in interleukin (IL)-1 beta, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) expression.
Main Methods:
- Exposed alveolar macrophages (AM) from control and pediatric interstitial lung disease patients to hyperoxia (95% O2).
- Utilized U937 cells for further experiments on cytokine expression under varying hyperoxia durations.
- Measured cytokine expression including IL-1 beta, IL-6, IL-8, and TNF-alpha.
Main Results:
- A 48-hour hyperoxia exposure decreased TNF-alpha, IL-1 beta, and IL-6 expression.
- Conversely, IL-8 expression increased after 48 hours of oxygen exposure.
- Short-term hyperoxia (first few hours) initially induced TNF-alpha, IL-1 beta, and IL-6.
Conclusions:
- Hyperoxia significantly alters inflammatory cytokine expression in macrophages.
- The duration of oxygen exposure influences the pattern of cytokine response.
- These cytokine modifications may impact lung repair mechanisms in oxidative stress-induced lung damage.