Evidence shows that hyperoxia influences the risk of infection, a

Evidence shows that hyperoxia influences the risk of infection, autoimmunity and alloreactivity and hence is a possible therapeutic option in a number of disorders. Regulatory T cells (Tregs) play a central role in tolerance maintenance, but their behaviour under hyperoxia is largely unknown. We investigated in vitro the impact of normobaric Inhibitor Library screening hyperoxia on human Tregs and their cellular network. Peripheral blood mononuclear

cells isolated from six healthy men were cultured under normoxia and escalating duration of normobaric hyperoxia (10 min, 1, 16, 88 h) under resting conditions and at the presence of anti-CD3/CD28 beads. Foxp3+ Tregs’ and other T cell subsets’ survival, proliferation, activation, maturation and Th1/Th2 markers were assessed by flow cytometry. We observed decreasing CD4+ cell survival with increasing duration of hyperoxia irrespectively of the presence of stimulators. The prevalence of CD4+CD45RA+ cells increased under stimulation (P = 0.001). In stimulated samples, the proliferation and induced Foxp3 expression decreased after 88 h of hyperoxia (both P = 0.001). BIBW2992 cost In conclusion, normobaric hyperoxia up to 16 h does not induce significant changes in basic human T cell subsets, including

the prevalence naturally occurring Tregs. Prolonged exposure to hyperoxia likely affects all unstimulated T cell subsets in a similar way. In stimulated T lymphocytes, the proliferation is hampered and cell death increases more evidently after prolonged hyperoxia (several days). Inducible Foxp3 expression is likely closely related to these processes. Naive CD4+ T cells are maintained Mirabegron by stimulation during exposure to hyperoxia. Oxygen tensions have been demonstrated to influence immune system reactions [1]. While the majority of experiments were performed under normoxic conditions, an emerging number of data are collected regarding immune cell functions under hypoxia. Limited evidence also supports, however, that hyperoxia

may modulate immune functions [2]. Existing studies indicate that hyperoxia, particularly hyperbaric oxygen exposure, modulate immune reactions. Under hyperoxia, phagocytosis and cytokine production of macrophages decrease [3], neutrophil cells migrate to regions with higher oxygen pressure [4], CD4/CD8 lymphocyte ratio and tissue distribution are altered [5, 6], while proliferation of haemopoietic cells is decreasing and apoptosis exaggerated [7]. As a net result of hyperoxic conditions, immune responses including autoimmunity and graft-versus-host reaction are suppressed [2, 8–10]. These data may be of particular clinical relevance as hyperoxia (particularly normobaric hyperoxia) frequently occurs during intensive care setting [11]. While several mechanisms contributing to immunomodulatory effects of hyperoxia have been revealed, other options have not been explored. These include the possible impact of hyperoxia on the induction of regulatory T cells (Tregs).

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