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Pulmonary production of such mediators may induce systemic responses.
ACTH-stimulated glucocorticoids and/or immunologic mediators may induce release of MIF by Th2 cells [ 5].
Alternatively, 15d-PGJ2, directly or through production of other mediators, may induce negative regulators of JAK activity, such as SOCS or SHP2.
Furthermore, systemic and local inflammatory mediators may induce structural and functional alterations in the peritoneal membrane, thus interfering with dialysis adequacy.
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Additional studies will be needed to clarify the roles of astrocytes and pericytes in BBB function and to identify molecular mediators that may induce BBB properties in cerebral endothelia.
BAL fluid from mice exposed to 6 ppm ozone immediately following exposure manifested little inflammation but exhibited AHR; we postulated that a mediator in BAL may induce AHR.
These mediators may have affected the activity of SP levels.
Sympathetic mediators such as epinephrine and norepinephrine may induce cytokine release from immune cells [ 6] and can enhance migration of immune cells to sites of inflammation as well as the degree of plasma extravasation [ 7].
Experimental studies have suggested that high tidal volume ventilation may induce various inflammatory mediators that leak into the circulation causing injury to distant organs including the heart [ 12, 13], with this effect being amplified in the setting of acute lung injury [ 14– 16].
We speculate that increased IFN-β, IL-6, and COX-2 expression in HBV WT-transfected /Phyllanthus extract-treated HepG2 cells may induce the expression of IFN-inducible genes and/or different inflammatory mediators, which then inhibit HBV replication.
In addition, efferocytosis may induce DCs to secrete immunosuppressive mediators, such as TGF-β, which triggers the differentiation of classical regulatory T lymphocytes, Foxp3+ Tregs [ 36, 37].
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