“…After 2h, IL-1b expression was restored to control levels, suggesting that it is rapidly regulated, TNFa remained unchanged and IL-6 and TGF-b1 expression were inhibited. This inhibition of cytokine expression is in concordance with the described inhibition of the pro-inflammatory cytokine expression by adrenaline stress in mammalian systems [62,63] and confirms the previously described important role of immuneendocrine interactions in the head kidney of fish [64,65]. However, we cannot disregard the possible effects of different adrenaline receptors in the head kidney (already described in other species, such as catfish [66] and rainbow trout [67] where head kidney leukocytes expressed both alpha and beta adrenergic receptors) that could be exerting differential and even opposite effects and therefore counteracting the expression of cytokines.…”
“…After 2h, IL-1b expression was restored to control levels, suggesting that it is rapidly regulated, TNFa remained unchanged and IL-6 and TGF-b1 expression were inhibited. This inhibition of cytokine expression is in concordance with the described inhibition of the pro-inflammatory cytokine expression by adrenaline stress in mammalian systems [62,63] and confirms the previously described important role of immuneendocrine interactions in the head kidney of fish [64,65]. However, we cannot disregard the possible effects of different adrenaline receptors in the head kidney (already described in other species, such as catfish [66] and rainbow trout [67] where head kidney leukocytes expressed both alpha and beta adrenergic receptors) that could be exerting differential and even opposite effects and therefore counteracting the expression of cytokines.…”
“…One of the functional consequences of adrenergic stimulation in macrophages (MØ) is the alteration in endotoxin mediated cytokine expression through intracellular signaling mechanisms (Bergmann, 2002;Cohen et al, 2004;Deng et al, 2004;Muthu et al, 2005a). Since all FACS defined hematopoietic myeloid progenitors were shown to express adrenergic receptors, we tested the functionality of the receptors in terms of cytokine expression that would indirectly indicate the coupling of adrenergic receptors.…”
Section: Functionality Of Adrenergic Receptorsmentioning
Association between the nervous and immune system is well documented. Immune cells originate within the bone marrow that is innervated. Thermal injury induces adrenergic stimulation, augments monocytopoiesis and alters the β-adrenergic receptor (AR) profile of bone marrow monocyte committed progenitors. This provides an impetus to study AR expression in hematopoietic progenitors along myeloid lineage. Using FACS analysis and confocal microscopy, we report the expression of α1-, α2-and β2-AR in enriched populations of ER-MP20+ and ER-MP12+ myeloid progenitors, CD117+ and CD34+ multi-potential progenitors and more importantly pluripotent stem cells suggesting a plausible role for catecholamine in hematopoietic development.
“…(D) To determine if norepinephrine-mediated changes in phagocytosis involve the protein kinase A (PKA) signaling pathway, cells were incubated with H-89 (10 −5 M, Sigma), a specific inhibitor of PKA, for two hours prior to norepinephrine treatment as above. The dosages and treatment durations employed were chosen to allow ease of comparison with previous studies (20,21,23). …”
Background-The systemic response to injury is characterized by massive release of norepinephrine (NE) into the circulation as a result of global sympathetic activation. We have recently demonstrated that NE modulates the recruitment of macrophages to the cutaneous wound. We hypothesized that NE suppresses wound macrophage phagocytic function through canonical adrenergic signaling pathways.
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