Dual mode of catecholamine action on splenic macrophage phagocytosis in wall lizard, Hemidactylus flaviviridis.
In the present study, in vitro concentration-related effect of catecholamines, dopamine (DA), norepinephrine (NE), and epinephrine (E) was observed on phagocytic activity of splenic macrophages to understand the impact of sympatho-adrenal-medullary (SAM) activation on innate immunity in wall lizard Hemidactylus flaviviridis under stress condition. Restraint stress for 1 h resulted in marked suppression of macrophage phagocytosis, suggesting that supra-physiological level of catecholamines in response to SAM activation under stress suppressed phagocytosis. This interpretation was reinforced since all the catecholamines considerably reduced phagocytosis at high concentrations ranging from 10(-7) to 10(-5)M. On the contrary, DA, NE, and E at low concentrations considerably stimulated phagocytosis, which increased with the decrease of concentrations ranging from 10(-11) to 10(-15)M. Further, effect of NE and E was blocked by beta-adrenergic blocker suggesting the beta-adrenoceptor-dependent regulating mechanism of NE and E. DA acts through both beta-adrenoceptor-dependent and D1/D2 class receptor-dependent mechanism, since beta-adrenergic blocker could partially block the DA effect. beta-Adrenoceptor-linked adenylate cyclase-mediated cAMP action in modulation of phagocytic activity was evident as 3-isobutyl-1-methyl-xanthine suppressed phagocytosis. Further, to delineate the mode of dual effect of catecholamines through beta-adrenergic receptors, in vitro concentration-related effect of cAMP was investigated on macrophage phagocytosis. cAMP depending on concentration had opposite effect on phagocytosis, and its stimulatory effect at low concentrations was reversed by actinomycin D and cycloheximide, whereas these transcription and translation inhibitors, respectively, failed to alter the inhibitory effect of cAMP at high concentrations. This suggests the concentration-related two different pathways of catecholamine action, classical non-genomic at high concentration while genomic pathway at low concentration.
Roy
Brototi
B
Department of Zoology, University of Delhi, Delhi 110 007, India.
Rai
Umesh
U
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003994:Bucladesine / Q000494:pharmacology; D002395:Catecholamines / Q000494:pharmacology*; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D018491:Dopamine Agonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D008116:Lizards / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D010587:Phagocytosis / Q000187:drug effects*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011954:Receptors, Dopamine / Q000187:drug effects; D013154:Spleen / Q000166:cytology*; D013312:Stress, Physiological
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D018491:Dopamine Agonists; D011500:Protein Synthesis Inhibitors; D011954:Receptors, Dopamine; D003609:Dactinomycin; D003994:Bucladesine; D003513:Cycloheximide; D001058:Apomorphine; D015056:1-Methyl-3-isobutylxanthine