Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effect of a range of adenosine receptor agonists on intracellular free calcium concentration ([Ca2+]i) has been studied in the hamster vas deferens smooth muscle cell line DDT1MF-2. 2. Adenosine receptor agonists elicited a rapid and maintained increase in [Ca2+]i in fura-2 loaded DDT1MF-2 cells. The initial rise could be maintained in the absence of extracellular calcium, whereas the maintained or plateau phase was dependent upon the presence of extracellular calcium and appeared to be associated with calcium influx. The rank order of agonist potencies was N6-cyclopentyladenosine > 5'-N-ethylcarboxamidoadenosine > 2-chloroadenosine > adenosine. 3. The response to 2-chloroadenosine was antagonized by the antagonists 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, KD 0.14 nM) and 8-phenyltheophylline (KD 112 nM). 4. Pretreatment with the 5-lipoxygenase inhibitor AA861 (20 microM) produced only a small (14 +/- 2%) inhibition of the [Ca2+]i response elicted by N6-cyclopentyladenosine (300 nM), in nominally Ca(2+)-free buffer containing 0.1 mM EGTA. The cyclo-oxygenase inhibitor, indomethacin (2 microM) was without effect. 5. The Ca(2+)-influx associated with the plateau phase required the continued presence of agonist on the receptor. The antagonist DPCPX (100 nM) attenuated the rise in [Ca2+]i observed when extracellular Ca2+ was re-applied after the cells had been stimulated with N6-cyclopentyladenosine (CPA; 300 nM) in experiments initiated in nominally Ca(2+)-free buffer. 6. Pretreatment with pertussis toxin (200 ng ml-1 for 4 h) inhibited the CPA (100 nM) stimulated intracellular Ca2+ release and Ca2+ influx but was without effect on the response to histamine (100 microM). 7.These data suggest that adenosine A(1)-receptor activation in DDT(1)MF-2 cells stimulates release of Ca(2+) from intracellular stores and influx of extracellular Ca(2+) through Ca(2+) entry pathways in the plasma membrane which required the continued presence of agonist on the receptor.
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PMID:Adenosine A1-receptor stimulated increases in intracellular calcium in the smooth muscle cell line, DDT1MF-2. 842 18

Eicosanoid lipid mediators, including prostaglandin E(2) (PGE(2)) and leukotrienes (LTs) B(4) and D(4), are produced in abundance in the infected lung. We have previously demonstrated that individually, PGE(2) suppresses while both classes of LTs augment alveolar macrophage (AM) innate immune functions. In this study, we sought to more appropriately model the milieu at a site of infection by studying the in vitro effects of these lipid mediators on Fc gammaR-mediated phagocytosis when they are present in combination. Consistent with their individual actions, both LTB(4) and LTD(4) opposed the suppressive effect of PGE(2) on phagocytosis, but only LTB(4) did so by mitigating the stimulatory effect of PGE(2) on intracellular cAMP production. Unexpectedly, we observed that IgG-opsonized targets themselves elicited a dose-dependent reduction in intracellular cAMP in AMs, but this was not observed in peritoneal macrophages or elicited peritoneal neutrophils; this effect in AMs was completely abolished by treatment with the LT synthesis inhibitor AA861, the BLT receptor 1 antagonist CP 105,696, and the G alpha i inhibitor pertussis toxin. Of two downstream cAMP effectors, protein kinase A and exchange protein activated by cAMP, the ability of PGE(2) to activate the latter but not the former was abrogated by both LTs B(4) and D(4). Taken together, our results indicate that both classes of LTs oppose the immune suppressive actions of PGE(2), with the stimulatory actions of LTB(4) reflecting combinatorial modulation of intracellular cAMP and those of LTD(4) being cAMP independent.
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PMID:Crosstalk between prostaglandin E2 and leukotriene B4 regulates phagocytosis in alveolar macrophages via combinatorial effects on cyclic AMP. 1910 85