Amplification of extracellular @entity377 -induced leukocyte(s) degranulation by contingent autocrine and paracrine mode of XXXX -mediated chemokine receptor activation.

@entity1 @entity1437 @entity8285 @entity2036 @entity4443 @entity9897 @entity377 @entity1426 @entity4352 @entity3900 @entity1317 @entity19960
Extracellular @entity377 -induced stimulation and activation of peripheral blood leukocytes and subsequent degranulation play a critical role in immediate-type hypersensitivity reaction and other inflammatory diseases. The extracellular @entity2036 stimulate a P2Y receptor(s) on @entity1 PMN with the pharmacological profile similar to that of the @entity9897 receptor. Upon activation of @entity9897 , @entity1426 , formed from the membrane bound lipids by @entity3900 , which subsequently metabolized by @entity1437 to form the @entity4443 . Of the several leukotrienes generated, @entity8285 is a potent pro-inflammatory chemokine. Upon its release @entity8285 binds to the PMN in a paracrine manner and also other leukocytes such as monocytes at the site of @entity1317 , leading to an accelerated rate of degranulation. It is known that LTA(4) formed in the @entity1437 pathway in PMN could be released from PMN by receptor-mediated transport. Upon its release, the monocytes, erythrocytes, platelet, endothelial or smooth muscle cells can take up LTA(4). The endogenous @entity19960 form the LTB(4) from LTA(4) in erythrocytes, platelet, endothelial or smooth muscle cells. As in PMN, @entity8285 is released from these cells via receptor-mediated transport to the extracellular milieu. Thus, released LTB(4) most likely acts as potentially accelerating factor in PMN and MN degranulation through its receptor-specific binding. It is not known whether any LTB(4) receptor exists in cytoplasm in any given cell type and also, the existence of any other signaling cascade for the extracellular @entity377 -induced leukocyte degranulation. Thus, it is convincing that the extracellular @entity2036 released from the activated platelets and other damaged cell types exacerbate the inflammatory response by @entity4352 generation. In turn the @entity4352 will act in both autocrine and paracrine manner to amplify the degranulation processes in leukocytes invoked by extracellular @entity2036 .
