Biological and kinetic characterization of recombinant human macrophage inflammatory peptides 2 alpha and beta and comparison with the neutrophil activating peptide 2 and interleukin 8
We examined the biological and kinetic characteristics of two new members of the intercrine family of cytokines. Human macrophage inflammatory peptides 2 α and β (huMIP-2α and β) were compared to human interleukin 8 (huIL-8), neutrophil activating peptide 2 (huNAP-2), and N-formyl-L-methionyl-L-leuc...
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Published in | Cytokine (Philadelphia, Pa.) Vol. 6; no. 2; pp. 124 - 134 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Ltd
01.03.1994
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Subjects | |
Online Access | Get full text |
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Summary: | We examined the biological and kinetic characteristics of two new members of the intercrine family of cytokines. Human macrophage inflammatory peptides 2 α and β (huMIP-2α and β) were compared to human interleukin 8 (huIL-8), neutrophil activating peptide 2 (huNAP-2), and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). The huMIP-2 peptides were the least potent cytokine tested in triggering neutrophil degranulation. They were also less potent neutrophil chemotaxins than fMLP or huIL-8. However, they were more effective than NAP-2 in stimulating chemotaxis of neutrophils. The binding studies showed that huMIP-2 peptides could interact with specific receptors on human blood neutrophils. Moreover, huMIP-2 peptides competed for up to 60% of the huIL-8 binding sites on neutrophils whereas huIL-8 competed for almost 100% of either of the huMIP-2 peptide binding sites. These data suggest the huMIP-2 peptides have little or no affinity for 40% of the huIL-8 receptors. In addition, detectable amounts of mRNA for huMIP-2α were found in samples from human alveolar macrophages stimulated with
Staphylococcus aureus, toxic shock syndrome toxin-1 (TSST), but not in samples stimulated with
S. aureus enterotoxin A (SEA) or
Escherichia coli endotoxin (lipopolysaccharide = LPS). In conclusion, huMIP-2α and β are weak neutrophil stimulating agents, which may increase inflammation in diseases such as toxic shock syndrome. |
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ISSN: | 1043-4666 1096-0023 |
DOI: | 10.1016/1043-4666(94)90033-7 |