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• W2022986843 startingPage "557" @default.
• W2022986843 abstract "Strong evidence suggests that neutrophils may play an active role in acute and chronic inflammatory disorders, such as rheumatoid arthritis and atherosclerosis. Given the role of pro-inflammatory cytokine TNF-α in these inflammatory processes, we planned the present study to investigate the effect of short term incubation with TNF-α on neutrophil migration to CCL3, a chemokine produced in inflammatory sites and normally devoid of neutrophil chemotactic properties. We found that TNF-α primed neutrophils for migration to CCL3 via CCR5. TNF-α-induced migration was a consequence of the TNF-α-induced up-regulation of integrin CD11b/CD18 (Mac-1) on neutrophil surface. Furthermore, TNF-α activity was found to be strictly dependent on the activation of ERK 1/2 p44, cooperating with the intracellular pathways involving Src kinases, PI3K/Akt, p38 MAPK, well known as activated in response to classical chemoattractants (CXCL8) or priming agents (GM-CSF). On the contrary, the effect of TNF-α on neutrophil migration to CCL3 was not dependent on JNK 1/2. In conclusion, the present report shows that TNF-α unveils a previously unknown capacity of neutrophils to migrate to CCL3 through the intervention of Mac-1. TNF-α regulates Mac-1 up-regulation through signalling pathways, involving various kinases, but not JNK 1/2. Although highly speculative, ERK 1/2 p44 may represent a selective target for the pharmacologic manipulation of neutrophil-mediated adverse activities in TNF-α-mediated inflammatory states." @default.
• W2022986843 created "2016-06-24" @default.
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• W2022986843 date "2008-03-01" @default.
• W2022986843 modified "2023-09-25" @default.
• W2022986843 title "Tumor necrosis factor-alpha (TNF-α) induces integrin CD11b/CD18 (Mac-1) up-regulation and migration to the CC chemokine CCL3 (MIP-1α) on human neutrophils through defined signalling pathways" @default.
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• W2022986843 doi "https://doi.org/10.1016/j.cellsig.2007.11.008" @default.
• W2022986843 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18164590" @default.
• W2022986843 hasPublicationYear "2008" @default.
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