Stimulation of adenosine receptors on myeloid cells enhances leukocyte migration at the site of burn injury
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Adenosine, endogenous purine nucleoside, is an ATP metabolite that also acts as an extracellular signaling molecule. The concentration of extracellular adenosine rises during hypoxia and cell damage leading to numerous pleiotropic effects. Although it has been shown that local adenosine concentrations are significantly increased during burn injury their effects at the site of the damage remain poorly investigated. Circulating myeloid cells express surface specific adenosine receptors and during burn injury they migrate to the damaged site. We have shown that during stimulation of the myeloid cells adenosine receptors for 72 h an alternative antigenic phenotype developed, which differed from that of (adenosine) unstimulated cells: the expression of the monocyte marker CD14 was preserved with already expressed dendritic cell markers (CD209, CD1a). These cells had also higher levels of mRNA expression of proinflammatory cytokines and chemoattractants (IL-6, IL-8, IL-1β). Being injected into the site of the burn injury the adenosine modified myeloid cells increased the bulk density of the mixed cellular infiltrate (granulocytes, monocytes, fibroblasts) by day 7. Thus, we have found that one of the effects of adenosine at the site of burn injury consists in increased migration of granulocytes and monocytes in response to the increased production of paracrine factors by myeloid cells.
Keywordsadenosine monocyte burn injury paracrine factor
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