Invertebrate innate immunity relies on both cellular and humoral components. Among humoral factors,there is less information on soluble molecules able to act as signals during the immune response (i.e.cytokines). In Drosophila melanogaster, the cytokine Unpaired (Upd)-3, is known to activate the JAK/STATpathway, but it is still not clear which molecules and pathways are responsible for its induction andsecretion. It has been proposed that highly chemotactic factors may increase the expression of upd-3.In this respect, we have studied the effects of the chemotactic human recombinant (hr) interleukin(IL)-8 on the immune functions of Drosophila SL2 macrophage-like cells. The hrIL-8 increases the percentageof phagocytic cells with a specific timing and enhances the expression of the cytokine, upd-3, as wellas that of the putative cytokine Drosophila helical factor (dhf). The antimicrobial peptides defensin, cecropinA1 and diptericin, are all influenced in their expression by the human chemokine, while hrIL-8 leavesunaffected the expression of drosomycin, i.e. the antimicrobial peptide more strictly connected with theToll pathway. Similar effects to those registered for hrIL-8 are also provoked by a specific activator of theImd pathway, i.e. the Escherichia coli peptidoglycan. RNAi experiments demonstrated that the silencing ofthe Imd pathway-associated kinase dTAK1, leaves unaffected the induction of upd-3, while it completelyabolishes the effects of hrIL-8-on the expression of dhf. Our data suggest that the Imd pathway is not fundamentalin regulating the levels of upd-3, whereas it controls the expression of the putative cytokine dhf.

unpaired (upd)-3 expression and other immune-related functions are stimulated by interleukin-8 in Drosophila melanogaster SL2 cell line / Malagoli, Davide; Sacchi, S; Ottaviani, Enzo. - In: CYTOKINE. - ISSN 1043-4666. - STAMPA. - 44:(2008), pp. 269-274. [10.1016/j.cyto.2008.08.011]

unpaired (upd)-3 expression and other immune-related functions are stimulated by interleukin-8 in Drosophila melanogaster SL2 cell line

MALAGOLI, Davide;OTTAVIANI, Enzo
2008

Abstract

Invertebrate innate immunity relies on both cellular and humoral components. Among humoral factors,there is less information on soluble molecules able to act as signals during the immune response (i.e.cytokines). In Drosophila melanogaster, the cytokine Unpaired (Upd)-3, is known to activate the JAK/STATpathway, but it is still not clear which molecules and pathways are responsible for its induction andsecretion. It has been proposed that highly chemotactic factors may increase the expression of upd-3.In this respect, we have studied the effects of the chemotactic human recombinant (hr) interleukin(IL)-8 on the immune functions of Drosophila SL2 macrophage-like cells. The hrIL-8 increases the percentageof phagocytic cells with a specific timing and enhances the expression of the cytokine, upd-3, as wellas that of the putative cytokine Drosophila helical factor (dhf). The antimicrobial peptides defensin, cecropinA1 and diptericin, are all influenced in their expression by the human chemokine, while hrIL-8 leavesunaffected the expression of drosomycin, i.e. the antimicrobial peptide more strictly connected with theToll pathway. Similar effects to those registered for hrIL-8 are also provoked by a specific activator of theImd pathway, i.e. the Escherichia coli peptidoglycan. RNAi experiments demonstrated that the silencing ofthe Imd pathway-associated kinase dTAK1, leaves unaffected the induction of upd-3, while it completelyabolishes the effects of hrIL-8-on the expression of dhf. Our data suggest that the Imd pathway is not fundamentalin regulating the levels of upd-3, whereas it controls the expression of the putative cytokine dhf.
2008
44
269
274
unpaired (upd)-3 expression and other immune-related functions are stimulated by interleukin-8 in Drosophila melanogaster SL2 cell line / Malagoli, Davide; Sacchi, S; Ottaviani, Enzo. - In: CYTOKINE. - ISSN 1043-4666. - STAMPA. - 44:(2008), pp. 269-274. [10.1016/j.cyto.2008.08.011]
Malagoli, Davide; Sacchi, S; Ottaviani, Enzo
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