1995
DOI: 10.1016/0165-5728(95)00050-c
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Enhancement of phagocytosis by dynorphin A in mouse peritoneal macrophages

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Cited by 39 publications
(27 citation statements)
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“…In the wall lizard H. flaviviridis, dyn A (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) by acting through the -opioid receptor inhibited the phagocytosis of yeast cells by splenic phagocytes. This is in contrast to data reported in fish (Singh and Rai, 2010) and mammals (Ichinose et al, 1995), wherein, dyn A (1-17) stimulated the phagocytosis of yeast cells by fish splenic phagocytes (Singh and Rai, 2010) and latex particles by murine peritoneal macrophages (Ichinose et al, 1995). With respect to receptormediated action, dyn A (1-17) stimulated the phagocytosis through a -opioid receptor in fish only.…”
Section: Discussioncontrasting
confidence: 55%
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“…In the wall lizard H. flaviviridis, dyn A (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) by acting through the -opioid receptor inhibited the phagocytosis of yeast cells by splenic phagocytes. This is in contrast to data reported in fish (Singh and Rai, 2010) and mammals (Ichinose et al, 1995), wherein, dyn A (1-17) stimulated the phagocytosis of yeast cells by fish splenic phagocytes (Singh and Rai, 2010) and latex particles by murine peritoneal macrophages (Ichinose et al, 1995). With respect to receptormediated action, dyn A (1-17) stimulated the phagocytosis through a -opioid receptor in fish only.…”
Section: Discussioncontrasting
confidence: 55%
“…With respect to receptormediated action, dyn A (1-17) stimulated the phagocytosis through a -opioid receptor in fish only. Interestingly, in mammals, the stimulatory effect of dyn A (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) was mediated through a non-opioid receptor as the non-selective opioid receptor blocker naltrexone failed to block the effect of dyn A (1-17) on phagocytosis (Ichinose et al, 1995). Nevertheless, a specific opioid-receptor-mediated inhibitory effect of dynorphin(s) and its receptor agonist on phagocytosis has been reported in mammals.…”
Section: Discussionmentioning
confidence: 99%
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“…Indeed, screening of several proteins stored in neutrophil granules as well as mammalian cathelicidins and other cationic peptides showed that they bind the a M I-domain 20 (and unpublished data). Consistent with this proposal, we have recently shown that the cationic peptide dynorphin A that was previously shown to enhance phagocytosis 56 opsonizes bacteria and promotes phagocytosis through Mac-1. 57 Since negatively charged residues are generally strongly disfavored in the Mac-1 recognition motifs, it is tempting to speculate that the absence of negatively charged residues in some cathelicidin peptides (eg, bovine SMAP-29 and BMAP-27 1 ) as compared to LL-37 may increase their Mac-1-binding activity.…”
Section: 9supporting
confidence: 63%
“…Furthermore, inhibition of LPS-induced NF-κB activation and subsequent IL-1β release following naloxone treatment in RAW264 cells was mediated by L-type calcium channels [16]. The enhancement of phagocytosis by DYN 1-17 in mouse peritoneal macrophages was reported to be dependent on intracellular calcium signalling [17], whereas in another study, the inhibition of LPS-induced production of nitric oxide and TNF-α by DYN 1-8 was not blocked by the KOR antagonist norbinaltorphimine (nor-BNI), indicative of the involvement of non-opioid mechanisms in these inhibitory effects [18].…”
Section: Introductionmentioning
confidence: 96%