Modulation of inflammatory responses by fractalkine signaling in microglia.

Modulation of inflammatory responses by fractalkine signaling in microglia.

Reactive microglia are suggested to be involved in neurological disorders, and the mechanisms underlying microglial activity may provide insights into therapeutic strategies for neurological diseases. Microglia produce immunological responses to various stimuli, which include fractalkine (FKN or CX3...

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Autores principales: Koichi Inoue, Hiroyuki Morimoto, Masahiro Ohgidani, Takatoshi Ueki
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2021
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Acceso en línea:https://doaj.org/article/cc2470ae2e0c460bb9515a695760febe
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spelling oai:doaj.org-article:cc2470ae2e0c460bb9515a695760febe2021-12-02T20:11:16ZModulation of inflammatory responses by fractalkine signaling in microglia.1932-620310.1371/journal.pone.0252118https://doaj.org/article/cc2470ae2e0c460bb9515a695760febe2021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0252118https://doaj.org/toc/1932-6203Reactive microglia are suggested to be involved in neurological disorders, and the mechanisms underlying microglial activity may provide insights into therapeutic strategies for neurological diseases. Microglia produce immunological responses to various stimuli, which include fractalkine (FKN or CX3CL1). CX3CR1, a FKN receptor, is present in microglial cells, and when FKN is applied before lipopolysaccharide (LPS) administration, LPS-induced inflammatory responses are inhibited, suggesting that the activation of the FKN signal is beneficial. Considering the practical administration for treatment, we investigated the influence of FKN on immunoreactive microglia using murine primary microglia and BV-2, a microglial cell line. The administration of LPS leads to nitric oxide (NO) production. NO was reduced when FKN was administered 4 h after LPS administration without a change in inducible nitric oxide synthase expression. In contrast, morphological changes, migratory activity, and proliferation were not altered by delayed FKN treatment. LPS decreases the CX3CR1 mRNA concentration, and the overexpression of CX3CR1 restores the FKN-mediated decrease in NO. CX3CR1 overexpression decreased the NO production that is mediated by LPS even without the application of FKN. ATP and ethanol also reduced CX3CR1 mRNA concentrations. In conclusion, the delayed FKN administration modified the LPS-induced microglial activation. The FKN signals were attenuated by a reduction in CX3CR1 by some inflammatory stimuli, and this modulated the inflammatory response of microglial cells, at least partially.Koichi InoueHiroyuki MorimotoMasahiro OhgidaniTakatoshi UekiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 5, p e0252118 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Koichi Inoue
Hiroyuki Morimoto
Masahiro Ohgidani
Takatoshi Ueki
Modulation of inflammatory responses by fractalkine signaling in microglia.
description Reactive microglia are suggested to be involved in neurological disorders, and the mechanisms underlying microglial activity may provide insights into therapeutic strategies for neurological diseases. Microglia produce immunological responses to various stimuli, which include fractalkine (FKN or CX3CL1). CX3CR1, a FKN receptor, is present in microglial cells, and when FKN is applied before lipopolysaccharide (LPS) administration, LPS-induced inflammatory responses are inhibited, suggesting that the activation of the FKN signal is beneficial. Considering the practical administration for treatment, we investigated the influence of FKN on immunoreactive microglia using murine primary microglia and BV-2, a microglial cell line. The administration of LPS leads to nitric oxide (NO) production. NO was reduced when FKN was administered 4 h after LPS administration without a change in inducible nitric oxide synthase expression. In contrast, morphological changes, migratory activity, and proliferation were not altered by delayed FKN treatment. LPS decreases the CX3CR1 mRNA concentration, and the overexpression of CX3CR1 restores the FKN-mediated decrease in NO. CX3CR1 overexpression decreased the NO production that is mediated by LPS even without the application of FKN. ATP and ethanol also reduced CX3CR1 mRNA concentrations. In conclusion, the delayed FKN administration modified the LPS-induced microglial activation. The FKN signals were attenuated by a reduction in CX3CR1 by some inflammatory stimuli, and this modulated the inflammatory response of microglial cells, at least partially.
format article
author Koichi Inoue
Hiroyuki Morimoto
Masahiro Ohgidani
Takatoshi Ueki
author_facet Koichi Inoue
Hiroyuki Morimoto
Masahiro Ohgidani
Takatoshi Ueki
author_sort Koichi Inoue
title Modulation of inflammatory responses by fractalkine signaling in microglia.
title_short Modulation of inflammatory responses by fractalkine signaling in microglia.
title_full Modulation of inflammatory responses by fractalkine signaling in microglia.
title_fullStr Modulation of inflammatory responses by fractalkine signaling in microglia.
title_full_unstemmed Modulation of inflammatory responses by fractalkine signaling in microglia.
title_sort modulation of inflammatory responses by fractalkine signaling in microglia.
publisher Public Library of Science (PLoS)
publishDate 2021
url https://doaj.org/article/cc2470ae2e0c460bb9515a695760febe
work_keys_str_mv AT koichiinoue modulationofinflammatoryresponsesbyfractalkinesignalinginmicroglia
AT hiroyukimorimoto modulationofinflammatoryresponsesbyfractalkinesignalinginmicroglia
AT masahiroohgidani modulationofinflammatoryresponsesbyfractalkinesignalinginmicroglia
AT takatoshiueki modulationofinflammatoryresponsesbyfractalkinesignalinginmicroglia
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