Opioid receptor activation suppresses the neuroinflammatory response by promoting microglial M2 polarization
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F22%3A10452635" target="_blank" >RIV/00216208:11310/22:10452635 - isvavai.cz</a>
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=7p0dLEZHQr" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=7p0dLEZHQr</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.mcn.2022.103744" target="_blank" >10.1016/j.mcn.2022.103744</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Opioid receptor activation suppresses the neuroinflammatory response by promoting microglial M2 polarization
Popis výsledku v původním jazyce
Activation of microglia is considered the most important component of neuroinflammation. Microglia can adopt a pro-inflammatory (M1) or anti-inflammatory (M2) phenotype. Opioid receptors (ORs) have been shown to control neurotransmission of various peptidergic neurons, but their potential role in regulating microglial function is largely unknown. Here, we aimed to investigate the effect of the OR agonists DAMGO, DADLE and U50488 on the polarization of C8-B4 microglial cells. We observed that opioids suppressed lipopolysaccharide (LPS)-triggered M1 polarization and promoted M2 polarization. This was reflected in lower phagocytic activity, lower production of NO, lower expression of TNF-α, IL-1β, IL-6, IL-86 and IL-12 beta p40 together with higher migration rate, and increased expression of IL-4, IL-10, arginase 1 and CD 206 in microglia, compared to cells affected by LPS. We demonstrated that the effect of opioids on microglial polarization is mediated by the TREM2/NF-κB signaling pathway. These results provide new insights into the anti-inflammatory and neuroprotective effects of opioids and highlight their potential in combating neurodegenerative diseases.
Název v anglickém jazyce
Opioid receptor activation suppresses the neuroinflammatory response by promoting microglial M2 polarization
Popis výsledku anglicky
Activation of microglia is considered the most important component of neuroinflammation. Microglia can adopt a pro-inflammatory (M1) or anti-inflammatory (M2) phenotype. Opioid receptors (ORs) have been shown to control neurotransmission of various peptidergic neurons, but their potential role in regulating microglial function is largely unknown. Here, we aimed to investigate the effect of the OR agonists DAMGO, DADLE and U50488 on the polarization of C8-B4 microglial cells. We observed that opioids suppressed lipopolysaccharide (LPS)-triggered M1 polarization and promoted M2 polarization. This was reflected in lower phagocytic activity, lower production of NO, lower expression of TNF-α, IL-1β, IL-6, IL-86 and IL-12 beta p40 together with higher migration rate, and increased expression of IL-4, IL-10, arginase 1 and CD 206 in microglia, compared to cells affected by LPS. We demonstrated that the effect of opioids on microglial polarization is mediated by the TREM2/NF-κB signaling pathway. These results provide new insights into the anti-inflammatory and neuroprotective effects of opioids and highlight their potential in combating neurodegenerative diseases.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30105 - Physiology (including cytology)
Návaznosti výsledku
Projekt
—
Návaznosti
S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2022
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Molecular and Cellular Neurosciences
ISSN
1044-7431
e-ISSN
1095-9327
Svazek periodika
121
Číslo periodika v rámci svazku
July
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
13
Strana od-do
103744
Kód UT WoS článku
000819175300005
EID výsledku v databázi Scopus
2-s2.0-85131455632