FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1998911644> ?p ?o ?g. }

• W1998911644 endingPage "10" @default.
• W1998911644 startingPage "10" @default.
• W1998911644 abstract "It is well appreciated that obtaining sufficient numbers of primary microglia for in vitro experiments has always been a challenge for scientists studying the biological properties of these cells. Supplementing culture medium with granulocyte-macrophage colony-stimulating factor (GM-CSF) partially alleviates this problem by increasing microglial yield. However, GM-CSF has also been reported to transition microglia into a dendritic cell (DC)-like phenotype and consequently, affect their immune properties.Although the concentration of GM-CSF used in our protocol for mouse microglial expansion (0.5 ng/ml) is at least 10-fold less compared to doses reported to affect microglial maturation and function (>/= 5 ng/ml), in this study we compared the responses of microglia derived from mixed glial cultures propagated in the presence/absence of low dose GM-CSF to establish whether this growth factor significantly altered the immune properties of microglia to diverse bacterial stimuli. These stimuli included the gram-positive pathogen Staphylococcus aureus (S. aureus) and its cell wall product peptidoglycan (PGN), a Toll-like receptor 2 (TLR2) agonist; the TLR3 ligand polyinosine-polycytidylic acid (polyI:C), a synthetic mimic of viral double-stranded RNA; lipopolysaccharide (LPS) a TLR4 agonist; and the TLR9 ligand CpG oligonucleotide (CpG-ODN), a synthetic form of bacteria/viral DNA.Interestingly, the relative numbers of microglia recovered from mixed glial cultures following the initial harvest were not influenced by GM-CSF. However, following the second and third collections of the same mixed cultures, the yield of microglia from GM-CSF-supplemented flasks was increased two-fold. Despite the ability of GM-CSF to expand microglial numbers, cells propagated in the presence/absence of GM-CSF demonstrated roughly equivalent responses following S. aureus and PGN stimulation. Specifically, the induction of tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-2 (MIP-2/CXCL2), and major histocompatibility complex (MHC) class II, CD80, CD86 expression by microglia in response to S. aureus were similar regardless of whether cells had been exposed to GM-CSF during the mixed culture period. In addition, microglial phagocytosis of intact bacteria was unaffected by GM-CSF. In contrast, upon S. aureus stimulation, CD40 expression was induced more prominently in microglia expanded in GM-CSF. Analysis of microglial responses to additional pathogen-associate molecular patterns (PAMPs) revealed that low dose GM-CSF did not significantly alter TNF-alpha or MIP-2 production in response to the TLR3 and TLR4 agonists polyI:C or LPS, respectively; however, cells expanded in the presence of GM-CSF produced lower levels of both mediators following CpG-ODN stimulation.We demonstrate that low levels of GM-CSF are sufficient to expand microglial numbers without significantly affecting their immunological responses following activation of TLR2, TLR4 or TLR3 signaling. Therefore, low dose GM-CSF can be considered as a reliable method to achieve higher microglial yields without introducing dramatic activation artifacts." @default.
• W1998911644 created "2016-06-24" @default.
• W1998911644 creator A5016119949 @default.
• W1998911644 creator A5022037144 @default.
• W1998911644 date "2007-01-01" @default.
• W1998911644 modified "2023-09-26" @default.
• W1998911644 title "Effects of low dose GM-CSF on microglial inflammatory profiles to diverse pathogen-associated molecular patterns (PAMPs)" @default.
• W1998911644 cites W1495090829 @default.
• W1998911644 cites W1533029876 @default.
• W1998911644 cites W1552686264 @default.
• W1998911644 cites W1557696362 @default.
• W1998911644 cites W1641259203 @default.
• W1998911644 cites W1646206347 @default.
• W1998911644 cites W1798758220 @default.
• W1998911644 cites W18573662 @default.
• W1998911644 cites W1886726419 @default.
• W1998911644 cites W1959886281 @default.
• W1998911644 cites W1964774089 @default.
• W1998911644 cites W1966871622 @default.
• W1998911644 cites W1972401206 @default.
• W1998911644 cites W1973312385 @default.
• W1998911644 cites W1978549020 @default.
• W1998911644 cites W1981310043 @default.
• W1998911644 cites W1982404230 @default.
• W1998911644 cites W1988740119 @default.
• W1998911644 cites W1991165501 @default.
• W1998911644 cites W1994318537 @default.
• W1998911644 cites W1995033968 @default.
• W1998911644 cites W1998776723 @default.
• W1998911644 cites W1999733628 @default.
• W1998911644 cites W2003491058 @default.
• W1998911644 cites W2006315864 @default.
• W1998911644 cites W2009230499 @default.
• W1998911644 cites W2010649971 @default.
• W1998911644 cites W2011539729 @default.
• W1998911644 cites W2016011359 @default.
• W1998911644 cites W2020428096 @default.
• W1998911644 cites W2022362212 @default.
• W1998911644 cites W2023635183 @default.
• W1998911644 cites W2024134968 @default.
• W1998911644 cites W2033042047 @default.
• W1998911644 cites W2034215339 @default.
• W1998911644 cites W2036742353 @default.
• W1998911644 cites W2038871743 @default.
• W1998911644 cites W2047412054 @default.
• W1998911644 cites W2049163438 @default.
• W1998911644 cites W2050707975 @default.
• W1998911644 cites W2055071429 @default.
• W1998911644 cites W2059579077 @default.
• W1998911644 cites W2064338748 @default.
• W1998911644 cites W2068384471 @default.
• W1998911644 cites W2071964449 @default.
• W1998911644 cites W2072632306 @default.
• W1998911644 cites W2074479550 @default.
• W1998911644 cites W2078257191 @default.
• W1998911644 cites W2079395100 @default.
• W1998911644 cites W2082786396 @default.
• W1998911644 cites W2088700961 @default.
• W1998911644 cites W2089380385 @default.
• W1998911644 cites W2089389165 @default.
• W1998911644 cites W2089427338 @default.
• W1998911644 cites W2097417855 @default.
• W1998911644 cites W2098797664 @default.
• W1998911644 cites W2108198131 @default.
• W1998911644 cites W2112293616 @default.
• W1998911644 cites W2112889163 @default.
• W1998911644 cites W2116369972 @default.
• W1998911644 cites W2122941682 @default.
• W1998911644 cites W2124667416 @default.
• W1998911644 cites W2129170329 @default.
• W1998911644 cites W2132382876 @default.
• W1998911644 cites W2137903322 @default.
• W1998911644 cites W2140139281 @default.
• W1998911644 cites W2141198052 @default.
• W1998911644 cites W2146543727 @default.
• W1998911644 cites W2160838897 @default.
• W1998911644 cites W2161142819 @default.
• W1998911644 cites W2162162759 @default.
• W1998911644 cites W2166628824 @default.
• W1998911644 cites W2270160657 @default.
• W1998911644 cites W2339773433 @default.
• W1998911644 cites W4210981518 @default.
• W1998911644 doi "https://doi.org/10.1186/1742-2094-4-10" @default.
• W1998911644 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1839084" @default.
• W1998911644 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17374157" @default.
• W1998911644 hasPublicationYear "2007" @default.
• W1998911644 type Work @default.
• W1998911644 sameAs 1998911644 @default.
• W1998911644 citedByCount "47" @default.
• W1998911644 countsByYear W19989116442012 @default.
• W1998911644 countsByYear W19989116442013 @default.
• W1998911644 countsByYear W19989116442014 @default.
• W1998911644 countsByYear W19989116442015 @default.
• W1998911644 countsByYear W19989116442016 @default.
• W1998911644 countsByYear W19989116442017 @default.
• W1998911644 countsByYear W19989116442018 @default.
• W1998911644 countsByYear W19989116442019 @default.
• W1998911644 countsByYear W19989116442020 @default.

• next