Evidence for lipopolysaccharideinduced differentiation of RAW264.7 murine macrophage cell line into dendritic like cells

Saxena, Rajiv K.; Vallyathan, Val; Lewis, Daniel M.

doi:10.1007/bf02970143

Cited by 82 publications

(66 citation statements)

References 15 publications

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“…LPS is known to induce a morphological change in RAW 264.7 cells (Saxena et al, 2003). Thus, we confirmed the change induced by LPS, and examined the effects of CKD712 on this change using optical microscopy.…”

Section: Ckd712 Inhibits Lps-induced Morphological Changes In Raw264supporting

confidence: 56%

(S)-Tetrahydroisoquinoline Alkaloid Inhibits LPS-Induced Arachidonic Acid Release through Downregulation of cPLA2 Expression

Choi

Kim

et al. 2013

Molecules and Cells

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Sepsis, a systemic inflammatory response syndrome, remains a potentially lethal condition. (S)-1-α-Naphthylmethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (CKD712) is noted as a drug candidate for sepsis. Many studies have demonstrated its significant anti-inflammatory effects. Here we first examined whether CKD712 inhibits lipopolysaccharide (LPS)-induced arachidonic acid (AA) release in the RAW 264.7 mouse monocyte cell line, and subsequently, its inhibitory mechanisms. CKD712 reversed LPS-associated morphological changes in the RAW 264.7 cells, and inhibited LPS-induced release of AA in a concentrationdependent manner. The inhibition was apparently due to the diminished expression of a cytosolic form of phospholipase A 2 (cPLA 2 ) by CKD712, resulting from reduced NF-κB activation. Furthermore, CKD712 inhibited the activation of ERK1/2 and SAP/JNK, but not of p38 MAPK. CKD712 had no effect on the activity or phosphorylation of cPLA 2 and on calcium influx. Our results collectively suggest that CKD712 inhibits LPS-induced AA release through the inhibition of a MAPKs/NF-κB pathway leading to reduced cPLA 2 expression in RAW 264.7 cells.

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Section: Ckd712 Inhibits Lps-induced Morphological Changes In Raw264supporting

confidence: 56%

(S)-Tetrahydroisoquinoline Alkaloid Inhibits LPS-Induced Arachidonic Acid Release through Downregulation of cPLA2 Expression

Choi

Kim

et al. 2013

Molecules and Cells

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“…Macrophages became largely elongated with stimulation by LPS, a typical proinflammatory stimulator of macrophages. It is reported that LPS by itself constitutes signals for differentiation, increases cell size and, change the morphology of macrophage [36]. RAW 264.7 cells treated with isoflavone glucoside (puerarin and daidzin) after LPS stimulation exhibited same elongated morphology as control induced by LPS (data not shown).…”

Section: Discussionmentioning

confidence: 52%

Suppression of arachidonic acid metabolism and nitric oxide formation by kudzu isoflavones in murine macrophages

Jun

Hong

Jeong

et al. 2005

Mol. Nutr. Food Res.

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Inhibitory effect of kudzu isoflavones on arachidonic acid metabolism and nitric oxide (NO) production in lipopolysaccharide activated RAW 264.7 macrophages were investigated. Isoflavone aglycones, such as daidzein, genistein, biochanin A, and formononetin significantly suppressed arachidonic acid release (50 microM). Biochanin A, which displayed the most active inhibition on arachidonic acid release in HT-29 human colon cancer cells, exhibited its most potent suppression in RAW 264.7 cell (by 86%) without showing cytotoxicity. However, isoflavone glucosides, puerarin and daidzin, showed lower inhibitory activities on the release of arachidonic acid and its metabolites. In NO formation, biochanin A showed marked inhibition, by 62% (50 microM), followed by genistein, daidzein, formononetin, and daidzin, 56, 39, 33, and 8%, respectively. 5,7-Dihydroxyl group in the A-ring of isoflavones could be a key functional group responsible for the strong inhibitory activity of biochanin A and genistein on NO production. These activities may contribute to the antiinflammatory and anticarcinogenic properties of kudzu isoflavones.

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“…*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (compared to media). # indicates P values calculated by an unpaired t-test or Mann-Whitney test between pairs of unstimulated (media) and CpG stimulated in (A) and between R848 and LPS stimulated in (C); # P < 0.05, ## P < 0.01, ### P < 0.001. macrophages, including MHCII, CD80, CD86 and CD40 (26,27). We have additionally shown that Poly I:C induced CD86, MHCII and CD40 on BMDMs.…”

Section: Discussionmentioning

confidence: 74%

TLR7 and TLR9 ligands regulate antigen presentation by macrophages

Celhar

Pereira-Lopes

Thornhill

et al. 2015

International Immunology

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The toll-like receptors (TLRs) are important innate receptors recognizing potentially pathogenic material. However, they also play a significant role in the development of Alzheimer's disease, cancer, autoimmunity and the susceptibility to viral infections. Macrophages are essential for an effective immune response to foreign material and the resolution of inflammation. In these studies, we examined the impact of different TLR ligands on macrophage cell function. We demonstrate that stimulation of all TLRs tested increases the phagocytosis of apoptotic cells by macrophages. TLR7 and TLR9 ligation decreased the levels of the surface co-expression molecules CD86 and MHCII, which was associated with a concomitant reduction in antigen presentation and proliferation of T cells. This down-regulation in macrophage function was not due to an increase in cell death. In fact, exposure to TLR7 or TLR9 ligands promoted cell viability for up to 9 days, in contrast to TLR3 or TLR4. Additionally, macrophages exposed to TLR7/TLR9 ligands had a significantly lower ratio of Il-12/Il-10 mRNA expression compared with those treated with the TLR4 ligand, LPS. Taken together, these data demonstrate that TLR7/TLR9 ligands push the macrophage into a phagocytic long-lived cell, with a decreased capacity of antigen presentation and reminiscent of the M2 polarized state.

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Evidence for lipopolysaccharideinduced differentiation of RAW264.7 murine macrophage cell line into dendritic like cells

Cited by 82 publications

References 15 publications

(S)-Tetrahydroisoquinoline Alkaloid Inhibits LPS-Induced Arachidonic Acid Release through Downregulation of cPLA2 Expression

(S)-Tetrahydroisoquinoline Alkaloid Inhibits LPS-Induced Arachidonic Acid Release through Downregulation of cPLA2 Expression

Suppression of arachidonic acid metabolism and nitric oxide formation by kudzu isoflavones in murine macrophages

TLR7 and TLR9 ligands regulate antigen presentation by macrophages

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