Protein Adsorption on Surfaces Functionalized with COOH Groups Promotes Anti-inflammatory Macrophage Responses

2021 ◽  
Vol 13 (6) ◽  
pp. 7021-7036
Author(s):  
Emily Buck ◽  
Seunghwan Lee ◽  
Laura S. Stone ◽  
Marta Cerruti
Keyword(s):  
Protein Adsorption ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

Anti-inflammatory macrophage induced MMP9 and ADAM8 expression increases invasion rate of pancreatic cancer cells

Pancreatology ◽  
2013 ◽  
Vol 13 (2) ◽  
pp. e72
Author(s):  
H. Seppänen ◽  
H. Mustonen ◽  
S. Vainionpää ◽  
Z.H. Shen ◽  
H. Repo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Invasion Rate ◽  
Pancreatic Cancer Cells ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

scholarly journals Probiotic Conditioned Media Induces an Anti-Inflammatory Macrophage Phenotype In Vivo and In Vitro

2011 ◽  
Vol 140 (5) ◽  
pp. S-19
Author(s):  
Michelle Taylor ◽  
Vandana Gambhir ◽  
Curtis Noordhof ◽  
Oliver Jones ◽  
Shu-Mei He ◽  
...  
Keyword(s):  
Conditioned Media ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

scholarly journals Free radical-decellularized tissue promotes enhanced antioxidant and anti-inflammatory macrophage response

Biomaterials ◽  
2019 ◽  
Vol 222 ◽  
pp. 119376 ◽  
Author(s):  
S.T. LoPresti ◽  
B. Popovic ◽  
M. Kulkarni ◽  
C.D. Skillen ◽  
B.N. Brown
Keyword(s):  
Free Radical ◽  
Macrophage Response ◽  
Decellularized Tissue ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

Keratin biomaterials augment anti-inflammatory macrophage phenotype in vitro

2018 ◽  
Vol 66 ◽  
pp. 213-223 ◽  
Author(s):  
Michele Waters ◽  
Pamela VandeVord ◽  
Mark Van Dyke
Keyword(s):  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

scholarly journals Haptoglobin Genotype-Dependent Anti-Inflammatory Signaling in CD163+Macrophages

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
R. Clive Landis ◽  
Pandelis Philippidis ◽  
Jan Domin ◽  
Joseph J. Boyle ◽  
Dorian O. Haskard
Keyword(s):  
Scavenger Receptor ◽  
Intraplaque Hemorrhage ◽  
Phosphatidylinositol 3 Kinase ◽  
Kinase Activation ◽  
Akt Phosphorylation ◽  
Increased Risk ◽  
Haptoglobin Genotype ◽  
Anti Inflammatory ◽  
Inflammatory Signalling ◽  
Inflammatory Macrophage

Intraplaque hemorrhage causes adaptive remodelling of macrophages towards a protective phenotype specialized towards handling iron and lipid overload, denoted Mhem. The Mhem phenotype expresses elevated levels of hemoglobin (Hb) scavenger receptor, CD163, capable of endocytosing pro-oxidant free Hb complexed to acute phase protein haptoglobin (Hp). It is notable that individuals homozygous for the Hp 2 allele (a poorer antioxidant) are at increased risk of cardiovascular disease compared to the Hp 1 allele. In this study, we examined whether scavenging of polymorphic Hp:Hb complexes differentially generated downstream anti-inflammatory signals in cultured human macrophages culminating in interleukin (IL)-10 secretion. We describe an anti-inflammatory signalling pathway involving phosphatidylinositol-3-kinase activation upstream of Akt phosphorylation (pSer473Akt) and IL-10 secretion. The pathway is mediated specifically through CD163 and is blocked by anti-CD163 antibody or phagocytosis inhibitor. However, levels of pSer473Akt and IL-10 were significantly diminished when scavenging polymorphic Hp2-2:Hb complexes compared to Hp1-1:Hb complexes(P<0.05). Impaired anti-inflammatory macrophage signaling through a CD163/pAkt/IL-10 axis may thus represent a possible Hp2-2 disease mechanism in atherosclerosis.

scholarly journals Chitosan drives anti-inflammatory macrophage polarisation and pro-inflammatory dendritic cell stimulation

2012 ◽  
Vol 24 ◽  
pp. 136-153 ◽  
Author(s):  
MI Oliveira ◽  
◽  
SG Santos ◽  
MJ Oliveira ◽  
AL Torres ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Cell Stimulation ◽  
Macrophage Polarisation ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

scholarly journals eIF6 Promotes Inflammatory Macrophage Phenotype, Foam Cell Formation and Atherosclerosise

2021 ◽  
Author(s):  
Junnian Zheng ◽  
Renjin Chen ◽  
Xuemei Xian ◽  
xiaoqiang Zhan ◽  
Jiajia Chang ◽  
...  
Keyword(s):  
Foam Cell ◽  
Cell Formation ◽  
Western Diet ◽  
Initiation Factor ◽  
Immunofluorescent Staining ◽  
Foam Cell Formation ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage ◽  
Novel Therapeutic

Abstract Background：Atherosclerosis is a chronic inflammatory disease, caused by accumulation of lipid-laden and inflammatory macrophages in the artery wall. Understanding its molecular mechanisms and developing novel therapeutic targets to promote atherosclerotic regression is an important clinical goal.Methods : ApoE-/- and eIF6+/-/ApoE-/- mice were fed Western diet (WD) for 16 weeks. Molecular biology technology were performed to analyze the differences between them.Results: The mechanism by which Eukaryotic initiation factor 6 (eIF6) affects macrophages and atherosclerosis remains to be elucidated. Western blotting and real-time polymerase chain reaction (PCR ) analysis indicated significantly higher expression levels of eIF6 than those in the control in RAW264.7 cells induced by Lipopolysaccharide (LPS) and Interleukin-4 (IL4). We constructed eIF6+/-/ApoE-/- mice, the hematoxylin (HE) and Oil Red O staining analysis indicated that these mice showed a significant decrease in atherosclerotic lesion formation increased anti-inflammatory cell content in aortas, and reduced necrotic core content compared with ApoE-/- mice on a western diet for 16 weeks. eIF6 deficiency suppressed foam cell formation and promoted the anti-inflammatory macrophage phenotype in primary macrophages. More anti-inflammatory populations were observed in blood and atherosclerotic aortas of eIF6+/- ApoE-/- mice by flow cytometry. Immunofluorescent staining analysis obtained the same results.Conclusions: eIF6 deficiency protects against atherosclerosis by promoting the anti-inflammatory macrophage phenotype and reducing macrophage uptake of low-density lipoprotein (LDL), indicating that new insight into eIF6 may reveal a potential novel therapeutic target for the resolution of inflammation in atherosclerosis.

scholarly journals O11.2. ELEVATION OF MACROPHAGE-RELATED TRANSCRIPTS IN THE MIDBRAIN IN SCHIZOPHRENIA

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S27-S28
Author(s):  
Tertia Purves-Tyson ◽  
Helen Cai ◽  
Danny Boerrigter ◽  
Debora Rothmond ◽  
Cynthia Shannon Weickert
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Immune Cells ◽  
Symptomatic Patient ◽  
Dopamine Neurons ◽  
Illness Duration ◽  
Macrophage Marker ◽  
Fresh Frozen ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

Abstract Background Neuroinflammation and dopamine dysregulation contribute to psychosis and cognitive deficits in schizophrenia. Approximately 50% of people with schizophrenia have elevated gene expression of proinflammatory cytokines in the postmortem midbrain, the location of the dopamine neurons. Infiltration of macrophages into the cortex was identified in a subset of high inflammatory schizophrenia cases. It is not known whether molecular measures of macrophages and cell adhesion molecules are increased in the midbrain in schizophrenia. We hypothesised that gene expression of macrophage markers CD163 (cluster of differentiation 163; perivascular macrophages), Fn1 (fibronectin 1; expressed by peripheral macrophages, not brain microglia), CD64 (pro-inflammatory macrophage), MRC1 (anti-inflammatory macrophage) and intracellular cell adhesion molecule 1 (ICAM1; enabling recruitment of peripheral macrophages into the brain), will be elevated in the midbrain of schizophrenia cases compared to controls. Methods Gene expression was examined by qRT-PCR in the midbrain from 28 schizophrenia cases (13 high inflammation, 15 low inflammation) and 29 healthy controls (low inflammation). ANCOVA, with age, PMI and RIN as covariates when correlations detected, were used to detect differences between diagnostic or diagnostic/inflammatory groups. For schizophrenia cases, antipsychotic doses were converted to chlorpromazine (CPZ) equivalents. Correlations were used to determine relationships between illness duration, antipsychotics and gene expression. CD163+ cells were identified in fresh frozen midbrain (14µm) from schizophrenia and control cases by immunohistochemistry to qualitatively assess their location relative to dopamine neurons. Results We found abundant macrophages (CD163+ cells) in and around blood vessels and in the schizophrenia midbrain parenchyma in close proximity to dopamine neurons. CD163, Fn1 and ICAM mRNAs were increased 237.6%, 39.67% and 137.7% respectively, in schizophrenia cases compared to control cases [all F(1,50 &gt;5.045, p&lt;0.05]. The pro-inflammatory macrophage marker (CD64 mRNA) was increased by 39% (F1,51=11.10, p=0.002), while the anti-inflammatory macrophage marker (MRC1 mRNA) was unchanged (F(1,52=2.97. p=0.09) in schizophrenia midbrain compared to control. CD163 and Fn1 mRNAs were not correlated in controls (R=0.319, p=0.112, n=24) but were correlated in schizophrenia cases (R=0.455, p=0.019, n=24). CD163 and ICAM mRNAs were positively correlated in controls (R=0.42, p=0.031, n=24) and schizophrenia cases (R=0.84, p&lt;0.0001, n=24), and the correlation was stronger in schizophrenia cases (p=0.014). CD163 and ICAM mRNAs were positively correlated with CPZ (Rho&gt;0.5, p&lt;0.02, n=21) but not illness duration (Rho=0.024, p&gt;0.05, n=28). Fn1 mRNA did not correlate with illness duration or antipsychotics. Discussion Increased ICAM1 may lead to increased transmigration of monocytes into the midbrain parenchyma. The increase in CD64 and the positive relationship between Fn1, expressed by peripheral monocytes/macrophages but not brain microglia, and CD163 expression in schizophrenia cases provides support that there is an increase in pro-inflammatory bone marrow-derived immune cells in the psychotic midbrain. These peripheral immune cells may be a source of increased cytokines identified in the midbrain schizophrenia cases and thus may contribute to dopamine neuron pathophysiology. Although the role of antipsychotics in increased macrophage marker expression in the midbrain is suggested, increased antipsychotics in patients displaying higher expression of inflammatory transcripts may indicate a more symptomatic patient requiring higher treatment doses.

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