LAIR-1 activation inhibits inflammatory macrophage phenotype in vitro

2018 ◽  
Vol 331 ◽  
pp. 78-84 ◽  
Author(s):  
Jingyi Jin ◽  
Ying Wang ◽  
Qianli Ma ◽  
Ning Wang ◽  
Wenwei Guo ◽  
...  
Keyword(s):  
Macrophage Phenotype ◽  
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

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 Context-enriched interactome powered by proteomics helps the identification of novel regulators of macrophage activation

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Arda Halu ◽  
Jian-Guo Wang ◽  
Hiroshi Iwata ◽  
Alexander Mojcher ◽  
Ana Luisa Abib ◽  
...  
Keyword(s):  
Macrophage Activation ◽  
The Novel ◽  
Macrophage Phenotype ◽  
Loss Of Function ◽  
Prioritization Method ◽  
Network Proximity ◽  
Network Approaches ◽  
Inflammatory Macrophage

The role of pro-inflammatory macrophage activation in cardiovascular disease (CVD) is a complex one amenable to network approaches. While an indispensible tool for elucidating the molecular underpinnings of complex diseases including CVD, the interactome is limited in its utility as it is not specific to any cell type, experimental condition or disease state. We introduced context-specificity to the interactome by combining it with co-abundance networks derived from unbiased proteomics measurements from activated macrophage-like cells. Each macrophage phenotype contributed to certain regions of the interactome. Using a network proximity-based prioritization method on the combined network, we predicted potential regulators of macrophage activation. Prediction performance significantly increased with the addition of co-abundance edges, and the prioritized candidates captured inflammation, immunity and CVD signatures. Integrating the novel network topology with transcriptomics and proteomics revealed top candidate drivers of inflammation. In vitro loss-of-function experiments demonstrated the regulatory role of these proteins in pro-inflammatory signaling.

scholarly journals Decellularized Porcine Achilles Tendon Induces Anti-inflammatory Macrophage Phenotype In Vitro and Tendon Repair In Vivo

2020 ◽  
Vol 8 ◽  
pp. 100027 ◽  
Author(s):  
Aysegul Dede Eren ◽  
Ravi Sinha ◽  
Egemen Deniz Eren ◽  
Yuan Huipin ◽  
Sultan Gulce-Iz ◽  
...  
Keyword(s):  
Achilles Tendon ◽  
Tendon Repair ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
Inflammatory Macrophage

scholarly journals Statins Directly Influence the Polarization of Adipose Tissue Macrophages: A Role in Chronic Inflammation

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 211
Author(s):  
Sona Kauerova ◽  
Hana Bartuskova ◽  
Barbora Muffova ◽  
Libor Janousek ◽  
Jiri Fronek ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Ldl Cholesterol ◽  
Macrophage Polarization ◽  
Inflammatory Activity ◽  
Human Macrophage ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage

Statins represent one of the most widely used classes of drugs in current medicine. In addition to a substantial decrease in atherogenic low density lipoprotein (LDL) particle concentrations, several large trials have documented their potent anti-inflammatory activity. Based on our preliminary data, we showed that statins are able to decrease the proportion of pro-inflammatory macrophages (CD14+16+CD36high) in visceral adipose tissue in humans. In the present study including 118 healthy individuals (living kidney donors), a very close relationship between the pro-inflammatory macrophage proportion and LDL cholesterol levels was found. This was confirmed after adjustment for the most important risk factors. The effect of statins on the proportion of pro-inflammatory macrophages was also confirmed in an experimental model of the Prague hereditary hypercholesterolemia rat. A direct anti-inflammatory effect of fluvastatin on human macrophage polarization in vitro was documented. Based on modifying the LDL cholesterol concentrations, statins are suggested to decrease the cholesterol inflow through the lipid raft of macrophages in adipose tissue and hypercholesterolemia to enhance the pro-inflammatory macrophage phenotype polarization. On the contrary, due to their opposite effect, statins respond with anti-inflammatory activity, affecting the whole organism.

Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

2017 ◽  
pp. 4-9
Author(s):  
С.В. Калиш ◽  
С.В. Лямина ◽  
А.А. Раецкая ◽  
И.Ю. Малышев
Keyword(s):  
Tumor Growth ◽  
Culture Medium ◽  
Ehrlich Carcinoma ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
M1 Macrophage ◽  
Ec Cells ◽  
Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

scholarly journals Interactome Analysis of iPSC Secretome and Its Effect on Macrophages In Vitro

2021 ◽  
Vol 22 (2) ◽  
pp. 958
Author(s):  
Luca Tamò ◽  
Kleanthis Fytianos ◽  
Fabienne Caldana ◽  
Cedric Simillion ◽  
Anis Feki ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Critical Role ◽  
Organ Injury ◽  
Macrophage Phenotype ◽  
Gene Interaction Network ◽  
Tissue Repair And Regeneration ◽  
Secretory Pattern

Induced pluripotent stem cell secretome (iPSC-CM) mitigate organ injury and help in repair. Macrophages play a critical role in tissue repair and regeneration and can be directed to promote tissue repair by iPSC-CM, although the exact mechanisms are not known. In the current investigative study, we evaluated the possible mechanism by which iPSC-CM regulates the phenotype and secretory pattern of macrophages in vitro. Macrophages were obtained from human peripheral blood mononuclear cells and differentiated to various subpopulations and treated with either iPSC-CM or control media in vitro. Macrophage phenotype was assessed by flow cytometry, gene expression changes by qRT PCR and secretory pattern by multiplex protein analysis. The protein and gene interaction network revealed the involvement of Amyloid precursor protein (APP) and ELAV-like protein 1 (ELAVL-1) both present in the iPSC-CM to play an important role in regulating the macrophage phenotype and their secretory pattern. This exploratory study reveals, in part, the possible mechanism and identifies two potential targets by which iPSC-CM regulate macrophages and help in repair and regeneration.

scholarly journals Lipodystrophy and obesity are associated with decreased number of T cells with regulatory function and pro-inflammatory macrophage phenotype

2017 ◽  
Vol 41 (11) ◽  
pp. 1676-1684 ◽  
Author(s):  
S Berger ◽  
G Ceccarini ◽  
G Scabia ◽  
I Barone ◽  
C Pelosini ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory Function ◽  
Macrophage Phenotype ◽  
Inflammatory Macrophage

scholarly journals Serum Amyloid A1 Induces Classically Activated Macrophages: A Role for Enhanced Fibril Formation

2021 ◽  
Vol 12 ◽  
Author(s):  
Ann-Kathrin Gaiser ◽  
Shanna Bauer ◽  
Stephanie Ruez ◽  
Karlheinz Holzmann ◽  
Marcus Fändrich ◽  
...  
Keyword(s):  
Amyloid Fibrils ◽  
Intervention Strategy ◽  
Serum Amyloid ◽  
Macrophage Phenotype ◽  
Aa Amyloidosis ◽  
Inflammatory Conditions ◽  
Serum Amyloid A1 ◽  
And Function

AA amyloidosis belongs to the group of amyloid diseases which can follow chronic inflammatory conditions of various origin. The disease is characterized by the deposition of insoluble amyloid fibrils formed by serum amyloid A1 (SAA1) leading eventually to organ failure. Macrophages are intimately involved in the fibrillogenesis as well as in the clearance of amyloid fibrils. In vivo, macrophages may occur as classically (M1) or alternatively activated (M2) macrophages. We investigate here how SAA1 might affect the macrophage phenotype and function. Gene microarray analysis revealed upregulation of 64 M1-associated genes by SAA1. M1-like polarization was further confirmed by the expression of the M1-marker MARCO, activation of the NF-κB transcription factor, and secretion of the M1-cytokines TNF-α, IL-6, and MCP-1. Additionally, we demonstrate here that M1-polarized macrophages exhibit enhanced fibrillogenic activity towards SAA1. Based on our data, we propose reconsideration of the currently used cellular amyloidosis models towards an in vitro model employing M1-polarized macrophages. Furthermore, the data suggest macrophage repolarization as potential intervention strategy in AA amyloidosis.

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