scholarly journals AN UNRESTRAINED PROINFLAMMATORY M1 MACROPHAGE POPULATION INDUCED BY IRON NANOCRYSTALS IMPAIRS MYOCARDIAL HEALING AFTER HEMORRHAGIC INFARCTION

2017 ◽  
Vol 69 (11) ◽  
pp. 1446
Author(s):  
Ivan Cokic ◽  
Avinash Kali ◽  
Richard Tang ◽  
Hsin-Jung Yang ◽  
Andreas Kumar ◽  
...  
Keyword(s):  
Macrophage Population ◽  
Hemorrhagic Infarction ◽  
M1 Macrophage ◽  
Iron Nanocrystals

scholarly journals Evaluation of Glycosylated PTGS2 in Colorectal Cancer for NSAIDS-Based Adjuvant Therapy

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 683
Author(s):  
Roberta Venè ◽  
Delfina Costa ◽  
Raffaella Augugliaro ◽  
Sebastiano Carlone ◽  
Stefano Scabini ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Interleukin 1 ◽  
Cost Benefit ◽  
Protective Role ◽  
Macrophage Population ◽  
M1 Macrophage ◽  
Luminal Area ◽  
Prostaglandin Endoperoxide Synthase ◽  
Positive Effect

Observational/retrospective studies indicate that prostaglandin-endoperoxide synthase-2 (PTGS2) inhibitors could positively affect colorectal cancer (CRC) patients’ survival after diagnosis. To obtain an acceptable cost/benefit balance, the inclusion of PTGS2 inhibitors in the adjuvant setting needs a selective criterion. We quantified the 72 kDa, CRC-associated, glycosylated form of PTGS2 in 100 frozen CRC specimens and evaluated PTGS2 localization by IHC in the same tumors, scoring tumor epithelial-derived and stroma-derived fractions. We also investigated the involvement of interleukin-1 beta (IL1β) in PTGS2 induction, both in vitro and in CRC lysates. Finally, we used overall survival (OS) as a criterion for patient selection. Glycosylated PTGS2 can be quantified with high sensibility in tissue lysates, but the expression in both tumor and stromal cells limits its use for predictive purposes. Immunohistochemistry (IHC) analysis indicates that stromal PTGS2 expression could exert a protective role on patient OS. Stromal PTGS2 was prevalently expressed by cancer-associated fibroblasts exerting a barrier function near the gut lumen, and it apparently favored the antitumor M1 macrophage population. IL1β was directly linked to gPTGS2 expression both in vitro and in tumors, but its activity was apparently prevalent on the stromal cell population. We suggest that stromal PTGS2 could exert a positive effect on patients OS when expressed in the luminal area of the tumor.

scholarly journals A Novel Treatment for Glomerular Disease: Targeting the Activated Macrophage Folate Receptor with a Trojan Horse Therapy in Rats

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2113
Author(s):  
Gabriela E. Garcia ◽  
Yingjuan J. Lu ◽  
Luan D. Truong ◽  
Carlos A. Roncal-Jiménez ◽  
Makoto Miyazaki ◽  
...  
Keyword(s):  
Folic Acid ◽  
Crescentic Glomerulonephritis ◽  
Inflammatory Diseases ◽  
Folate Receptor ◽  
Kidney Injury ◽  
Macrophage Population ◽  
Novel Treatment ◽  
M1 Macrophage ◽  
Kidney Protection ◽  
Activated Macrophage

Since activated macrophages express a functional folate receptor β (FRβ), targeting this macrophage population with folate-linked drugs could increase selectivity to treat inflammatory diseases. Using a macrophage-mediated anti-glomerular basement membrane (anti-GBM) glomerulonephritis (GN) in WKY rats, we investigated the effect of a novel folic acid-aminopterin (AMT) conjugate (EC2319) designed to intracellularly deliver AMT via the FR. We found that treatment with EC2319 significantly attenuated kidney injury and preserved renal function. Kidney protection with EC2319 was blocked by a folate competitor, indicating that its mechanism of action was specifically FRβ-mediated. Notably, treatment with methotrexate (MTX), another folic acid antagonist related to AMT, did not protect from kidney damage. EC2319 reduced glomerular and interstitial macrophage infiltration and decreased M1 macrophage recruitment but not M2 macrophages. The expression of CCL2 and the pro-fibrotic cytokine TGF-β were also reduced in nephritic glomeruli with EC2319 treatment. In EC2319-treated rats, there was a significant decrease in the deposition of collagens. In nephritic kidneys, FRβ was expressed on periglomerular macrophages and macrophages present in the crescents, but its expression was not observed in normal kidneys. These data indicate that selectively targeting the activated macrophage population could represent a novel means for treating anti-GBM GN and other acute crescentic glomerulonephritis.

scholarly journals Probiotic Bifidobacterium bifidum G9-1 Has a Preventive Effect on the Acceleration of Colonic Permeability and M1 Macrophage Population in Maternally Separated Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 641
Author(s):  
Xuan Wang ◽  
Hirokazu Fukui ◽  
Ying Ran ◽  
Xin Xu ◽  
Nobuhiko Ebisutani ◽  
...  
Keyword(s):  
Maternal Separation ◽  
Ussing Chamber ◽  
Bifidobacterium Bifidum ◽  
Preventive Effect ◽  
Mucosal Permeability ◽  
Macrophage Population ◽  
Mucosal Integrity ◽  
Caco2 Cells ◽  
M1 Macrophage ◽  
Ifn Γ

Although probiotics may be useful for the treatment of irritable bowel syndrome (IBS), it is unclear how probiotics play a role in colonic mucosal integrity and immunity. Here, we aimed to investigate the effect of Bifidobacterium bifidum G9-1 (BBG9-1) on colonic mucosal integrity and macrophage behavior in rats subjected to maternal separation (MS) as a model of IBS. MS pups were individually separated from their mother rats, and a proportion of the MS rats were orally administered BBG9-1. The colonic mucosal permeability was evaluated by Ussing chamber assay. The expression of tight junction proteins and cytokines and the population of CD80-positive cells was examined in the colonic tissues by real-time reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. Caco2 cells were stimulated with cytokines and the transepithelial electric resistance (TEER) was measured. MS rats showed significantly higher colonic permeability and lower claudin 4 expression in the colonic epithelium relative to controls. The number of CD80-positive macrophages was significantly increased in the colonic mucosa of MS rats, accompanied by the increase of IL-6 and IFN-γ expression. BBG9-1 treatment ameliorated the increase of M1 macrophage and IL-6/IFN-γ expression in the colonic tissue of MS rats. Simultaneously, BBG9-1 treatment improved the enhanced mucosal permeability and the decreased claudin 4 expression in the colon of MS rats. IL-6 and IFN-γ, whose expression is enhanced in the colon of MS rats, significantly decreased TEER in Caco2 cells in vitro. Probiotic BBG9-1 has a preventive effect on the acceleration of colonic permeability and M1 macrophage population in maternally separated rats.

scholarly journals An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice

2011 ◽  
Vol 121 (3) ◽  
pp. 985-997 ◽  
Author(s):  
Anca Sindrilaru ◽  
Thorsten Peters ◽  
Stefan Wieschalka ◽  
Corina Baican ◽  
Adrian Baican ◽  
...  
Keyword(s):  
Wound Healing ◽  
Macrophage Population ◽  
M1 Macrophage

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.

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