scholarly journals A Review of Macrophage MicroRNAs’ Role in Human Asthma

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 420 ◽  
Author(s):  
Gavriela Feketea ◽  
Corina I Bocsan ◽  
Cristian Popescu ◽  
Mihaela Gaman ◽  
Luminita A Stanciu ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Critical Role ◽  
Human Macrophage ◽  
Published Data ◽  
M2 Macrophage ◽  
Macrophage Phenotype ◽  
Activated Macrophages ◽  
Novel Therapy ◽  
Alternatively Activated Macrophages ◽  
Classically Activated Macrophages

There is an imbalance in asthma between classically activated macrophages (M1 cells) and alternatively activated macrophages (M2 cells) in favor of the latter. MicroRNAs (miRNAs) play a critical role in regulating macrophage proliferation and differentiation and control the balance of M1 and M2 macrophage polarization, thereby controlling immune responses. Here we review the current published data concerning miRNAs with known correlation to a specific human macrophage phenotype and polarization, and their association with adult asthma. MiRNA-targeted therapy is still in the initial stages, but clinical trials are under recruitment or currently running for some miRNAs in other diseases. Regulating miRNA expression via their upregulation or downregulation could show potential as a novel therapy for improving treatment efficacy in asthma.

scholarly journals Effects of Eltrombopag on In Vitro Macrophage Polarization in Pediatric Immune Thrombocytopenia

2020 ◽  
Vol 22 (1) ◽  
pp. 97
Author(s):  
Alessandra Di Paola ◽  
Giuseppe Palumbo ◽  
Pietro Merli ◽  
Maura Argenziano ◽  
Chiara Tortora ◽  
...  
Keyword(s):  
Immune Thrombocytopenia ◽  
Macrophage Polarization ◽  
Macrophage Phenotype ◽  
Activated Macrophages ◽  
T Helper ◽  
T Helper 1 ◽  
Alternatively Activated Macrophages ◽  
Effector Cells ◽  
Anti Inflammatory

Immune Thrombocytopenia (ITP) is an autoimmune disease characterized by autoantibodies-mediated platelet destruction, a prevalence of M1 pro-inflammatory macrophage phenotype and an elevated T helper 1 and T helper 2 lymphocytes (Th1/Th2) ratio, resulting in impairment of inflammatory profile and immune response. Macrophages are immune cells, present as pro-inflammatory classically activated macrophages (M1) or as anti-inflammatory alternatively activated macrophages (M2). They have a key role in ITP, acting both as effector cells, phagocytizing platelets, and, as antigen presenting cells, stimulating auto-antibodies against platelets production. Eltrombopag (ELT) is a thrombopoietin receptor agonist licensed for chronic ITP to stimulate platelet production. Moreover, it improves T and B regulatory cells functions, suppresses T-cells activity, and inhibits monocytes activation. We analyzed the effect of ELT on macrophage phenotype polarization, proposing a new possible mechanism of action. We suggest it as a mediator of macrophage phenotype switch from the M1 pro-inflammatory type to the M2 anti-inflammatory one in paediatric patients with ITP, in order to reduce inflammatory state and restore the immune system function. Our results provide new insights into the therapy and the management of ITP, suggesting ELT also as immune-modulating drug.

scholarly journals FIZZ1 and Ym as Tools to Discriminate between Differentially Activated Macrophages

2002 ◽  
Vol 9 (3) ◽  
pp. 151-159 ◽  
Author(s):  
Geert Raes ◽  
Wim Noël ◽  
Alain Beschin ◽  
Lea Brys ◽  
Patrick de Baetselier ◽  
...  
Keyword(s):  
Mouse Strains ◽  
Molecular Characteristics ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Different Populations ◽  
Classically Activated Macrophages ◽  
Macrophage Populations ◽  
Alternatively Activated

Although it is well-established that macrophages can occur in distinct activation states, the molecular characteristics of differentially activated macrophages, and particularly those of alternatively activated macrophages (aaMφ), are still poorly unraveled. Recently, we demonstrated that the expression of FIZZ1 and Ym is induced in aaMφ as compared with classically activated macrophages (caMφ), elicitedin vitroor developedin vivoduring infection withTrypanosoma brucei brucei. In the present study, we analyzed the expression of FIZZ1 and Ym in caMφ and aaMφ elicited duringTrypanosoma congolenseinfection and show that the use of FIZZ1 and Ym for the identification of aaMφ is not limited toT. b. bruceiinfection and is independent of the organ sources from which macrophages are obtained. We also demonstrate that FIZZ1 can be used to discriminate between different populations of aaMφ. Furthermore, we studied the effects of various stimuli, and combinations thereof, on the expression of FIZZ1 and Ym in macrophages from different mouse strains and demonstrate that regulation of the expression of FIZZ1 and Ym in macrophages is not dependent on the mouse strain. Finally, we show that these genes can be used to monitor the macrophage activation status without the need to obtain pure macrophage populations.

scholarly journals Gaucher Cells Demonstrate a Distinct Macrophage Phenotype and Resemble Alternatively Activated Macrophages

2004 ◽  
Vol 122 (3) ◽  
pp. 359-369 ◽  
Author(s):  
Leonie A. Boven ◽  
Marjan van Meurs ◽  
Rolf G. Boot ◽  
Atul Mehta ◽  
Louis Boon ◽  
...  
Keyword(s):  
Macrophage Phenotype ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Alternatively Activated

scholarly journals Analysis of the Influence of Jaw Periosteal Cells on Macrophages Phenotype Using an Innovative Horizontal Coculture System

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1753
Author(s):  
Fang He ◽  
Felix Umrath ◽  
Christiane von Ohle ◽  
Siegmar Reinert ◽  
Dorothea Alexander
Keyword(s):  
Macrophage Polarization ◽  
Maxillofacial Surgery ◽  
Inflammatory Factors ◽  
Osteogenic Potential ◽  
Oral And Maxillofacial Surgery ◽  
M2 Macrophage ◽  
Macrophage Phenotype ◽  
Flow Cytometric ◽  
Coculture System ◽  
Gene And Protein Expression

Jaw periosteum-derived mesenchymal stem cells (JPCs) represent a promising cell source for bone tissue engineering in oral and maxillofacial surgery due to their high osteogenic potential and good accessibility. Our previous work demonstrated that JPCs are able to regulate THP-1-derived macrophage polarization in a direct coculture model. In the present study, we used an innovative horizontal coculture system in order to understand the underlying paracrine effects of JPCs on macrophage phenotype polarization. Therefore, JPCs and THP-1-derived M1/M2 macrophages were cocultured in parallel chambers under the same conditions. After five days of horizontal coculture, flow cytometric, gene and protein expression analyses revealed inhibitory effects on costimulatory and proinflammatory molecules/factors as well as activating effects on anti-inflammatory factors in M1 macrophages, originating from multiple cytokines/chemokines released by untreated and osteogenically induced JPCs. A flow cytometric assessment of DNA synthesis reflected significantly decreased numbers of proliferating M1/M2 cells when cocultured with JPCs. In this study, we demonstrated that untreated and osteogenically induced JPCs are able to switch macrophage polarization from a classical M1 to an alternative M2-specific phenotype by paracrine secretion, and by inhibition of THP-1-derived M1/M2 macrophage proliferation.

scholarly journals Rapamycin and FTY720 Alleviate Atherosclerosis by Cross Talk of Macrophage Polarization and Autophagy

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Rui-zhen Sun ◽  
Ying Fan ◽  
Xiao Liang ◽  
Tian-tian Gong ◽  
Qi Wang ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Macrophage Polarization ◽  
Foam Cells ◽  
Peritoneal Macrophages ◽  
Macrophage Phenotype ◽  
Activated Macrophages ◽  
Activated Macrophage ◽  
Phenotype Markers ◽  
Alternatively Activated ◽  
Classically Activated

Foam cell formation and macrophage polarization are involved in the pathologic development of atherosclerosis, one of the most important human diseases affecting large and medium artery walls. This study was designed to assess the effects of rapamycin and FTY720 (fingolimod) on macrophages and foam cells. Mouse peritoneal macrophages were collected and treated with rapamycin and FTY720 to study autophagy, polarization, and lipid accumulation. Next, foam cells were formed by oxidizing low-density lipoprotein to observe changes in lipid accumulation, autophagy, and polarization in rapamycin-treated or FTY720-treated foam cells. Lastly, foam cells that had been treated with rapamycin and FTY720 were evaluated for sphingosine 1-phosphate receptor (S1prs) expression. Autophagy microtubule-associated protein 1 light chain 3- (LC3-) II was increased, and classically activated macrophage phenotype markers interleukin- (IL-) 6, cyclooxygenase-2 (COX2), and inducible nitric oxide synthase (iNOS) were increased, whereas alternatively activated macrophage phenotype markers transforming growth factor- (TGF-)β, arginase 1 (Arg1), and mannose receptor C-type 1 (Mrc1) were decreased by rapamycin in peritoneal macrophages. LC3-II was also obviously enhanced, though polarization markers were unchanged in rapamycin-treated foam cells. Moreover, lipid accumulation was inhibited in rapamycin-treated macrophage cells but was unchanged in rapamycin-treated foam cells. For FTY720, LC3-II did not change, whereas TGF-β, Arg1 and Mrc1 were augmented, and IL-6 was suppressed in macrophages. However, LC3-II was increased, and TGF-β, ARG1 and MRC1 were strikingly augmented, whereas IL-6, COX2 and iNOS could be suppressed in foam cells. Furthermore, lipid accumulation was alleviated in FTY720-treated foam cells. Additionally, S1pr1 was markedly decreased in foam cells (P< .05); S1pr2, S1pr3, S1pr4 and S1pr5 were unchanged in rapamycin-treated foam cells. In FTY720-treated foam cells, S1pr3 and S1pr4 were decreased, and S1pr1, S1pr2 and S1pr5 were unchanged. Therefore, we deduced that rapamycin stimulated classically activated macrophages and supressed early atherosclerosis. Rapamycin may also stabilize artery plaques by preventing apoptosis and S1PR1 in advanced atherosclerosis. FTY720 allowed transformation of foam cells into alternatively activated macrophages through the autophagy pathway to alleviate advanced atherosclerosis.

scholarly journals IL10 Alters Peri-Collateral Macrophage Polarization and Hind-Limb Reperfusion in Mice after Femoral Artery Ligation

2020 ◽  
Vol 21 (8) ◽  
pp. 2821 ◽  
Author(s):  
Alexander M. Götze ◽  
Christian Schubert ◽  
Georg Jung ◽  
Oliver Dörr ◽  
Christoph Liebetrau ◽  
...  
Keyword(s):  
Femoral Artery ◽  
Hind Limb ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
Doppler Imaging ◽  
Activated Macrophages ◽  
Artery Ligation ◽  
Alternatively Activated Macrophages ◽  
Collateral Growth ◽  
Alternatively Activated

Arteriogenesis is a process by which a pre-existing arterioarterial anastomosis develops into a functional collateral network following an arterial occlusion. Alternatively activated macrophages polarized by IL10 have been described to promote collateral growth. This study investigates the effect of different levels of IL10 on hind-limb reperfusion and the distribution of perivascular macrophage activation types in mice after femoral artery ligation (FAL). IL10 and anti-IL10 were administered before FAL and the arteriogenic response was measured by Laser-Doppler-Imaging perioperatively, after 3, 7, and 14 d. Reperfusion recovery was accelerated when treated with IL10 and impaired with anti-IL10. Furthermore, symptoms of ischemia on ligated hind-limbs had the highest incidence after application of anti-IL10. Perivascular macrophages were immunohistologically phenotyped using CD163 and CD68 in adductor muscle segments. The proportion of alternatively activated macrophages (CD163+/CD68+) in relation to classically activated macrophages (CD163−/CD68+) observed was the highest when treated with IL10 and suppressed with anti-IL10. This study underlines the proarteriogenic response with increased levels of IL10 and demonstrates an in-vivo alteration of macrophage activation types in the perivascular bed of growing collaterals.

scholarly journals Similarity and Diversity in Macrophage Activation by Nematodes, Trematodes, and Cestodes

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
Stephen J. Jenkins ◽  
Judith E. Allen
Keyword(s):  
Macrophage Activation ◽  
Helminth Infection ◽  
Current Knowledge ◽  
Host Tissue ◽  
Macrophage Phenotype ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Helminth Infections ◽  
Host Metabolism ◽  
Alternatively Activated

This review summarizes current knowledge of macrophages in helminth infections, with a focus not only on delineating the striking similarities in macrophage phenotype between diverse infections but also on highlighting the differences. Findings from many different labs illustrate that macrophages in helminth infection can act as anti-parasite effectors but can also act as powerful immune suppressors. The specific role for their alternative (Th2-mediated) activation in helminth killing or expulsion versus immune regulation remains to be determined. Meanwhile, the rapid growth in knowledge of alternatively activated macrophages will require an even more expansive view of their potential functions to include repair of host tissue and regulation of host metabolism.

Methamphetamine causes neurotoxicity by promoting polarization of macrophages and inflammatory response

2017 ◽  
Vol 37 (5) ◽  
pp. 486-495 ◽  
Author(s):  
X Li ◽  
F Wu ◽  
L Xue ◽  
B Wang ◽  
J Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Macrophage Polarization ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neuronal System ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Raw264.7 Macrophages ◽  
Gene And Protein Expression ◽  
Anti Inflammatory

Macrophages, especially their activation state, are closely related to the progression of neurotoxicity. Classically activated macrophages (M1) are proinflammatory effectors, while alternatively activated macrophages (M2) exhibit anti-inflammatory properties. As a powerful addictive psychostimulant drug, coupled with its neurotoxicity, methamphetamine (Meth) abuse may lead to long-lasting abnormalities in the neuronal system. The present study investigated the effect of Meth at subtoxic concentration on macrophage activation state and its underlying toxicity to neuronal cells. PC12 and Murine RAW264.7 cells were coincubated with Meth to test its toxicity. 3-(4,5-Dimethylthiazol)-2,5-diphenyltetrazolium-bromide, enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot assays were performed to evaluate the toxicity, cytokine secretion, gene, and protein expression. Results showed that cytotoxicity was enhanced on PC12 cells after coculturing with RAW264.7 stimulated with Meth. RAW264.7 macrophages tended to switch to the M1 phenotype, releasing more nitric oxide and proinflammatory cytokines, including tumor necrosis factor α (TNFα), interleukin (IL)-12, and IL-1β, while decreasing the release of anti-inflammatory cytokine IL-10 after treatment with Meth. Meth upregulated the gene expression of IL-6, IL-1β, and TNFα and downregulated the expression of Arg-1, IL-10, and KLF4. Meth could also upregulate the protein expression of IL-1β and TNF α and downregulate the expression of Arg-1 and KLF4. However, the abovementioned effects induced by Meth were abolished by the addition of dopamine receptor D3 antagonist. In conclusion, our study demonstrated that Meth promoted macrophage polarization from M0 to M1 and enhanced inflammatory response, which provided the scientific rationale for the neurotoxicity caused by the chronic use of Meth.

scholarly journals Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xian Jin ◽  
Tongqing Yao ◽  
Zhong’e Zhou ◽  
Jian Zhu ◽  
Song Zhang ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Advanced Glycation ◽  
Alternatively Activated Macrophages ◽  
M1 Macrophage ◽  
Glycation End Products ◽  
End Products ◽  
Patients With Diabetes ◽  
M1 Phenotype

Atherosclerotic lesions are accelerated in patients with diabetes. M1 (classically activated in contrast to M2 alternatively activated) macrophages play key roles in the progression of atherosclerosis. Since advanced glycation end products (AGEs) are major pathogenic factors and active inflammation inducers in diabetes mellitus, this study assessed the effects of AGEs on macrophage polarization. The present study showed that AGEs significantly promoted macrophages to express IL-6 and TNF-α. M1 macrophage markers such as iNOS and surface markers including CD11c and CD86 were significantly upregulated while M2 macrophage markers such as Arg1 and CD206 remained unchanged after AGEs stimulation. AGEs significantly increased RAGE expression in macrophages and activated NF-κB pathway, and the aforementioned effects were partly abolished by administration of anti-RAGE antibody or NF-κB inhibitor PDTC. In conclusion, our results suggest that AGEs enhance macrophage differentiation into proinflammatory M1 phenotype at least partly via RAGE/NF-κB pathway activation.

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