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Search Results: 1 - 10 of 518 matches for " macrophage "
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Pyroglutamated Apelin-13 Inhibits Lipopolysaccharide-Induced Production of Pro-Inflammatory Cytokines in Murine Macrophage J774.1 Cells  [PDF]
Shigeyuki Obara, Sumio Akifusa, Wataru Ariyoshi, Toshinori Okinaga, Michihiko Usui, Keisuke Nakashima, Tatsuji Nishihara
Modern Research in Inflammation (MRI) , 2014, DOI: 10.4236/mri.2014.32007
Abstract:

Apelin, recently identified as an endogenous ligand of the orphan G protein-coupled receptor APJ, has multiple pathophysiological properties. In the present study, we investigated whether pyroglutamated apelin-13 ([Pyr1]-apelin-13), the most highly active isoform among the mature apelin peptide family, modulates the effect of bacterial lipopolysaccharide (LPS) on cytokine induction in a murine macrophage-like cell line, J774.1 cells. J774.1 cells expressed the APJ protein in a stationary state, and the expression of APJ was not affected by LPS stimulation. No significant effect of [Pyr1]-apelin-13 treatment alone was observed on the proliferation or cytokine production of J774.1 cells in the stationary state. However, prior to LPS stimulation, pretreatment with [Pyr1]apelin-13 for 16 h significantly diminished mRNA expression and protein secretion of inflammatory cytokine interleukin-6, which was confirmed by RT-PCR and ELISA, respectively. Western blot analysis revealed that the phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, but not extracellular signal-regulated kinase, which was induced by LPS, significantly decreased in [Pyr1]-apelin-13-pretreated J774.1 cells compared with untreated cells. These observations suggest that [Pyr1]-apelin-13 functions as a negative regulator of LPS-mediated pro-inflammatory responses in macrophages.

Fc receptors: Cell activators of antibody functions  [PDF]
Carlos Rosales, Eileen Uribe-Querol
Advances in Bioscience and Biotechnology (ABB) , 2013, DOI: 10.4236/abb.2013.44A004
Abstract:

At the onset of an infection early defense systems, such as complement, get into action. Specialized leukocytes (white blood cells) of the innate immune system, including monocytes, macrophages, and neutrophils also participate as a first line of defense against infections. These early responses are rapid but not very specific and are usually not enough to clear completely many infections. The adaptive immune system is also needed to finish the job against many microorganisms. Antibody molecules, produced during the adaptive immune response, are crucial for preventing recurrent infections. Although, IgG antibodies are essential for controlling infections, these molecules do not directly damage the microorganisms they recognize. Today, it is established that leukocytes of the innate immune system are responsible for the protective effects of these antibodies. IgG molecules bind to their cognate antigens and are in turn recognized by specific receptors (Fcγ receptors) on the membrane of leukocytes. Crosslinking these receptors on the surface of leukocytes leads to activation of several effector cell functions. These effector functions are geared toward the destruction of microbial pathogens and the induction of an inflammatory state that is beneficial during infections. However, in autoimmune diseases, antibodies can direct these effector functions against normal tissues and cause severe tissue damage. In recent years, several factors that can modulate the IgG-FcγR interaction have been elucidated. In this review, we describe the main types of Fcγ receptors, and our current view of how antibody variants interact with these receptors to initiate different cell responses. In addition, new findings on the signaling role of individual Fcγ receptors are also discussed.

Silicosis and Smoking: Intrinsic Phenomenon in the Respiratory System  [PDF]
Diemen Delgado Garcia, Nayab Mahmood Sultan, Oscar Ramirez Yerba, Sofia Jimenez Castro, Enmanuel Agila Palacios, Ashley Delgado Cano
Advances in Applied Sociology (AASoci) , 2018, DOI: 10.4236/aasoci.2018.810039
Abstract: Purpose of the Review: Some physiopathological mechanisms that could support the relationship between tobacco and silicosis have been postulated but exact pathogenesis remains unknown. Recent Findings: Local inflammation in workers with silicosis is a complex process characterized by an infiltration of inflammatory cells in the respiratory alveolus, accompanied by an increase in the expression of cytokines, chemokines, enzymes, growth factors and adhesion molecules. Although in smokers without silicosis a similar pattern of inflammation can be observed, in workers with silicosis this process seems to be characterized by more pronounced increases in structural damage in the lungs. Altered balance of innate and adaptive immunity both play key roles in the pathogenesis of extensive fibrosis in a molecular level, influenced by individual susceptibilities and genetic traits. Conclusion: The identification of the molecular mechanism and a potential protective genotype for silicosis opens a window for the eradication of this occupational respiratory disease. This should encourage us to continue exploring and searching for the relation between the genetic polymorphism and the inorganic silica particle.
PLGA-Polymer Encapsulating Tumor Antigen and CpG DNA Administered into the Tumor Microenvironment Elicits a Systemic Antigen-Specific IFN-γ Response and Enhances Survival  [PDF]
Kevin P. Nikitczuk, Rene S. Schloss, Martin L. Yarmush, Edmund C. Lattime
Journal of Cancer Therapy (JCT) , 2013, DOI: 10.4236/jct.2013.41035
Abstract:

Critical to the generation of an effective therapeutic antitumor immune response is the elicitation of effective antigen presentation coupled with overcoming tumor-immune escape mechanisms. Towards this end, we aimed to understand the therapeutic effectiveness of a polymer based vaccine approach at enhancing the anti-tumor responses in a tumor-bearing mouse model. While we and others have previously demonstrated the effectiveness of PLGA based systems in delivering antigen etc., studies scarcely focus on understanding the immunological mechanisms of polymer based therapies in tumor bearing treatment models. Considering tumors modulate the immune system and consequently the efficacy of therapies, understanding treatment mechanisms in the presence of tumor will help lead to more efficacious treatment options. We demonstrate here that a poly(lactic-co-glycolic acid) (PLGA) based delivery system encapsulating tumor antigen (OVA) and the TLR9 agonist CpG motif DNA administered into the tumor microenvironment initiates an effective type 1 mediated (IFN-γ producing) anti-tumor response in a syngeneic murine model of T cell lymphoma (E.G7-OVA). Although E.G7-OVA tumors spontaneously generate antigen specific CTLs in draining lymph nodes (LN), tumors progress rapidly. Modulation of the tumor microenvironment via local PLGA based therapy led to the generation of a systemic antigen specific Th1 response, absent in the non-polymer delivery method, subsequently associated with reduced tumor growth and prolongation of survival. These studies provide further insight into the use of a PLGA-based therapeutic approach at modulating the tumor microenvironment and highlight the need for analyzing the treatment effects in a tumor bearing model.

Proposal for a new evaluation of phagocytosis using different sizes of fluorescent polystyrene microspheres  [PDF]
Riyo Enomoto, Makoto Imamori, Ayoumi Seon, Kozue Yoshida, Aya Furue, Hirofumi Tsuruda, Eibai Lee-Hiraiwa
Advances in Biological Chemistry (ABC) , 2013, DOI: 10.4236/abc.2013.36064
Abstract:

To investigate phagocytosis, peritoneal-resident and J774.1 macrophages were incubated with fluorescent polystyrene microspheres measuring 1.0 μm in diamter at 200 particles per cell. The amount of phagocytized microspheres increased with incubation time, and both cell types had similar phagocytic activity. Further, we investigated the phagocytosis of different sizes of microspheres by J774.1 macrophages. To adequately evaluate phagocytosis, varying amounts of different sizes of microspheres were added to J774.1 cells, and their phagocytic activities were evaluated. When the microspheres were added at a density of 20 particles per cell, few small microspheres (<1.0 μm in diameter) were phagocytized. This result suggested that their low amount caused difficulty in evaluating phagocytosis. In contrast, when the same variety of microspheres was added at a density of 200 particles per cell, phagocytosis of large microspheres (>3 μm in diameter) could not be evaluated because of cytotoxicity. Thus, the amount of different sizes of microspheres added is important for precisely evaluating phagocytic activity. When the amount of different sizes of microspheres added was standardized to provide a set amount of total surface area, phagocytosis of these microspheres could be adequately evaluated and compared. To determine the effects of phagocytosis on cell viability and proliferation, cells incubated with different sizes of microspheres were assayed using a cell counting kit. We found that phagocytosis had no effect on cell viability or proliferation and was independent of particle size. Furthermore, cells already phagocytized microspheres retained their phagocytic activity.

 

The Phenotypic Conversion of Macrophage Detected by FACS in EAE Mice Treated with or without Fasudil  [PDF]
Chunyun Liu, Yong Xie, Yanhua Li, Jiezhong Yu, Ling Feng, Shaowei Hou, Haifei Zhang, Cungen Ma, Baoguo Xiao
Engineering (ENG) , 2013, DOI: 10.4236/eng.2013.510B101
Abstract:

We studied the changes of macrophage populations in splenic mononuclear cells of experimental autoimmune ence-phalomyelitis (EAE) mice treated with or without Fasudil. Phenotypic analysis using flow cytometry showed that the levels of TLR4, CD11c and CD40 which represent the type 1 macrophage, were depressed in Fasudil-treated mice. Incontrast, it was observed the expressions of CD200 and CD14 which typify the type 2 macrophage were elevated in Fasudil-treated mice as compared to EAE mice. And we also found that Fasudil at dose of 40 mg/kg alleviated the se-verity of symptom in EAE mice. Based on the evidence that M1 macrophages are neurotoxic and M2 macrophages promote a regenerative growth, indicating that polarization and shifting of macrophages into M2 cells may also play key roles in treatment of EAE.

Effects of oleic acid on murine macrophage dysfunction  [PDF]
Naofumi Shiomi, Keiko Watanabe
Journal of Biomedical Science and Engineering (JBiSE) , 2013, DOI: 10.4236/jbise.2013.66080
Abstract:

Obese individuals exhibit much higher risks not only for metabolic syndrome, but also for cancer and allergies, than normal-weight subjects. This fact suggests that signals secreted from adipocytes change the characteristics of lymphocytes, such as macrophages and T-cells. We focused on a free fatty acid, oleic acid, as a signal inducing such changes and examined its effects on murine J774.2 macrophages. When the cells were cultured in medium containing high concentrations (1, 2 and 4 mM) of oleic acid, apoptosis occurred, and the apoptotic cells were gathered into clusters of very large size by the work of enzymes for phagocytosis. When the cells were cultured in medium containing 0.5 mM of oleic acid, the fatty acid did not affect cell growth; however, it inhibited nitrogen monoxide (NO) secretion and the gene expressions of interleukins and TNF-α. NO disturbs the invasion of macrophages into blood vessels, and interleukins promote the differentiation and proliferation of T- and B-cells. Therefore, these results suggest that the high risks for cancer and allergies observed in obese subjects are associated with the dysfunction of macrophages induced by fatty acids. Moreover, we also examined the protective effects of carnitine against dysfunction. However, carnitine did not exhibit sufficient effects.

Down Regulation of MyD88 in Macrophages Treated with Liposomes Composed of Phosphatidylserine  [PDF]
Yuka Takasugi, Futoshi Kurai, Issei Kazume, Masaki Otsuka, Yoichi Negishi, Rui Tada, Yukihiko Aramaki
Pharmacology & Pharmacy (PP) , 2013, DOI: 10.4236/pp.2013.42035
Abstract: We have recently demonstrated that liposomes composed of phosphatidylserine (PS-liposomes) suppressed nitric oxide and inflammatory cytokine productions following LPS stimulation in macrophages. In this study, we examined the effect of PS-liposomes on expressions of TLR-4 and MyD88, which are essential for the signal transduction in LPS stimulation. Expression of MyD88 was suppressed when macrophages were treated with PS-liposomes, but not with liposomes of phosphatidylcholine. No change in TLR-4 expression was observed. MyD88 suppression was restored to the control levels when cells were pre-treated with anti-TGF-β antibody, suggesting that TGF-β plays an important role in down-regulation of MyD88 following PS-liposome treatment.
Tyrosine phosphorylation of monocyte-derived macrophage proteins in buffalo (Bubalus bubalis): A potential phenotype of natural resistance  [PDF]
Maria Miarelli, Federica Signorelli, Giovanna de Matteis
Open Journal of Animal Sciences (OJAS) , 2013, DOI: 10.4236/ojas.2013.32019
Abstract:

The aim of this work was to explore the possibility of using the presence of tyrosine-phosphorylated macrophage proteins as a phenotype of natural resistance. Tyrosine-phosphorylation of macrophage proteins was investigated in 18 buffaloes, that carried either the resistant, or the non-resistant, Natural Resistance-Associated Macrophage Protein one (NRAMP1) genotype, that various authors have associated with susceptibility to intracellular bacterial diseases. Monocyte-derived macrophages were Interferon-gamma (IFN-γ) stimulated and tyrosine-phosphorylation was assessed by Western blotting. Evidence of phosphorylation after IFN-γ stimulation was shown by 75% of the buffaloes carriers of the resistant genotype, and by 20% of the carriers of the non-resistant genotype (Chisquare value between the groups = 5.44; P = 0.02). The study of the Proteoma of monocyte-derived macrophages might open the way to the genetic control of disease resistance.

IL-10 Inhibits LPS-Induced Expression of miR-147 in Murine Macrophages  [PDF]
Leah N. Cardwell, Brian K. Weaver
Advances in Biological Chemistry (ABC) , 2014, DOI: 10.4236/abc.2014.44032
Abstract: Interleukin-10 (IL-10) mediates an anti-inflammatory response that constrains immune responses and limits inflammation-associated pathology. IL-10 does so, in part, by selectively inhibiting pro-inflammatory cytokine and chemokine expression induced in macrophages in response to Toll-like receptor (TLR) signaling. The IL-10-mediated anti-inflammatory response is executed through the activation of STAT3 leading to induction of target genes referred to as IL-10-induced genes. As miRNAs have emerged as important negative regulators of gene expression in various systems, we sought to address whether the IL-10-mediated anti-inflammatory response acts through regulated expression of miRNA genes. Using quantitative PCR-based arrays, we examined 140 miRNA genes with putative roles in inflammation for changes in expression in response to IL-10 and lipopoly-saccharide (LPS) in primary mouse macrophages. IL-10 stimulation resulted in the inhibition of miR-147 expression induced in response to LPS, while having a potentiating effect on the induction of miR-455. miR-147 is the second TLR-induced miRNA, in addition to miR-155, identified to be counter-regulated by IL-10. Its suppression by IL-10 suggests that miR-147 may have an unknown pro-inflammatory function in TLR-triggered macrophages. The results extend the notion that IL-10 selectively regulates expression of miRNA genes, and that miRNA-mediated pathways are a component of the IL-10-mediated anti-inflammatory response.
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