BioAssay record AID 135371 submitted by ChEMBL: Inhibitory activity against LPS-induced NO production in mouse peritoneal macrophages was evaluated.
Wiltrout, R H.; Brunda, M J.; Gorelik, E; Peterson, E S.; Dunn, O J.; Leonhardt, J; Varesio, L; R; and Holden, H T., "Distribution of peritoneal macrophage populations after intraven- ous injection in mice: differential effects of eliciting and activating agents." (1983). Subject Strain Bibliography 1983. 1806 ...
Cytotoxic effects of MWCNTs-COOH and MWCNTs-PEG on macrophages.(A) RAW 264.7 cells and (B) primary rat peritoneal macrophages were incubated with or without ind
The system for this is not recognized but could be triggering crucial generic pathways that suppress the proliferation of T. gondii. A latest review, using
Hamilton, T.A.; Weiel, J.E.; Adams, D.O., 1984: Expression of the transferrin receptor in murine peritoneal macrophages is modulated in the different stages of activation
The transport of cystine has been investigated in mouse peritoneal macrophages cultured in vitro. The transport activity for cystine was very low in freshly isolated macrophages but was potently induced during culture in the presence of bacterial lipopolysaccharide (LPS) at concentrations as low as 0.1 ng/ml. The transport activity for cystine was enhanced when the cells were incubated with tumour necrosis factor-alpha (TNF-alpha), but not with interferon-gamma (IFN-gamma) or interleukin-1. IFN-gamma was rather repressive in the induction of the activity by LPS or TNF-alpha. The transport activity for cystine induced by LPS has been characterized. Cystine was transported mainly by Na(+)-independent system and the uptake of cystine was inhibited by extracellular glutamate and homocysteate, but not by aspartate, indicating that the transport of cystine in macrophages treated with LPS is mediated by System xc-. Glutathione content of the macrophages increased when they were exposed to LPS, and this ...
Schwartz, R H.; Horton, C L.; and Paul, W E., "T-lymphocyte-enriched murine peritoneal exudate cells. IV. Genetic control of cross-stimuation at the t-cell level." (1977). Subject Strain Bibliography 1977. 1668 ...
inproceedings{226715, author = {BRUYNINCKX, W and BLANQUAERT, AM and Ysebaert, Maria and Vanneste, Walter}, language = {eng}, title = {Phagocytosis-induced functional heterogeneity of resident peritoneal macrophages. Proc. Conference of the Federation of the American Societies for Experimental Biology, Atlanta, april 1992 ...
The adjuvant muramyl dipeptide (MDP) has been shown to affect a number of macrophage functions in vitro. We studied the effect of subcutaneous injection of MDP into mice. Cultured peritoneal macrophages from treated mice displayed increased spreading, total cell protein, and specific activity of beta-glucosaminidase a constituent of macrophage lysosomes, and of lactate dehydrogenase. Generation of superoxide anion (O2-) by MDP-treated macrophages stimulated by contact with phorbol myristate acetate was enhanced by over fivefold to levels achieved by macrophages from bacillus Calmette-Guérin-infected mice. The enhancement in stimulated O2- release was noted by 1 h after injection of MDP, peaked by 3 h, and remained high for at least 48 h. Priming for enhancement of O2- release by MDP was similar in athymic nude mice and in normal littermates, suggesting that mature T lymphocytes are not involved in this MDP effect. Priming for enhanced stimulated O2- release, and morphologic and enzymic changes, ...
Summary Mouse peritoneal macrophages from C57 Bl and NIH mice were examined after infection with polyoma virus. Cell DNA synthesis was stimulated in both cell types to the same extent between two and three days after addition of virus. Morphological changes appearing soon after infection were reversed by the second or third day. The cells did not acquire other properties associated with the transformed state. Treatment with mouse interferon up to 48 h after infection inhibited the virus-induced host DNA synthesis while morphological changes were not affected.
The diverse functions of macrophages as participants in innate and acquired immune responses are regulated by the specific milieu of environmental factors, cytokines, and other signaling molecules that are encountered at sites of inflammation. Microarray analysis of the transcriptional response of mouse peritoneal macrophages to the T(H)2 cytokine interleukin-4 (IL-4) identified Ym1 and arginase as the most highly up-regulated genes, exhibiting more than 68- and 88-fold induction, respectively. Molecular characterization of the Ym1 promoter in transfected epithelial and macrophage cell lines revealed the presence of multiple signal transducers and activators of transcription 6 (STAT6) response elements that function in a combinatorial manner to mediate transcriptional responses to IL-4. The participation of STAT6 as an obligate component of protein complexes binding to these sites was established by analysis of nuclear extracts derived from STAT6-deficient macrophages. Macrophage expression of Ym1 was
Graduate Student. Receptor tyrosine kinase RON, besides being expressed on tumor cells is also expressed on host macrophages and epithelial cells. My project is focused on deciphering the role of Ron (receptor tyrosine kinase) expressing resident peritoneal macrophages in breast cancer metastasis. I am using immune competent in vivo mouse models to address this question. I am also interested in delineating the developmental origin of Ron expressing resident peritoneal macrophages. Contrary to the previously well-established dogma that all macrophages originate from bone marrow derived monocytes recent studies has shown embryonic origins of certain tissue resident macrophages. I am using in vivo lineage tracing models to address this question. And outside of the lab, I love kayaking. ...
... : Phagocytic activity of peritoneal macrophages from knockout mice. Phagocytic activity of macrophages from wild type C57BL/6 (black bar), TLR2 -/- C57BL/6 (grey bar), TLR4-/- C57BL/6 (dark-grey bar), and MyD88-/- C57BL/6 (light-grey bar) mice stimulated previously with Lactobacillus casei CRL 431 by 7 consecutive days of administration and probiotic fermented milk, 5 consecutive days of administration. a,b,c,dMeans values for peritoneal macrophages without a common letter differ significantly (P,0.05). The error bars indicate standard deviations for 3 independent determinations per mouse ...
Subcellular localization of the Nramp1 protein in macrophages. Peritoneal macrophages from normal 129/sv mice (A) and from 129/sv Nramp1−/− mutants (B) w
In this study, we have shown that after peritoneal injection of [3H]-cholesterol-labeled mouse primary peritoneal macrophages, L1-KO mice expressing hepatic NPC1L1 (L1LivOnly) accumulated more [3H]-tracer in blood and tissues and secreted significantly reduced amounts of [3H]-neutral sterols in gallbladder bile and feces, when compared with L1-KO mice expressing no hepatic NPC1L1. Ezetimibe treatment reversed the accumulation of [3H]-tracer in blood and tissues and restored biliary and fecal excretion of [3H]-neutral sterols in L1LivOnly mice. Our results demonstrate an essential role of biliary sterol secretion in mediating macrophage-to-feces RCT in mice deficient in intestinal cholesterol absorption. Given that human livers express NPC1L1,8,10,15 our findings suggest that ezetimibe may have a previously unappreciated action: promoting macrophage RCT via direct inhibition of hepatic NPC1L1 in humans.. Recent studies on mice genetically or surgically deficient in biliary cholesterol secretion ...
In this study, we designed and synthesized 48 CAPE derivatives and evaluated their anti-inflammatory activities in mouse primary peritoneal macrophages (MPMs) activated by LPS. The most active compound, 10s, was found to bind with MD2 with high affinity, which prevented formation of the LPS/MD2/TLR4 complex. The binding mode of 10s revealed that the major interactions with MD2 were established via two key hydrogen bonds and hydrophobic interactions. Furthermore, 10s showed remarkable protective effects against LPS-caused ALI (acute lung injury) in vivo ...
Macrophages are usually found in tumor infiltrates where they exert cytostatic/cytotoxic activities against tumor cells. The tumoricidal activity is enhanced by activation of macrophages with bacterial products or cytokines (1,2). Recently nitric oxide (NO) has been indicated as a critical effector molecule for macrophage anti-tumor activity (3,4). Macrophages can be induced to release NO upon stimulation with a variety of stimuli such as bacterial products or cytokines (3,5). More recently it has been reported that mycoplasma-treated macrophages release large amounts of NO (6).. YAC-1 tumor cells have been classically used as targets for natural killer (NK) cells. Resident macrophages do not present anti-YAC-1 activity, but lymphokine-activated macrophages are able to kill YAC-1 cells (7). The mechanism by which lymphokine-activated macrophages kill YAC-1 cells remains unsettled.. Based on these observations, we asked whether mycoplasma-infected YAC-1 tumor cells could stimulate macrophages to ...
It is widely known that macrophages can be activated to kill tumor cells. It is also known that tumor-infiltrating macrophages can be immunosuppressed. The mechanisms of both tumor killing by activated macrophages and tumor-induced macrophage suppression are not entirely clear. To better understand the mechanisms that macrophages use to kill tumor cells, a murine macrophage cell line, RAW264.7, was fixed with paraformaldehyde, subsequently stimulated with lipopolysaccharide (LPS) and co-cultured with tumor cells. Macrophage activity was assessed by nitric oxide (NO) production and tumor cell growth inhibition in the 3H-thymidine incorporation assay. It was found that fixed macrophages were still able to suppress the proliferation of tumor cells while the production of NO was abrogated. Additionally, a model of tumor-induced suppression of macrophages was developed by co-culturing them with tumor cell conditioned media before adding LPS. Inhibition of macrophage activity by tumor cell products ...
Abstract: Glucagon and concanavalin A were administered into cell cultures of mice peritoneal macrophages and human intima aorta simultaneously with atherogenous blood serum, obtained from patients with ischemic heart disease, or with acetylated and native low density lipo-proteins. Their effect was dissimilar: glucagon decreased accumulation of intracellular cholesterol and the rate of 3H-thymidine incorporation into these cells, while concanavalin A increased the patterns studied. Cellular lysosomes appear to participate in atherogenesis, these results suggest that regulation of lysosomal apparatus may occur at the step of secondary lysosomes formation ...
Soluble products from antigen stimulated Trypanosoma cruzi-immune spleen cells enhanced the expression of Ia antigens on proteose-peptone-elicited mouse peritoneal macrophages (M phi). Acquisition of Ia paralleled M phi activation, previously shown to be mediated by this same source of lymphokine (LK). Expression of Ia and four other plasma membrane antigens was monitored by quantitative binding and radioautographic studies with 125I-monoclonal antibodies. Immune LK selectively enhanced expression of Ia and, to a lesser extent, H-2D relative to control LK from antigen-stimulated noninfected spleen. The levels of three other non-major histocompatibility complex (MHC) antigens, including the trypsin-resistant Fc receptor, were similar in cells exposed to both sources of LK. As little as 1% immune LK induced one-half maximal expression of Ia. Kinetic studies revealed that much of the Ia on freshly explanted peritoneal M phi was lost during the 1st d of culture. In the continued presence of immune ...
1. Macrophage Stimulating Protein (MSP), a serum factor related to Hepatocyte Growth Factor, was originally discovered to stimulate chemotaxis of murine resident peritoneal macrophages. MSP is the ligand for Ron, a member of the Met subfamily of tyrosine kinase receptors. The effects of MSP on human …
Macrophages display remarkable plasticity, with the ability to undergo dynamic transition between different functional phenotypes.63,64 Macrophages activated by TLR ligands and IFN-γ are called M1 macrophages (also referred to as classically activated macrophages).63-65 Conversely, stimulation of macrophages with Th2 cytokines, such as IL-4 or IL-13, immune complexes plus TLR ligands, IL-10, transforming growth factor-β, or glucocorticoids induces the generation of M2-type macrophages (also called alternatively activated macrophages).63-65 M1 macrophages produce high amounts of proinflammatory cytokines and NO by expressing inducible NO synthase and are important for eradicating bacterial, viral, and fungal infections.63-65 M2 macrophages are characterized by their high expression of markers of alternative activation, such as arginase-1, Chitinase 3-like 3 (also called YM-1), and found in inflammatory zone 1 (FIZZ1), and regulate responses to parasite infection, tissue remodeling, ...
In this study, we have shown that peritoneal macrophages, obtained from patients with cirrhosis and AF, and the presence of bactDNA are primed to synthesise significantly higher amounts of NO than macrophages obtained from patients without bactDNA, and this is associated with marked activation of the cytokines implicated in the type 1 immune response.. Bacterial infections are common complications in patients with advanced cirrhosis, and SBP is the most frequent and clinically relevant.1 The classical pathogenic theory of SBP suggests that bacteria of intestinal origin move across the intestinal wall,5 reaching mesenteric lymph nodes and other organs. Bacteria can then obtain access to AF, and a SBP episode may eventually develop if the local bactericidal mechanisms are insufficient to mount an adequate response.16,17. We have recently described the presence of bactDNA in patients with cirrhosis and culture negative non-neutrocytic AF, a fact that we interpret as molecular evidence of BT.6 It is ...
Polarization has been a useful concept for describing activated macrophage phenotypes and gene expression profiles. However, macrophage activation status within tumors and other settings are often inferred based on only a few markers. Complicating matters for relevance to human biology, many macrophage activation markers have been best characterized in mice and sometimes are not similarly regulated in human macrophages. To identify novel markers of activated human macrophages, gene expression profiles for human macrophages of a single donor subjected to 33 distinct activating conditions were obtained and a set of putative activation markers were subsequently evaluated in macrophages from multiple donors using integrated fluidic circuit (IFC)-based RT-PCR. Using unsupervised hierarchical clustering of the microarray screen, highly altered transcripts (>4-fold change in expression) sorted the macrophage transcription profiles into two major and 13 minor clusters. Among the 1874 highly altered transcripts,
Macrophages are found in most tissues of the body, where they have tissue- and context-dependent roles in maintaining homeostasis as well as coordinating adaptive responses to a variety of stresses. Their capacity for specialized functions is controlled by polarizing signals, which activate (or polarize) macrophages by upregulating transcriptional programs that encode distinct effector functions. An important conceptual advance in the field of macrophage biology, emerging from recent studies, is that macrophage activation is critically supported by metabolic shifts. Metabolic shifts fuel multiple aspects of macrophage activation, and preventing these shifts impairs appropriate activation. These findings raise the exciting possibility that macrophage functions in various contexts could be regulated by manipulating their metabolism. Here we review the rapidly evolving field of macrophage metabolism, discussing how polarizing signals trigger metabolic shifts and how these shifts enable appropriate
Dave: To isolate resident peritoneal macrophages, kill the mouse, and immediately inject the peritoneum with about 5 mls of pre-warmed HBSS or other media. Keeping the needle in the peritoneum, gently massage the mouse to suspend the cells. Remove as much of the media as you can, and place it into a centrifuge tube. Spin the cells gently to pellet them, and resuspend them in about 1 ml of 0.83% ammonium chloride, pH 7. This lyses rbcs. Incubate at room temp for 2-3 minutes, dilute with HBSS or media, and wash the cells twice. Resuspend the cells in MEM with 10% FBS at a concentration of 10(5)/ml, and plate. After 24 hrs, gently wash off the non-adherent cells. This procedure usually gets you ,95% pure macrophages by non-specific esterase staining. If you want inflammatory macrophages, simply inject 2 mls of thioglycollate broth into the peritoneum 3-4 days before harvest. Good luck. Let me know if you need more info. Jay Mone Millersville University ...
Accumulation of lipid-laden macrophages is a hallmark of atherosclerosis. The relevance of the key transcription factor nuclear factor κB (NF-κB) for macrophage-derived foam-cell formation has not been unequivocally resolved. Transgenic mice lines were generated in which NF-κB activation is specifically inhibited in macrophages by overexpressing a trans-dominant, non-degradable form of IκBα (IκBα (32A/36A)) under control of the macrophage-specific SR-A promoter. Alanine substitution of serines 32 and 36 prevents degradation and retains the inactive NF-κB/IκBα (32A/36A) complex in the cytoplasm. Similarly, stable human THP1 monocytic cell lines were generated with integrated copies of IκBα (32A/36A) cDNA. Upon treatment with oxidized low-density lipoprotein (ox-LDL), murine peritoneal macrophages from transgenic IκBα (32A/36A) mice, as well as THP1/IκBα (32A/36A) clones, display decreased lipid loading after differentiation into macrophages. This is accompanied by increased ...
The most abundant immune cell types of the tumor microenvironment macrophages recruited there by tumor-eluted factors. The role of these immune cells in tumor progression, and the interplay between tumor and immune cells is an emerging field of research with potential for novel treatment strategies. Here, a TIE2 expressing macrophage (TEM) subtype is integrated into a virtual tumor model. Within the 2D microenvironment, the TEM will differentiate from an extravasated monocyte precursor, congregate around the abluminal side of the vasculature in response to a chemoattractant gradient, secrete cytokines which favor differentiation of a separate angiogenic macrophage subtype [1]. The effects of macrophage populations on tumor progression on angiogenic activity and tumor growth will be examined.
The roles of A8 in inflammation are still unclear. In the mouse, A8 is induced in Mac by LPS, IFN, and TNF in the absence of A9 (17, 18), whereas the human counterparts are generally coexpressed and the A8/A9 heterodimer is implicated as the functional form (5, 6). Murine A8 is chemotactic for monocytes and neutrophils at picomolar levels in vitro, but the human homologue does not share this function (13). In contrast, A8 from both species is highly susceptible to oxidation by hypochlorite, a property not shared with A9 (22). We suggested that, in acute inflammation, A8 expressed in enormous amounts by neutrophils and released at inflammatory sites (7, 8) may protect the host against excessive oxidative damage. Here we show that induction of murine A8 is differentially regulated by agents that generally down-regulate proinflammatory Mac functions.. IL-4 and IL-13 inhibited mRNA induced by LPS in Mac (Fig. 1⇑) and MEC (Fig. 2⇑) by ∼50%. Transient transfection analysis of an A8 reporter ...
Hi I am a beginner in immunology. Please let me know how to prepare thioglycolate sol. for peritoneal macrophage migration. As I know, the sol. has activity in several days after autoclave. If somebody knows the full method for this experiment. Also I want to know what kind of mice is good for this, such as sex, age, etc.... Thank you for your regard ...
AB0069 TIE2 signalling induces a pro-inflammatory and pro-angiogenic phenotype in differentiated macrophages, independently of macrophage polarization conditions ...
Macrophages are extremely versatile cells, distributed throughout all tissues, involved in numerous functions, and equipped with many sensing receptors and effector molecules
Hi everyone! Does anyone have a good quality antibody/protocol to detect macrophages in FFPE mouse tissues? Thank you!! Noelle Linke, BS, HTL(ASCP)QIHC Allergan, Inc 2525 Dupont Drive RD-2A Irvine, CA 92612 714-246-5568 _______________________________________________ Histonet mailing list [email protected] http://lists.utsouthwestern.edu/mailman/listinfo/histonet ...
As we reported in an article yesterday, researchers are becoming increasingly interested in the potential of changing the ratio of types of macrophages pre...
Aujourdhui/today I have begun the back work to project 1 C.H.H (which will be named at a much later date) for now Ill posting usef ...
The cover for issue 33 of Oncotarget features Figure 5, Microglia and macrophages are more pro-inflammatory in IDH-MUT compared to IDH-WT GBMs, by Poon, et al.
Endotoxin-associated protein (EP) from Salmonella typhi activated murine resident peritoneal macrophages to produce prostaglandin E2 (PGE2). Cells from both endotoxin nonresponder (C3H/HeJ) and the endotoxin responder (C3H/OuJ) mouse strains were activated by EP. This EP-induced prostaglandin E2 production was blocked by the protein kinase C (PKC) inhibitor H-7 as well as the tyrosine kinase inhibitor genistein, suggesting the involvement of both serine and threonine phosphorylation and tyrosine phosphorylation pathways in the activation of resident peritoneal macrophages by EP. Immunoblot analysis using antiphosphoserine and antiphosphothreonine antibodies showed that EP induced the serine and threonine phosphorylation of a 14-kDa protein (p14). This phosphorylation was not induced by phorbol myristic acid or by lipopolysaccharide endotoxin. Inhibitors of PKC, PKA, and PKG did not block the phosphorylation of p14. However, the tyrosine kinase inhibitor piceatannol blocked p14 serine and ...
TY - JOUR. T1 - Acceleration of diabetes in young NOD mice with peritoneal macrophages. AU - Shimada, Akira. AU - Takei, Izumi. AU - Maruyama, Taro. AU - Kasuga, Akira. AU - Kasatani, Tomohiro. AU - Watanabe, Kenji. AU - Asaba, Yoshiaki. AU - Ishii, Toshiharu. AU - Tadakuma, Takushi. AU - Habu, Sonoko. AU - Miyazaki, Jun ichi. AU - Saruta, Takao. PY - 1994. Y1 - 1994. N2 - To elucidate the roles of macrophages in the pathogenesis of NOD murine diabetes, peritoneal macrophages from NOD mice were injected into young NOD mice. We used 12 to 20 week-old NOD mice of both sexes as donors, and sex-matched 2-week-old NOD mice as recipients. Cyclophosphamide (CY), 200 mg/kg, was intraperitoneally injected into the donors. Two weeks later, peritoneal exudate cells (PEC) were collected from the diabetic donors. Macrophagerich fractions (MRF) were collected by adherence. Then PEC(5-8 × 106) or MRF(3-7 × 106) were transferred, intraperitoneally, to the recipients. Two weeks later, some of the recipients ...
BioAssay record AID 309254 submitted by ChEMBL: Reduction of Mycobacterium tuberculosis H37Rv growth in mouse peritoneal macrophage monolayers after 7 days.
ER stress occurs in macrophage-rich areas of advanced atherosclerotic lesions and contributes to macrophage apoptosis and subsequent plaque necrosis. Therefore, signaling pathways that alter ER stressinduced apoptosis may affect advanced atherosclerosis. Here we placed Apoe/ mice deficient in macrophage p38α MAPK on a Western diet and found that they had a marked increase in macrophage apoptosis and plaque necrosis. The macrophage p38αdeficient lesions also exhibited a significant reduction in collagen content and a marked thinning of the fibrous cap, which suggests that plaque progression was advanced in these mice. Consistent with our in vivo data, we found that ER stressinduced apoptosis in cultured primary mouse macrophages was markedly accelerated under conditions of p38 inhibition. Pharmacological inhibition or genetic ablation of p38 suppressed activation of Akt in cultured macrophages and in atherosclerotic lesions. In addition, inhibition of Akt enhanced ER stressinduced macrophage ...
Using cDNA array analysis, we have identified spi2a as a protein that is induced in macrophages activated during infection with intracellular bacteria. The cDNA for spi2a was originally cloned from a chondrocyte cell line (6) and subsequently demonstrated to be expressed in hemopoietic progenitor cells (7). Interestingly, Hampson et al. (7) found spi2a mRNA to be down-regulated during granulocyte macrophage differentiation of a multipotential hemopoietic progenitor cell line and during macrophage differentiation of bipotential granulocyte/macrophage precursor cells isolated from mouse bone marrow. They found that spi2a mRNA was absent from mature macrophages differentiated from the progenitor cell line, which is consistent with our results showing that spi2a mRNA and protein are undetectable in unstimulated resident peritoneal macrophages.. Up-regulation of spi2a appears to be a general response of macrophages to bacterial infection both in vivo and in vitro. In addition to BCG, both ...
Interferons (IFNs) are potent antiviral cytokines capable of reprogramming the macrophage phenotype through the induction of interferon-stimulated genes (ISGs). Here we have used targeted RNA interference to suppress the expression of a number of key genes associated with IFN signalling in murine macrophages prior to stimulation with interferon-gamma. Genome-wide changes in transcript abundance caused by siRNA activity were measured using exon-level microarrays in the presence or absence of IFNγ. Transfection of murine bone-marrow derived macrophages (BMDMs) with a non-targeting (control) siRNA and 11 sequence-specific siRNAs was performed using a cationic lipid transfection reagent (Lipofectamine2000) prior to stimulation with IFNγ. Total RNA was harvested from cells and gene expression measured on Affymetrix GeneChip Mouse Exon 1.0 ST Arrays. Network-based analysis of these data revealed six siRNAs to cause a marked shift in the macrophage transcriptome in the presence or absence IFNγ. These six
Immortalized Murine Macrophage Cell Line as a Model for Macrophage Polarization into Classically Activated M(IFNγ+LPS) or Alternatively Activated M(IL-4) Macrophages Abstract.
Tumor-associated macrophages (TAMs) are the multifarious group of cells that originate mainly from the peritumoral tissue or bone marrow and can be divided into two main types: M1 and M2. Among them are the infiltrating M1 tumor-associated macrophages present in the early stages of tumorigenesis, which can secrete proinflammatory cytokines and in turn inhibit tumor growth. On the contrary, M2 tumor-associated macrophages are predominant in the late stage of tumor formation. Type II cytokines, which are secreted by them, can promote anti-inflammatory reaction and thus promote tumor growth. However, it remains unclear when M1 tumor-associated macrophages are transformed to M2 tumor-associated macrophages, but tumor hypoxia is currently thought to be associated with such a shift. M2 tumor-associated macrophages secrete many proteases such as cathepsin, cytokines, and an epidermal growth factor. The presence of M2 TAMs make the tumor prone to growth and angiogenesis, which in turn damages other ...
The interactions established between macrophages and cancer cells are largely dependent on instructions from the tumour microenvironment. Macrophages may differentiate into populations with distinct inflammatory profiles, but knowledge on their role on cancer cell activities is still very scarce. In this work, we investigated the influence of pro-inflammatory (LPS-stimulated) and anti-inflammatory (IL-10-stimulated) macrophages on gastric and colorectal cancer cell invasion, motility/migration, angiogenesis and proteolysis, and the associated molecular mechanisms. Following exposure of gastric and colon cancer cell lines to LPS- and IL-10-stimulated human macrophages, either by indirect contact or conditioned media, we analyzed the effect of the different macrophage populations on cancer cell invasion, migration, motility and phosphorylation status of EGFR and several interacting partners. Cancer-cell induced angiogenesis upon the influence of conditioned media from both macrophage populations was
Macrophages were first identified by Elie Metchnikoff more than a century ago as cells essential for host defense. Despite the fact that macrophages are one of the oldest immune cells known to man, this field is currently undergoing a thrilling revival as recent technological advances have revealed the fascinating diversity of macrophages and their essential functions in tissue homeostasis, wound healing, morphogenesis, cancer and metabolism. Importantly, it is now clear that macrophages in inflamed tissues comprise distinct subsets that differ in cellular origin and functional specialization.. This complexity has forced researchers to develop new tools to study the role of these intriguing cells in health and disease. Technological advances now permit the transcriptomic profiling and precise tissue localization of macrophages at the single-cell level, but these advances also bring puzzling questions regarding the inter- and intracellular networks that control macrophage function.. To help meet ...
The chemotactic response of murine peritoneal macrophages to RANTES/CCL5 was inhibited significantly following pretreatment with delta-9-tetrahydrocannabinol (THC), the main psychoactive component in marijuana. peritoneal macrophages from human beings, rats or mice pursuing or contact with weed or THC likewise have been reported. These modifications have included reduces in cell motility, Telavancin capability to pass on and (Huber et al., 1975; Chari-Briton, 1976; McCarthy et al., 1976; Drath et al., 1979; Huber et al., 1978; Lopez-Cepero et al., 1986; Specter et al., 1991; Tang et al., 1992). Furthermore, THC continues to be reported to influence macrophage digesting of soluble proteins antigens (McCoy et al., 1995; 1999). A crucial activity of macrophages thats exerted early in the inflammatory procedure is the capability to migrate in response to stimuli. This migratory activity can be exclusive from that of stimulus-independent arbitrary mobile movement (Lauffenburger and Horwitz, 1996; ...
Rat C-reactive protein (CRP) is a serum glycoprotein belonging to the pentraxin family of proteins. In this study we have shown the specific binding of 125I-CRP to rat peritoneal macrophages at 4 degrees C. This binding was dependent upon incubation time, CRP and cell concentrations, and was not inhibited by either phosphorylcholine or human IgG. At 37 degrees C, the surface-bound 125I-CRP was internalized and degraded. The degradation of 125I-CRP was measured by the formation of 125I-labelled trichloroacetic-acid-soluble CRP peptides by either precipitation assays or by h.p.l.c. of the incubation medium using a gel-filtration column. Since chloroquine and leupeptin inhibited CRP degradation, it was concluded that degradation of CRP occurred in the lysosomal compartment of the macrophage. There was an absolute requirement for the presence of bivalent cations (Ca2+ and Mg2+) in the incubation medium for the binding and degradation of CRP, which could be inhibited by EDTA but not by ...
TY - JOUR. T1 - Intracellular bacteria recognition contributes to maximal interleukin (IL)-12 production by IL-10-deficient macrophages. AU - Naruse, H.. AU - Hisamatsu, T.. AU - Yamauchi, Y.. AU - Chang, J. E.. AU - Matsuoka, K.. AU - Kitazume, M. T.. AU - Arai, K.. AU - Ando, S.. AU - Kanai, Takanori. AU - Kamada, N.. AU - Hibi, T.. PY - 2011/4. Y1 - 2011/4. N2 - Interleukin (IL)-12 is a key factor that induces T helper cell type 1-mediated immunity and inflammatory diseases. In some colitis models, such as IL-10 knock-out (KO) mice, IL-12 triggers intestinal inflammation. An abundant amount of IL-12 is produced by intestinal macrophages in response to stimulation by commensal bacteria in IL-10 KO mice. Intact bacteria are more potent inducers of macrophage IL-12 production than cell surface components in this model. This suggested that cell surface receptor signalling and intracellular pathogen recognition mechanisms are important for the induction of IL-12. We addressed the importance of ...
IFN-γ is so far the only cytokine able to induce by its own the synthesis of iNOS and the release of NO from MPM. However, it has been shown recently that IFN-γ-induced TNF-α is a prerequisite for in vitro production of NO released by MPM [2,4]. In addition to TNF-α, many other cytokines and bacterial products including transforming growth factor β, IL-10, TNF-α/β, GM-CSF and LPS [5-8,13,16,22,25] can also trigger NO production by acting in synergistic pairs on IFN-γ-activated MPM. We recently demonstrated that representative members of the cystatin superfamily, and particularly CC, can stimulate the release of NO from IFN-γ-activated MPM by stimulating the iNOS/NO system [12]. The results reported here show that CC stimulates the synthesis of TNF-α and IL-10 and upregulates the NO production by IFN-γ-activated MPM. The early iNOS induction by IFN-γ, followed by a CC stimulation, leads to maximal production of NO by MPM. This suggests that CC acts as an amplifier, but only if the ...