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Journal articles on the topic 'Macrophages'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Stojadinović, Marija. "Macrophage polarization and infectious diseases." Biologia Serbica 45, no. 2 (2023): 38–43. https://doi.org/10.5281/zenodo.10402369.

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<strong>Summary. </strong>Macrophages are a heterogeneous cell population present in most mammalian tissues with a wide range of functions. They are an essential component of optimal tissue homeostasis and an essential first line of defense against pathogens. Activated macrophages are typically divided into two phenotypes, M1 macrophages and M2 macrophages, which are influenced by microorganisms, the tissue microenvironment, and cytokine signals from physiological conditions to infections. The management of macrophage polarity is crucial for the prevention and treatment of infections and infla

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Rodriguez, Eric, Frederic Boudard, Michele Mallié, Jean-Marie Bastide, and Madeleine Bastide. "Murine macrophage elastolytic activity induced by Aspergillus fumigatus strains in vitro: evidence of the expression of two macrophage-induced protease genes." Canadian Journal of Microbiology 43, no. 7 (1997): 649–57. http://dx.doi.org/10.1139/m97-092.

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The interaction between Aspergillus fumigatus conidia and murine macrophages of various origins was investigated. Cocultures were carried out between A. fumigatus strains and freshly isolated murine pulmonary alveolar macrophages or two murine macrophage cell-lines: murine alveolar cell-line MALU and murine astrocytoma cell-line J774. By measuring the variation of elastolytic activity in the coculture supernatants with two elastin substrates, we demonstrated that either viable or fixed A. fumigatus or C. albicans yeasts or nonspecific particles induced significant macrophage elastolytic activi

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Lu, Yufei, Leiming Guo, and Gaofeng Ding. "PD1+ tumor associated macrophages predict poor prognosis of locally advanced esophageal squamous cell carcinoma." Future Oncology 15, no. 35 (2019): 4019–30. http://dx.doi.org/10.2217/fon-2019-0519.

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Aim: Tumor associated macrophages are the most abundant cancer immune cells. However, little was known about the identity of CD68+PD1+ macrophages as well as the contributions in the prognosis of esophageal squamous cell carcinoma (ESCC). Methods & methods: Immunofluorescence, flowcytometry and RT-PCR were used to analysis PD1+ macrophages in ESCC. Results: CD68+PD1+ macrophages which can express higher M2 markers in cancer tissues, increased about 4.2-times compared with para-cancer tissues. Additionally, PD1high macrophages were significantly correlated with more malignant phenotypes and

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Hargarten, Jessica C., Tyler C. Moore, Thomas M. Petro, Kenneth W. Nickerson, and Audrey L. Atkin. "Candida albicans Quorum Sensing Molecules Stimulate Mouse Macrophage Migration." Infection and Immunity 83, no. 10 (2015): 3857–64. http://dx.doi.org/10.1128/iai.00886-15.

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The polymorphic commensal fungusCandida albicanscauses life-threatening disease via bloodstream and intra-abdominal infections in immunocompromised and transplant patients. Although host immune evasion is a common strategy used by successful human fungal pathogens,C. albicansprovokes recognition by host immune cells less capable of destroying it. To accomplish this,C. albicanswhite cells secrete a low-molecular-weight chemoattractive stimulant(s) of macrophages, a phagocyte that they are able to survive within and eventually escape from.C. albicansopaque cells do not secrete this chemoattracti

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Yadav, Mahesh, та Jeffrey S. Schorey. "The β-glucan receptor dectin-1 functions together with TLR2 to mediate macrophage activation by mycobacteria". Blood 108, № 9 (2006): 3168–75. http://dx.doi.org/10.1182/blood-2006-05-024406.

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AbstractPattern recognition receptors (PRRs) play an essential role in a macrophage's response to mycobacterial infections. However, how these receptors work in concert to promote this macrophage response remains unclear. In this study, we used bone marrow–derived macrophages isolated from mannose receptor (MR), complement receptor 3 (CR3), MyD88, Toll-like receptor 4 (TLR4), and TLR2 knockout mice to examine the significance of these receptors in mediating a macrophage's response to a mycobacterial infection. We determined that mitogen-activated protein kinase (MAPK) activation and tumor necr

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Gallego, Carolina, Douglas Golenbock, Maria Adelaida Gomez, and Nancy Gore Saravia. "Toll-Like Receptors Participate in Macrophage Activation and Intracellular Control of Leishmania (Viannia) panamensis." Infection and Immunity 79, no. 7 (2011): 2871–79. http://dx.doi.org/10.1128/iai.01388-10.

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ABSTRACTToll-like receptors (TLRs) play a central role in macrophage activation and control of parasitic infections. Their contribution to the outcome ofLeishmaniainfection is just beginning to be deciphered. We examined the interaction ofLeishmania panamensiswith TLRs in the activation of host macrophages.L. panamensisinfection resulted in upregulation of TLR1, TLR2, TLR3, and TLR4 expression and induced tumor necrosis factor alpha (TNF-α) secretion by human primary macrophages at comparable levels and kinetics to those of specific TLR ligands. The TLR dependence of the host cell response was

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McKenzie, C. G. J., U. Koser, L. E. Lewis, et al. "Contribution of Candida albicans Cell Wall Components to Recognition by and Escape from Murine Macrophages." Infection and Immunity 78, no. 4 (2010): 1650–58. http://dx.doi.org/10.1128/iai.00001-10.

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ABSTRACT The pathogenicity of the opportunistic human fungal pathogen Candida albicans depends on its ability to escape destruction by the host immune system. Using mutant strains that are defective in cell surface glycosylation, cell wall protein synthesis, and yeast-hypha morphogenesis, we have investigated three important aspects of C. albicans innate immune interactions: phagocytosis by primary macrophages and macrophage cell lines, hyphal formation within macrophage phagosomes, and the ability to escape from and kill macrophages. We show that cell wall glycosylation is critically importan

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Wilson, Justin E., Bhuvana Katkere, and James R. Drake. "Francisella tularensis Induces Ubiquitin-Dependent Major Histocompatibility Complex Class II Degradation in Activated Macrophages." Infection and Immunity 77, no. 11 (2009): 4953–65. http://dx.doi.org/10.1128/iai.00844-09.

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ABSTRACT The intracellular bacterium Francisella tularensis survives and replicates within macrophages, ultimately killing the host cell. Resolution of infection requires the development of adaptive immunity through presentation of F. tularensis antigens to CD4+ and CD8+ T cells. We have previously established that F. tularensis induces macrophage prostaglandin E2 (PGE2) production, leading to skewed T-cell responses. PGE2 can also downregulate macrophage major histocompatibility complex (MHC) class II expression, suggesting that F. tularensis-elicited PGE2 may further alter T-cell responses v

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Careau, Éric, Léa-Isabelle Proulx, Philippe Pouliot, Annie Spahr, Véronique Turmel, and Élyse Y. Bissonnette. "Antigen sensitization modulates alveolar macrophage functions in an asthma model." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 5 (2006): L871—L879. http://dx.doi.org/10.1152/ajplung.00219.2005.

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We have previously demonstrated that adoptive transfer of alveolar macrophages from allergy-resistant rats to alveolar macrophage-depleted allergic rats prevents airway hyperresponsiveness development, suggesting an important role for alveolar macrophages in asthma pathogenesis. Given that ovalbumin sensitization can modulate alveolar macrophage cytokine production, we investigated the role of sensitized and unsensitized alveolar macrophages in an asthma model. Alveolar macrophages from unsensitized or sensitized Brown Norway rats were transferred to alveolar macrophage-depleted sensitized rat

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Shinonaga, Masamichi, Cha Cheng Chang, Noriyuki Suzuki, Masazumi Sato, and Takeo Kuwabara. "Immunohistological evaluation of macrophage infiltrates in brain tumors." Journal of Neurosurgery 68, no. 2 (1988): 259–65. http://dx.doi.org/10.3171/jns.1988.68.2.0259.

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✓ Peritumoral edema is one of the most serious complications of intracranial neoplasms; however, the exact pathogenesis of this condition is still unknown. To explore the effect of macrophages in brain tumors on the pathogenesis of peritumoral edema, 42 specimens of primary or metastatic brain tumors were studied. Frozen sections were examined by an immunoperoxidase staining technique with anti-Leu-M3 monoclonal antibody. Eight of 14 gliomas demonstrated Leu-M3-positive cell (macrophage) infiltration. The two glioblastomas showed a moderate or marked degree of macrophage infiltration. Twelve o

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Fedorov, A. A., N. A. Ermak, T. S. Gerashchenko, et al. "Polarization of macrophages: mechanisms, markers and factors of induction." Siberian journal of oncology 21, no. 4 (2022): 124–36. http://dx.doi.org/10.21294/1814-4861-2022-21-4-124-136.

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Macrophages are key components of the innate immune system. The variability of the macrophage’s participation in tumor progression, determined by their functional polarization, opens up a wide prospect for modulating their functional profile, primarily in the direction of increasing antitumor activity. The purpose of the study was to provide up-to-date data on the process of macrophage polarization, mechanisms of its regulation, polarization markers and induction factors. Material and methods. A search was made for available literature sources published in Web of Science, Scopus and other data

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García-Rodas, Rocío, Fernando González-Camacho, Juan Luis Rodríguez-Tudela, Manuel Cuenca-Estrella, and Oscar Zaragoza. "The Interaction between Candida krusei and Murine Macrophages Results in Multiple Outcomes, Including Intracellular Survival and Escape from Killing." Infection and Immunity 79, no. 6 (2011): 2136–44. http://dx.doi.org/10.1128/iai.00044-11.

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ABSTRACTCandida kruseiis a fungal pathogen of interest for the scientific community for its intrinsic resistance to fluconazole. Little is known about the interaction of this yeast with host immune cells. In this work, we have characterized the outcome of the interaction betweenC. kruseiand murine macrophages. OnceC. kruseiwas internalized, we observed different phenomena. In a macrophage-like cell line,C. kruseisurvived in a significant number of macrophages and induced filamentation and macrophage explosion. Phagocytosis ofC. kruseiled to actin polymerization around the yeast cells at the si

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Xu, Jiawei, Lanya Fu, Junyao Deng, et al. "miR-301a Deficiency Attenuates the Macrophage Migration and Phagocytosis through YY1/CXCR4 Pathway." Cells 11, no. 24 (2022): 3952. http://dx.doi.org/10.3390/cells11243952.

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(1) Background: the miR-301a is well known involving the proliferation and migration of tumor cells. However, the role of miR-301a in the migration and phagocytosis of macrophages is still unclear. (2) Methods: sciatic nerve injury, liver injury models, as well as primary macrophage cultures were prepared from the miR-301a knockout (KO) and wild type (WT) mice to assess the macrophage’s migration and phagocytosis capabilities. Targetscan database analysis, Western blotting, siRNA transfection, and CXCR4 inhibition or activation were performed to reveal miR301a’s potential mechanism. (3) Result

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DiNapoli, Sarah R., Vanessa M. Hirsch, and Jason M. Brenchley. "Macrophages in Progressive Human Immunodeficiency Virus/Simian Immunodeficiency Virus Infections." Journal of Virology 90, no. 17 (2016): 7596–606. http://dx.doi.org/10.1128/jvi.00672-16.

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The cells that are targeted by primate lentiviruses (HIV and simian immunodeficiency virus [SIV]) are of intense interest given the renewed effort to identify potential cures for HIV. These viruses have been reported to infect multiple cell lineages of hematopoietic origin, including all phenotypic and functional CD4 T cell subsets. The two most commonly reported cell types that become infectedin vivoare memory CD4 T cells and tissue-resident macrophages. Though viral infection of CD4 T cells is routinely detected in both HIV-infected humans and SIV-infected Asian macaques, significant viral i

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Bonetti, Justine, Alessandro Corti, Lucie Lerouge, Alfonso Pompella, and Caroline Gaucher. "Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis—Nitro-Redox Interconnections." Antioxidants 10, no. 4 (2021): 516. http://dx.doi.org/10.3390/antiox10040516.

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Monocytes/macrophages and vascular smooth muscle cells (vSMCs) are the main cell types implicated in atherosclerosis development, and unlike other mature cell types, both retain a remarkable plasticity. In mature vessels, differentiated vSMCs control the vascular tone and the blood pressure. In response to vascular injury and modifications of the local environment (inflammation, oxidative stress), vSMCs switch from a contractile to a secretory phenotype and also display macrophagic markers expression and a macrophagic behaviour. Endothelial dysfunction promotes adhesion to the endothelium of m

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Taylor, Sarah A., Shang-Yang Chen, Gaurav Gadhvi, et al. "Transcriptional profiling of pediatric cholestatic livers identifies three distinct macrophage populations." PLOS ONE 16, no. 1 (2021): e0244743. http://dx.doi.org/10.1371/journal.pone.0244743.

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Background & aims Limited understanding of the role for specific macrophage subsets in the pathogenesis of cholestatic liver injury is a barrier to advancing medical therapy. Macrophages have previously been implicated in both the mal-adaptive and protective responses in obstructive cholestasis. Recently two macrophage subsets were identified in non-diseased human liver; however, no studies to date fully define the heterogeneous macrophage subsets during the pathogenesis of cholestasis. Here, we aim to further characterize the transcriptional profile of macrophages in pediatric cholestatic

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Deng, Lishuang, Zhijie Jian, Tong Xu, et al. "Macrophage Polarization: An Important Candidate Regulator for Lung Diseases." Molecules 28, no. 5 (2023): 2379. http://dx.doi.org/10.3390/molecules28052379.

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Macrophages are crucial components of the immune system and play a critical role in the initial defense against pathogens. They are highly heterogeneous and plastic and can be polarized into classically activated macrophages (M1) or selectively activated macrophages (M2) in response to local microenvironments. Macrophage polarization involves the regulation of multiple signaling pathways and transcription factors. Here, we focused on the origin of macrophages, the phenotype and polarization of macrophages, as well as the signaling pathways associated with macrophage polarization. We also highl

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Ulndreaj, Antigona, Angela Li, Yonghong Chen, et al. "Adventitial recruitment of Lyve-1− macrophages drives aortic aneurysm in an angiotensin-2-based murine model." Clinical Science 135, no. 10 (2021): 1295–309. http://dx.doi.org/10.1042/cs20200963.

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Abstract Objective: Aortic macrophage accumulation is characteristic of the pathogenesis of abdominal aortic aneurysm (AAA) but the mechanisms of macrophage accumulation and their phenotype are poorly understood. Lymphatic vessel endothelial receptor-1 (Lyve-1+) resident aortic macrophages independently self-renew and are functionally distinct from monocyte-derived macrophages recruited during inflammation. We hypothesized that Lyve-1+ and Lyve-1− macrophages differentially contribute to aortic aneurysm. Approach and results: Angiotensin-2 and β-aminopropionitrile (AT2/BAPN) were administered

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Yaparla, Amulya, Milan Popovic, Kelsey A. Hauser, Louise A. Rollins-Smith, and Leon Grayfer. "Amphibian (Xenopus laevis) Macrophage Subsets Vary in Their Responses to the Chytrid Fungus Batrachochytrium dendrobatidis." Journal of Fungi 11, no. 4 (2025): 311. https://doi.org/10.3390/jof11040311.

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The chytrid fungus, Batrachochytrium dendrobatidis (Bd), infects amphibian skin, causing chytridiomycosis, which is a contributing cause of worldwide declines and extinctions of amphibians. Relatively little is known about the roles of amphibian skin-resident immune cells, such as macrophages, in these antifungal defenses. Across vertebrates, macrophage differentiation is controlled through the activation of colony-stimulating factor-1 (CSF1) receptor by CSF1 and interleukin-34 (IL34) cytokines. While the precise roles of these respective cytokines in macrophage development remain to be fully

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Randolph, Gwendalyn J. "Monocyte Trafficking, Inflammation, and Atherosclerosis." Blood 122, no. 21 (2013): SCI—53—SCI—53. http://dx.doi.org/10.1182/blood.v122.21.sci-53.sci-53.

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Abstract Macrophages are central to the progression of atherosclerosis. An increased number of macrophages in plaque are associated with larger, more stenotic lesions. Furthermore, activated plaque macrophages promote rupture, the most significant clinical event affecting mortality. Plaque macrophages derive from monocytes that are recruited from blood. We have thus focused our efforts on understanding the mechanisms that regulate plaque macrophages, with emphasis on how macrophage-burden might be reduced to lower disease risk. We have developed techniques to discern whether macrophage contrac

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Wang, Jianjun, Yongliang Yao, Jing Xiong, Jianhong Wu, Xin Tang, and Guangxin Li. "Evaluation of the Inflammatory Response in Macrophages Stimulated with Exosomes Secreted byMycobacterium avium-Infected Macrophages." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/658421.

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Exosomes secreted fromMycobacterium avium-infected macrophages contain numerous antigens of bothM. aviumand the host cell and are involved in the induction and expression of the inflammatory responses in macrophages. The interaction between exosomes secreted fromM. avium-infected macrophages and macrophage phagocytosis, cytokine secretion, immunostimulation, and apoptosis was analyzed. Upon stimulation with exosomes secreted fromM. avium-infected macrophages, the phagocytosis of dextran by treated macrophages was increased. Furthermore, the expression of CD40, CD80, CD81, CD86, HLA-DR, and mos

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Li, Wei, Yaomei Wang, Huizhi Zhao, et al. "Identification, Isolation and Transcriptome Analyses of Mouse, Rat and Man Erythroblastic Island Central Macrophages." Blood 132, Supplement 1 (2018): 841. http://dx.doi.org/10.1182/blood-2018-99-114188.

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Abstract Erythroblastic island (EBI), composed of a central macrophage and surrounding erythroid cells, is the first hematopoietic niche discovered for erythropoiesis. Yet, the identity of the central macrophage has so far remained elusive. Based on the previous findings that F4/80, VCAM1 and CD169 are potential mouse central macrophage markers, we first calculated the number of F4/80+VCAM1+CD169+ mouse macrophages in the mouse bone marrow and compared it to the number of Ter119+ erythroblasts. We found that the ratio of F4/80+VCAM1+CD169+ macrophage and erythroblasts is about 1:2. Given the f

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AlQasrawi, Dania, and Saleh A. Naser. "Nicotine Modulates MyD88-Dependent Signaling Pathway in Macrophages during Mycobacterial Infection." Microorganisms 8, no. 11 (2020): 1804. http://dx.doi.org/10.3390/microorganisms8111804.

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Recently, we reported that cigarette smoking, and especially nicotine, increases susceptibility to mycobacterial infection and exacerbates inflammation in patients with Crohn’s disease (CD). The macrophagic response to Mycobacterium avium subspecies paratuberculosis (MAP) in CD and Mycobacteria tuberculosis (MTB) continues to be under investigation. The role of toll-like-receptors (TLRs) and cytoplasmic adaptor protein (MyD88) in proinflammatory response during Mycobacterial infection has been suggested. However, the mechanism of how nicotine modulates macrophage response during infection in C

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Lu, Chunxia, P. Anil Kumar, Yong Fan, Mark A. Sperling, and Ram K. Menon. "A Novel Effect of Growth Hormone on Macrophage Modulates Macrophage-Dependent Adipocyte Differentiation." Endocrinology 151, no. 5 (2010): 2189–99. http://dx.doi.org/10.1210/en.2009-1194.

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The GH receptor (GHR) is expressed on macrophages. However, the precise role of GH in regulation of macrophage function is unclear. We hypothesized that soluble factors including cytokines produced by macrophages in a GH-dependent manner regulate adipogenesis. We confirmed expression and functional integrity of the GHR in the J774A.1 macrophage cells. Conditioned medium (CM) from macrophages inhibited adipogenesis in a 3T3-L1 adipogenesis assay. CM from GH-treated macrophages decreased the inhibitory effect of CM from macrophages on adipogenesis. This effect on preadipocyte differentiation was

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Cotechini, Tiziana, Aline Atallah, and Arielle Grossman. "Tissue-Resident and Recruited Macrophages in Primary Tumor and Metastatic Microenvironments: Potential Targets in Cancer Therapy." Cells 10, no. 4 (2021): 960. http://dx.doi.org/10.3390/cells10040960.

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Macrophages within solid tumors and metastatic sites are heterogenous populations with different developmental origins and substantially contribute to tumor progression. A number of tumor-promoting phenotypes associated with both tumor- and metastasis-associated macrophages are similar to innate programs of embryonic-derived tissue-resident macrophages. In contrast to recruited macrophages originating from marrow precursors, tissue-resident macrophages are seeded before birth and function to coordinate tissue remodeling and maintain tissue integrity and homeostasis. Both recruited and tissue-r

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Fischer, Carrie D., Jennifer K. Beatty, Stephanie C. Duquette, Douglas W. Morck, Merlyn J. Lucas, and André G. Buret. "Direct and Indirect Anti-Inflammatory Effects of Tulathromycin in Bovine Macrophages: Inhibition of CXCL-8 Secretion, Induction of Apoptosis, and Promotion of Efferocytosis." Antimicrobial Agents and Chemotherapy 57, no. 3 (2013): 1385–93. http://dx.doi.org/10.1128/aac.01598-12.

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ABSTRACTRecent evidence indicates that immunomodulation by antibiotics may enhance their clinical efficacy. Specifically, drug-induced leukocyte apoptosis and macrophage efferocytosis have been shown to promote the resolution of inflammation in a variety of disease settings. Tulathromycin is a new macrolide antibiotic for the treatment of bovine respiratory disease. The direct antimicrobial effects of the drug alone do not fully justify its superior clinical efficacy, and we hypothesize that tulathromycin may have immunomodulating properties. We recently reported that tulathromycin promotes ap

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Gautier, Emmanuel L., Stoyan Ivanov, Jesse W. Williams, et al. "Gata6 regulates aspartoacylase expression in resident peritoneal macrophages and controls their survival." Journal of Experimental Medicine 211, no. 8 (2014): 1525–31. http://dx.doi.org/10.1084/jem.20140570.

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The transcription factor Gata6 regulates proliferation and differentiation of epithelial and endocrine cells and cancers. Among hematopoietic cells, Gata6 is expressed selectively in resident peritoneal macrophages. We thus examined whether the loss of Gata6 in the macrophage compartment affected peritoneal macrophages, using Lyz2-Cre x Gata6flox/flox mice to tackle this issue. In Lyz2-Cre x Gata6flox/flox mice, the resident peritoneal macrophage compartment, but not macrophages in other organs, was contracted, with only a third the normal number of macrophages remaining. Heightened rates of d

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Dende, Chaitanya, Mihir Pendse, Daniel Propheter, Gabriella Quinn, and Lora V. Hooper. "Vitamin A regulates phagocytosis by resident macrophages of the small intestine." Journal of Immunology 208, no. 1_Supplement (2022): 113.23. http://dx.doi.org/10.4049/jimmunol.208.supp.113.23.

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Abstract Intestinal Tim4+ CD4+ macrophages are a distinctive macrophage subset that express Tim4, a receptor for phosphatidylserine on dying apoptotic cells, Unlike other macrophage subsets, they do not depend on blood monocytes for their turnover, instead self-maintained in the small intestine. The signal(s) responsible for the self-maintenance and function of Tim4+ CD4+ macrophages is not known. We have discovered that maintenance of the gut resident Tim4+ CD4+ macrophage population depends on dietary vitamin A and its derivative retinoic acid (RA). Retinoic acid receptors, which direct RA-d

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Knuth, Anne-Kathrin, Arnaud Huard, Zumer Naeem, et al. "Apoptotic Cells induce Proliferation of Peritoneal Macrophages." International Journal of Molecular Sciences 22, no. 5 (2021): 2230. http://dx.doi.org/10.3390/ijms22052230.

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The interaction of macrophages with apoptotic cells is required for efficient resolution of inflammation. While apoptotic cell removal prevents inflammation due to secondary necrosis, it also alters the macrophage phenotype to hinder further inflammatory reactions. The interaction between apoptotic cells and macrophages is often studied by chemical or biological induction of apoptosis, which may introduce artifacts by affecting the macrophages as well and/or triggering unrelated signaling pathways. Here, we set up a pure cell death system in which NIH 3T3 cells expressing dimerizable Caspase-8

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Misharin, Alexander V., Luisa Morales-Nebreda, Paul A. Reyfman, et al. "Monocyte-derived alveolar macrophages drive lung fibrosis and persist in the lung over the life span." Journal of Experimental Medicine 214, no. 8 (2017): 2387–404. http://dx.doi.org/10.1084/jem.20162152.

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Little is known about the relative importance of monocyte and tissue-resident macrophages in the development of lung fibrosis. We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis. Using transcriptomic profiling of flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously over the course of fibrosis and its resolution. During the fibrotic phase, monocyte-derived alveolar macrophages diff

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Peng, Yuan, Mengxian Zhou, Hong Yang, et al. "Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases." Mediators of Inflammation 2023 (June 8, 2023): 1–20. http://dx.doi.org/10.1155/2023/8821610.

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Macrophages are innate immune cells in the organism and can be found in almost tissues and organs. They are highly plastic and heterogeneous cells and can participate in the immune response, thereby playing a crucial role in maintaining the immune homeostasis of the body. It is well known that undifferentiated macrophages can polarize into classically activated macrophages (M1 macrophages) and alternatively activated macrophages (M2 macrophages) under different microenvironmental conditions. The directions of macrophage polarization can be regulated by a series of factors, including interferon

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Singh, Gyanesh, U. C. Pachouri, Chirag Chopra, Preeti Bajaj, and Pushplata Singh. "Macrophage Gene Therapy: opening novel therapeutic avenues for immune disorders." F1000Research 4 (August 6, 2015): 495. http://dx.doi.org/10.12688/f1000research.6817.1.

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Macrophages are probably the most important cells of the mammalian immune system, and compromised macrophage function is known to cause several diseases. Their involvement in arthritis, cancer, infections, atherosclerosis, diabetes, and autoimmune disorders is well known. There has been a constantly growing need to transfer therapeutic genes into macrophages. Like most non-macrophage gene therapies,in vitrogene transfer has been attempted much more frequently in case of macrophages. However, primary macrophages are still somewhat recalcitrant to transfection. Macrophage-specific synthetic prom

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Xie, Linglin, M. Teresa Ortega, Silvia Mora, and Stephen K. Chapes. "Interactive Changes between Macrophages and Adipocytes." Clinical and Vaccine Immunology 17, no. 4 (2010): 651–59. http://dx.doi.org/10.1128/cvi.00494-09.

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ABSTRACT Obesity is associated with a proinflammatory state, with macrophage infiltration into adipose tissue. We tested the hypothesis that communication between macrophages and adipocytes affects insulin resistance by disrupting insulin-stimulated glucose transport, adipocyte differentiation, and macrophage function. To test this hypothesis, we cocultured 3T3-L1 adipocytes with C2D macrophages or primary peritoneal mouse macrophages and examined the impacts of macrophages and adipocytes on each other. Adipocytes and preadipocytes did not affect C2D macrophage TNF- α, IL-6, or IL-1 β transcri

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Xu, Rong, Hong-Fan Sun, David W. Williams та ін. "IL-34 SuppressesCandida albicansInduced TNFαProduction in M1 Macrophages by Downregulating Expression of Dectin-1 and TLR2". Journal of Immunology Research 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/328146.

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Candida albicansis a fungus that is an opportunistic pathogen of humans. Normally,C. albicansexists as a harmless commensal and does not trigger inflammatory responses by resident macrophages in skin mucosa, which may be caused by a tolerance of skin macrophage toC. albicans. IL-34 is a recently discovered cytokine, constitutively expressed by keratinocytes in the skin. IL-34 binds to the receptor of M-CSF, thereby stimulating tissue macrophage maturation and differentiation. Resident macrophages exhibit phenotypic plasticity and may transform into inflammatory M1 macrophages for immunity or a

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Tian, Ying, Sheri E. Kelemen, and Michael V. Autieri. "Inhibition of AIF-1 expression by constitutive siRNA expression reduces macrophage migration, proliferation, and signal transduction initiated by atherogenic stimuli." American Journal of Physiology-Cell Physiology 290, no. 4 (2006): C1083—C1091. http://dx.doi.org/10.1152/ajpcell.00381.2005.

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Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic, calcium-binding, inflammation-responsive scaffold protein. Several studies have reported increased AIF-1 expression in activated macrophages and have implicated AIF-1 as a marker of activated macrophages. However, the function of AIF-1 in macrophages and the mechanism whereby it participates in macrophage activation are unknown at this time. Immunohistochemical analysis colocalized AIF-1 expression with CD68-positive macrophages in atherosclerotic human coronary arteries. Subsequent experiments were designed to determine a role for AIF-

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GREGORY, D. J., and M. OLIVIER. "Subversion of host cell signalling by the protozoan parasiteLeishmania." Parasitology 130, S1 (2005): S27—S35. http://dx.doi.org/10.1017/s0031182005008139.

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The protozoaLeishmaniaspp. are obligate intracellular parasites that inhabit the macrophages of their host. Since macrophages are specialized for the identification and destruction of invading pathogens, both directly and by triggering an innate immune response,Leishmaniahave evolved a number of mechanisms for suppressing some critical macrophage activities. In this review, we discuss how various species ofLeishmaniadistort the host macrophage's own signalling pathways to repress the expression of various cytokines and microbicidal molecules (nitric oxide and reactive oxygen species), and anti

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Hamrick, Terri S., Edward A. Havell, John R. Horton, and Paul E. Orndorff. "Host and Bacterial Factors Involved in the Innate Ability of Mouse Macrophages To Eliminate Internalized UnopsonizedEscherichia coli." Infection and Immunity 68, no. 1 (2000): 125–32. http://dx.doi.org/10.1128/iai.68.1.125-132.2000.

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ABSTRACT In an effort to better understand genetic and cellular factors that influence innate immunity, we examined host and bacterial factors involved in the nonopsonic phagocytosis and killing ofEscherichia coli K-12 by mouse macrophages. Unelicited (resident) peritoneal macrophages from five different mouse strains, BALB/c, C57BL/6, CD-1, C3H/HeJ, and C3H/HeN, were employed. Additional macrophage populations were obtained from CD-1 mice (bone marrow-derived macrophages). Also, for BALB/c and C57BL/6 mice, peritoneal macrophages elicited with either thioglycolate or proteose peptone, bone ma

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Bauerle, Kevin Thomas, Jisu Oh, Amy Elizabeth Riek, et al. "Vitamin D Deficiency Induces Macrophage Pro-Inflammatory Phenotype via ER Stress-Mediated Activation of Renin-Angiotensin System." Journal of the Endocrine Society 5, Supplement_1 (2021): A304—A305. http://dx.doi.org/10.1210/jendso/bvab048.620.

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Abstract Chronic inflammation and local activation of the renin-angiotensin-aldosterone system (RAAS) play a pivotal role in the pathogenesis and progression of diabetic complications. In patients with type 2 diabetes (T2DM), the prevalence of vitamin D deficiency is almost twice that of non-diabetics, and vitamin d deficiency nearly doubles the risk of developing hypertension and cardiovascular complications compared to diabetics with normal vitamin D levels. Interestingly, mice lacking the vitamin D receptor (VDR) in macrophages (KODMAC) develop renin-dependent hypertension, insulin resistan

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Aziz, Athar, Laurent Vanhille, Peer Mohideen, et al. "Development of Macrophages with Altered Actin Organization in the Absence of MafB." Molecular and Cellular Biology 26, no. 18 (2006): 6808–18. http://dx.doi.org/10.1128/mcb.00245-06.

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ABSTRACT In the hematopoietic system the bZip transcription factor MafB is selectively expressed at high levels in monocytes and macrophages and promotes macrophage differentiation in myeloid progenitors, whereas a dominant-negative allele can inhibit this process. To analyze the requirement of MafB for macrophage development, we generated MafB-deficient mice and, due to their neonatal lethal phenotype, analyzed macrophage differentiation in vitro, in the embryo, and in reconstituted mice. Surprisingly we observed in vitro differentiation of macrophages from E14.5 fetal liver (FL) cells and E1

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Hashimoto, Shin-ichi, Takuji Suzuki, Hong-Yan Dong, Nobuyuki Yamazaki, and Kouji Matsushima. "Serial Analysis of Gene Expression in Human Monocytes and Macrophages." Blood 94, no. 3 (1999): 837–44. http://dx.doi.org/10.1182/blood.v94.3.837.413k02_837_844.

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Monocytes/macrophages serve as sentinels involved in chronic inflammation and the eradication of various pathogens. To define molecularly the differentiation of blood monocytes into macrophages, we conducted serial analysis of gene expression (SAGE) in human blood monocytes/macrophages induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) or M-CSF. SAGE analysis of 57,560, 57,463, and 55,856 tags from monocytes, GM-CSF–, and M-CSF–induced macrophages, respectively, allowed identification of 35,037 different transcripts. Interestingly, the genes with the highest expression during

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Luo, Qianting, Xingyang Li, Wenchao Zhong, et al. "Dicalcium silicate-induced mitochondrial dysfunction and autophagy-mediated macrophagic inflammation promotes osteogenic differentiation of BMSCs." Regenerative Biomaterials, December 13, 2021. http://dx.doi.org/10.1093/rb/rbab075.

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Abstract Dicalcium silicate (Ca2SiO4, C2S) has osteogenic potential but induces macrophagic inflammation. Mitochondrial function plays a vital role in macrophage polarization and macrophagic inflammation. The mitochondrial function of C2S-treated macrophages is still unclear. This study hypothesized: (1) the C2S modulates mitochondrial function and autophagy in macrophages to regulate macrophagic inflammation, and (2) C2S-induced macrophagic inflammation regulates osteogenesis. We used RAW264.7 cells as a model of macrophage. The C2S (75-150 μg/mL) extract was used to analyze the macrophagic m

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Bo, Haotian, Ulrich Aymard Ekomi Moure, Yuanmiao Yang, et al. "Mycobacterium tuberculosis-macrophage interaction: Molecular updates." Frontiers in Cellular and Infection Microbiology 13 (March 3, 2023). http://dx.doi.org/10.3389/fcimb.2023.1062963.

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Mycobacterium tuberculosis (Mtb), the causative agent of Tuberculosis (TB), remains a pathogen of great interest on a global scale. This airborne pathogen affects the lungs, where it interacts with macrophages. Acidic pH, oxidative and nitrosative stressors, and food restrictions make the macrophage’s internal milieu unfriendly to foreign bodies. Mtb subverts the host immune system and causes infection due to its genetic arsenal and secreted effector proteins. In vivo and in vitro research have examined Mtb-host macrophage interaction. This interaction is a crucial stage in Mtb infection becau

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Yi, D. ‐Y, Q. ‐Y Xu, Y. He, X. ‐Q Zheng, T. ‐C Yang, and Y. Lin. "Treponema pallidum protein Tp47 induced prostaglandin E2 to inhibit the phagocytosis in human macrophages." Journal of the European Academy of Dermatology and Venereology, January 23, 2024. http://dx.doi.org/10.1111/jdv.19809.

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AbstractBackgroundDuring Treponema pallidum (T. pallidum) infection, the host's immune system actively engages in pursuit and elimination of T. pallidum, while T. pallidum skillfully employs various mechanisms to evade immune recognition. Macrophages exhibit incomplete clearance of T. pallidum in vitro and the underlying mechanism of how T. pallidum resists the attack of macrophage remains unclear.ObjectivesTo investigate the effect of T. pallidum membrane protein Tp47 on the phagocytosis of macrophages.MethodsTHP‐1‐derived macrophages were used to investigate the role of Tp47 in the secretion

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Luque-Campos, Noymar, Felipe A. Bustamante-Barrientos, Carolina Pradenas, et al. "The Macrophage Response Is Driven by Mesenchymal Stem Cell-Mediated Metabolic Reprogramming." Frontiers in Immunology 12 (June 4, 2021). http://dx.doi.org/10.3389/fimmu.2021.624746.

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Mesenchymal stem cells (MSCs) are multipotent adult stromal cells widely studied for their regenerative and immunomodulatory properties. They are capable of modulating macrophage plasticity depending on various microenvironmental signals. Current studies have shown that metabolic changes can also affect macrophage fate and function. Indeed, changes in the environment prompt phenotype change. Therefore, in this review, we will discuss how MSCs orchestrate macrophage’s metabolic plasticity and the impact on their function. An improved understanding of the crosstalk between macrophages and MSCs w

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Muhammad, Sajjad, Shafqat Rasul Chaudhry, Gergana Dobreva, Michael T. Lawton, Mika Niemelä, and Daniel Hänggi. "Vascular Macrophages as Therapeutic Targets to Treat Intracranial Aneurysms." Frontiers in Immunology 12 (March 8, 2021). http://dx.doi.org/10.3389/fimmu.2021.630381.

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Aneurysmal subarachnoid hemorrhage (aSAH) is a highly fatal and morbid type of hemorrhagic strokes. Intracranial aneurysms (ICAs) rupture cause subarachnoid hemorrhage. ICAs formation, growth and rupture involves cellular and molecular inflammation. Macrophages orchestrate inflammation in the wall of ICAs. Macrophages generally polarize either into classical inflammatory (M1) or alternatively-activated anti-inflammatory (M2)-phenotype. Macrophage infiltration and polarization toward M1-phenotype increases the risk of aneurysm rupture. Strategies that deplete, inhibit infiltration, ameliorate m

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Xiao, Qiuqun, Jinyan Huang, Xing Wang, et al. "Supramolecular Peptide Amphiphile Nanospheres Reprogram Tumor‐associated Macrophage to Reshape the Immune Microenvironment for Enhanced Breast Cancer Immunotherapy." Small, December 15, 2023. http://dx.doi.org/10.1002/smll.202307390.

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AbstractTumor immunotherapy has become a research hotspot in cancer treatment, with macrophages playing a crucial role in tumor development. However, the tumor microenvironment restricts macrophage functionality, limiting their therapeutic potential. Therefore, modulating macrophage function and polarization is essential for enhancing tumor immunotherapy outcomes. Here, a supramolecular peptide amphiphile drug‐delivery system (SPADS) is utilized to reprogram macrophages and reshape the tumor immune microenvironment (TIM) for immune‐based therapies. The approach involved designing highly specif

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van Stijn, Caroline M., Jason Kim, and Rajendra K. Tangirala. "Abstract 549: Adiponectin Modulation of Macrophage Inflammatory and Metabolic Properties is Regulated by Macrophage Polarization Status and Adiponectin Receptor Expression." Arteriosclerosis, Thrombosis, and Vascular Biology 33, suppl_1 (2013). http://dx.doi.org/10.1161/atvb.33.suppl_1.a549.

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Adiponectin, an adipose-derived adipokine, exerts metabolic, anti-inflammatory and anti-atherogenic effects to ameliorate metabolic syndrome, diabetes and cardiovascular disease. Monocytes/macrophages play a crucial pathogenic role in these inflammatory and metabolic disorders. We identified that macrophage polarization profoundly alters their adiponectin receptor expression and functional responses to adiponectin. We addressed the hypothesis that macrophage activation status which affects adiponectin receptor expression leads to differential adiponectin-mediated inflammatory and metabolic res

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Heaster, Tiffany M., Alexa R. Heaton, Paul M. Sondel, and Melissa C. Skala. "Intravital Metabolic Autofluorescence Imaging Captures Macrophage Heterogeneity Across Normal and Cancerous Tissue." Frontiers in Bioengineering and Biotechnology 9 (April 20, 2021). http://dx.doi.org/10.3389/fbioe.2021.644648.

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Macrophages are dynamic immune cells that govern both normal tissue function and disease progression. However, standard methods to measure heterogeneity in macrophage function within tissues require tissue excision and fixation, which limits our understanding of diverse macrophage function in vivo. Two-photon microscopy of the endogenous metabolic co-enzymes NAD(P)H and flavin adenine dinucleotide (FAD) (metabolic autofluorescence imaging) enables dynamic imaging of mouse models in vivo. Here, we demonstrate metabolic autofluorescence imaging to assess cell-level macrophage heterogeneity in re

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Zhao, Zhenzhen, Yuelong Qin, Rui Wu, Wenwu Li, and Yujiang Dong. "Single-cell analysis identified key macrophage subpopulations associated with atherosclerosis." Open Medicine 19, no. 1 (2024). https://doi.org/10.1515/med-2024-1088.

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Abstract Background Atherosclerosis is a lipid-driven inflammatory disease characterized by plaque formation in major arteries. These plaques contain lipid-rich macrophages that accumulate through monocyte recruitment, local macrophage differentiation, and proliferation. Objective We identify the macrophage subsets that are closely related to atherosclerosis and reveal the key pathways in the progression of atherosclerotic disease. Materials and methods In this study, we characterize the single-cell landscape of atherosclerosis, identifying macrophage subsets closely related to the disease and

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Zhang, Minni, Kun Liu, Qiuyue Zhang, et al. "Alpha fetoprotein promotes polarization of macrophages towards M2-like phenotype and inhibits macrophages to phagocytize hepatoma cells." Frontiers in Immunology 14 (February 23, 2023). http://dx.doi.org/10.3389/fimmu.2023.1081572.

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Alpha-fetoprotein(AFP) is a cancer biomarker for the diagnosis of hepatocellular carcinoma(HCC); however, its role in macrophage polarization and phagocytosis remains unclear. In the present study, we explored the correlation between AFP regulation of macrophage function and the possible regulatory mechanisms. Human mononuclear leukemia cells (THP-1) and monocytes from healthy donors were used to analyze the effect of AFP on the macrophages’ phenotype and phagocytosis. THP-1 cells and healthy human donor-derived monocytes were polarized into M0 macrophages induced by phorbol ester (PMA), and M

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