Macrophage

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F L Wormley - One of the best experts on this subject based on the ideXlab platform.

  • Classical versus alternative Macrophage activation: the Ying and the Yang in host defense against pulmonary fungal infections
    Mucosal Immunology, 2014
    Co-Authors: C M Leopold Wager, F L Wormley
    Abstract:

    Macrophages are innate immune cells that possess unique abilities to polarize toward different phenotypes. Classically activated Macrophages are known to have major roles in host defense against various microbial pathogens, including fungi, while alternatively activated Macrophages are instrumental in immune-regulation and wound healing. Macrophages in the lungs are often the first responders to pulmonary fungal pathogens, and the Macrophage polarization state has the potential to be a deciding factor in disease progression or resolution. This review discusses the distinct Macrophage polarization states and their roles during pulmonary fungal infection. We focus primarily on Cryptococcus neoformans and Pneumocystis model systems as disease resolution of these two opportunistic fungal pathogens is linked to classically or alternatively activated Macrophages, respectively. Further research considering Macrophage polarization states that result in anti-fungal activity has the potential to provide a novel approach for the treatment of fungal infections.

Hiromasa Nikai - One of the best experts on this subject based on the ideXlab platform.

  • distribution of Macrophage lineage cells in rat gingival tissue after topical application of lipopolysaccharide an immunohistochemical study using monoclonal antibodies ox6 ed1 and ed2
    Journal of Periodontal Research, 1998
    Co-Authors: Mutsumi Miyauchi, Ikuko Ogawa, Yasusel Kudo, Toshitsugu Takekoshi, Takashi Takata, Hiromasa Nikai
    Abstract:

    To discuss the role of Macrophage lineage cells on the periodontal tissue destruction, we immunohistochemically examined the phenotype and the dynamics of Macrophage lineage cells 1 or 3 h or 1, 2, 3 or 7 d after topical application of LPS (5 mg/ml in physiological saline) from the rat gingival sulcus using 3 monoclonal antibodies: OX6 (antigen-presenting cells), ED1 (monocytes, Macrophages and dendritic cells) and ED2 (resident Macrophages). We could detect at least 3 different types of Macrophage lineage cells, namely OX6+/ED1+/ED2− dendritic cells and exudate Macrophages and ED2+ resident Macrophages. After LPS application the majority of Macrophage lineage cells accumulated in the subjunctional epithelial area were newly extravasated OX6+/ED1+/ED2− dendritic cells or Macrophages. The number Department of Oral Pathology, Hiroshima of these cells increased progressively with time and reached a maximum level at University School of Dentistry, d 2. On the other hand, number and tissue distribution of ED2+ resident Macrophages did not change. These results indicate that several types of Macrophage lineage cells exist in rat gingival tissue and suggest that dendritic cells and exudate Macrophages transiently accumulated after LPS application are responsible for various host immune response and tissue destruction caused by LPS.

Hakim M. Lukman - One of the best experts on this subject based on the ideXlab platform.

  • Annexin-A1 enhances breast cancer growth and migration by promoting alternative Macrophage polarization in the tumour microenvironment
    Scientific Reports, 2017
    Co-Authors: Leonardo A. Moraes, Sok Lin Foo, Shreya Kar, Yi Qian Toh, Patrick B. Ampomah, Gracemary Yap, Olga Zharkova, Karishma Sachaphibulkij, Tong Gu, Hakim M. Lukman
    Abstract:

    Macrophages are potent immune cells with well-established roles in the response to stress, injury, infection and inflammation. The classically activated Macrophages (M1) are induced by lipopolysaccharide (LPS) and express a wide range of pro-inflammatory genes. M2 Macrophages are induced by T helper type 2 cytokines such as interleukin-4 (IL4) and express high levels of anti-inflammatory and tissue repair genes. The strong association between Macrophages and tumour cells as well as the high incidences of leukocyte infiltration in solid tumours have contributed to the discovery that tumour-associated Macrophages (TAMs) are key to tumour progression. Here, we investigated the role of Annexin A1 (ANXA1), a well characterized immunomodulatory protein on Macrophage polarization and the interaction between Macrophages and breast cancer cells. Our results demonstrate that ANXA1 regulates Macrophage polarization and activation. ANXA1 can act dually as an endogenous signalling molecule or as a secreted mediator which acts via its receptor, FPR2, to promote Macrophage polarization. Furthermore, ANXA1 deficient mice exhibit reduced tumour growth and enhanced survival in vivo, possibly due to increased M1 Macrophages within the tumor microenvironment. These results provide new insights into the molecular mechanisms of Macrophage polarization with therapeutic potential to suppress breast cancer growth and metastasis.

Siamon Gordon - One of the best experts on this subject based on the ideXlab platform.

  • Macrophage activation and polarization nomenclature and experimental guidelines
    Immunity, 2014
    Co-Authors: Peter J Murray, Subhra K. Biswas, Siamon Gordon, Judith E Allen, Edward A Fisher, Derek W Gilroy, Sergij Goerdt, John A Hamilton, Lionel B Ivashkiv, Toby Lawrence
    Abstract:

    Description of Macrophage activation is currently contentious and confusing. Like the biblical Tower of Babel, Macrophage activation encompasses a panoply of descriptors used in different ways. The lack of consensus on how to define Macrophage activation in experiments in vitro and in vivo impedes progress in multiple ways, including the fact that many researchers still consider there to be only two types of activated Macrophages, often termed M1 and M2. Here, we describe a set of standards encompassing three principles—the source of Macrophages, definition of the activators, and a consensus collection of markers to describe Macrophage activation—with the goal of unifying experimental standards for diverse experimental scenarios. Collectively, we propose a common framework for Macrophage-activation nomenclature.

  • Macrophage fusion induced by il 4 alternative activation is a multistage process involving multiple target molecules
    European Journal of Immunology, 2007
    Co-Authors: Laura Helming, Siamon Gordon
    Abstract:

    Multinucleated giant cells, characteristic of granulomatous infections, originate from fusion of Macrophages, however, little is known about the underlying mechanism. Alternative activation of Macrophages by exposure to IL-4 and IL-13 induces Macrophage homokaryon formation. We have established a new quantitative bifluorescent system to study IL-4-induced fusion of primary murine Macrophages in vitro. Using this assay, we could show that Macrophage fusion is not mediated by a single molecule, but involves multiple functional components. Although several murine Macrophage populations were not competent to form giant cells, indicating that they fail to display the full fusion machinery, these non-fusogenic Macrophages could fuse with fusion-competent Macrophages in a heterophilic manner. Since IL-4 induced molecules were needed on both fusion partners, we conclude that at least two functionally distinct molecules mediate Macrophage homokaryon formation with each present on one fusion partner. In addition, though IL-4 treatment led to induction of a fusogenic status, Macrophages could only fuse efficiently when adherent to a permissive substratum. Based on our findings, we conclude that Macrophage fusion is a multistage process involving multiple target molecules. The model we describe will allow analysis of the molecular basis of membrane fusion and possible insight into alternative activation of Macrophages. See accompanying commentary: http://dx.doi.org/10.1002/eji.200636910

Anthony W Ferrante - One of the best experts on this subject based on the ideXlab platform.

  • Macrophage specific pparγ controls alternative activation and improves insulin resistance
    Nature, 2007
    Co-Authors: Justin I Odegaard, Roberto R Ricardogonzalez, Matthew H Goforth, Christine R Morel, Vidya Subramanian, Lata Mukundan, Alex Red Eagle, Divya Vats, Frank Brombacher, Anthony W Ferrante
    Abstract:

    Obesity and insulin resistance, the cardinal features of metabolic syndrome, are closely associated with a state of low-grade inflammation1,2. In adipose tissue chronic overnutrition leads to Macrophage infiltration, resulting in local inflammation that potentiates insulin resistance3,4. For instance, transgenic expression of Mcp1 (also known as chemokine ligand 2, Ccl2) in adipose tissue increases Macrophage infiltration, inflammation and insulin resistance5,6. Conversely, disruption of Mcp1 or its receptor Ccr2 impairs migration of Macrophages into adipose tissue, thereby lowering adipose tissue inflammation and improving insulin sensitivity5,7. These findings together suggest a correlation between Macrophage content in adipose tissue and insulin resistance. However, resident Macrophages in tissues display tremendous heterogeneity in their activities and functions, primarily reflecting their local metabolic and immune microenvironment8. While Mcp1 directs recruitment of pro-inflammatory classically activated Macrophages to sites of tissue damage5,8, resident Macrophages, such as those present in the adipose tissue of lean mice, display the alternatively activated phenotype9. Despite their higher capacity to repair tissue10, the precise role of alternatively activated Macrophages in obesity-induced insulin resistance remains unknown. Using mice with Macrophage-specific deletion of the peroxisome proliferator activated receptor-γ (PPARγ), we show here that PPARγ is required for maturation of alternatively activated Macrophages. Disruption of PPARγ in myeloid cells impairs alternative Macrophage activation, and predisposes these animals to development of diet-induced obesity, insulin resistance, and glucose intolerance. Furthermore, gene expression profiling revealed that downregulation of oxidative phosphorylation gene expression in skeletal muscle and liver leads to decreased insulin sensitivity in these tissues. Together, our findings suggest that resident alternatively activated Macrophages have a beneficial role in regulating nutrient homeostasis and suggest that Macrophage polarization towards the alternative state might be a useful strategy for treating type 2 diabetes.