Macrophage Response

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Dmitry M Shayakhmetov - One of the best experts on this subject based on the ideXlab platform.

  • virus binding to a plasma membrane receptor triggers interleukin 1α mediated proinflammatory Macrophage Response in vivo
    Immunity, 2009
    Co-Authors: Nelson C Di Paolo, Kaja Muralikrishna, Alan Aderem, Edward A Miao, Richard A Flavell, Thalia Papayannopoulou, Yoichiro Iwakura, Dmitry M Shayakhmetov
    Abstract:

    Summary The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune Response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that Macrophages in vivo activated an innate immune Response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In Response to Ad, Macrophage-derived IL-1α triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1α-mediated Response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with Macrophage β 3 integrins. Thus, these data identify IL-1α-IL-1RI as a key pathway allowing for the activation of proinflammatory Responses to the virus, independently of its genomic nucleic acid recognition.

  • virus binding to a plasma membrane receptor triggers interleukin 1α mediated proinflammatory Macrophage Response in vivo
    Immunity, 2009
    Co-Authors: Nelson C Di Paolo, Kaja Muralikrishna, Alan Aderem, Edward A Miao, Richard A Flavell, Thalia Papayannopoulou, Yoichiro Iwakura, Dmitry M Shayakhmetov
    Abstract:

    The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune Response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that Macrophages in vivo activated an innate immune Response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In Response to Ad, Macrophage-derived IL-1 alpha triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1 alpha-mediated Response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with Macrophage beta(3) integrins. Thus, these data identify IL-1 alpha-IL-1RI as a key pathway allowing for the activation of proinflammatory Responses to the virus, independently of its genomic nucleic acid recognition.

Paul Chuchana - One of the best experts on this subject based on the ideXlab platform.

  • The transcriptomic analytical level determines the human monocyte-derived Macrophage Response toward either the infectious agent or the host.
    Infection Genetics and Evolution, 2016
    Co-Authors: Philippe Holzmuller, Frédéric Vezilier, Philippe Nirdé, Paul Chuchana
    Abstract:

    Macrophages exhibit multifunctional activity and play a central role in the Response to infectious agents. It is commonly accepted that the plasticity of the Response of Macrophages depends on the type of stimuli. Here we re-evaluate whether the Macrophage Response is only dependent on the stimulus. We analyzed the transcriptomic profile of monocyte-derived Macrophages (MDMs) that were activated with several pathogens and multiple in vitro-stimulations. The transcriptomic data were normalized using matched-pair analysis. Further analysis showed a clustering association with (i) specific signatures of the infectious agent and its strategy as well as (ii) a preponderance of MDM overall Responses related to individuals. Currently, the null hypothesis H0 is that the innate MDM Response is globally associated with the pathogen. Our results reveal that the global innate MDM Response is intrinsically and predominantly associated with the individual. Thus, the hypothesis is supported or negated depending on the transcriptomic analytical level. Author summary In modern medicine, diagnosis is based on objective criteria. Scientists are focused on the common denominators indicative of an infection. Analytical studies are based on this oriented approach, which defines the null hypothesis H0: the host immune Response depends on the stimulus. We observe that the Macrophage Response to a given pathogen represents

  • The transcriptomic analytical level determines the human monocyte-derived Macrophage Response toward either the infectious agent or the host
    Infection Genetics and Evolution, 2016
    Co-Authors: Philippe Holzmuller, Frédéric Vezilier, Philippe Nirdé, Paul Chuchana
    Abstract:

    Macrophages exhibit multifunctional activity and play a central role in the Response to infectious agents. It is commonly accepted that the plasticity of the Response of Macrophages depends on the type of stimuli. Here we re-evaluate whether the Macrophage Response is only dependent on the stimulus. We analyzed the transcriptomic profile of monocyte-derived Macrophages (MDMs) that were activated with several pathogens and multiple in vitrostimulations. The transcriptomic data were normalized using matched-pair analysis. Further analysis showed a clustering association with (i) specific signatures of the infectious agent and its strategy as well as (ii) a preponderance of MDM overall Responses related to individuals. Currently, the null hypothesis H0 is that the innate MDM Response is globally associated with the pathogen. Our results reveal that the global innate MDM Response is intrinsically and predominantly associated with the individual. Thus, the hypothesis is supported or negated depending on the transcriptomic analytical level.

Nelson C Di Paolo - One of the best experts on this subject based on the ideXlab platform.

  • virus binding to a plasma membrane receptor triggers interleukin 1α mediated proinflammatory Macrophage Response in vivo
    Immunity, 2009
    Co-Authors: Nelson C Di Paolo, Kaja Muralikrishna, Alan Aderem, Edward A Miao, Richard A Flavell, Thalia Papayannopoulou, Yoichiro Iwakura, Dmitry M Shayakhmetov
    Abstract:

    Summary The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune Response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that Macrophages in vivo activated an innate immune Response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In Response to Ad, Macrophage-derived IL-1α triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1α-mediated Response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with Macrophage β 3 integrins. Thus, these data identify IL-1α-IL-1RI as a key pathway allowing for the activation of proinflammatory Responses to the virus, independently of its genomic nucleic acid recognition.

  • virus binding to a plasma membrane receptor triggers interleukin 1α mediated proinflammatory Macrophage Response in vivo
    Immunity, 2009
    Co-Authors: Nelson C Di Paolo, Kaja Muralikrishna, Alan Aderem, Edward A Miao, Richard A Flavell, Thalia Papayannopoulou, Yoichiro Iwakura, Dmitry M Shayakhmetov
    Abstract:

    The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune Response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that Macrophages in vivo activated an innate immune Response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In Response to Ad, Macrophage-derived IL-1 alpha triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1 alpha-mediated Response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with Macrophage beta(3) integrins. Thus, these data identify IL-1 alpha-IL-1RI as a key pathway allowing for the activation of proinflammatory Responses to the virus, independently of its genomic nucleic acid recognition.

Ludovic Tailleux - One of the best experts on this subject based on the ideXlab platform.

  • Tri-mannose grafting of chitosan nanocarriers remodels the Macrophage Response to bacterial infection
    Journal of Nanobiotechnology, 2019
    Co-Authors: Juan Manuel Coya, Laura De Matteis, Alexandre Giraud-gatineau, Anne Biton, Inés Serrano-sevilla, Anne Danckaert, Marie-agnès Dillies, Brigitte Gicquel, Jesus De La Fuente, Ludovic Tailleux
    Abstract:

    Background: Infectious diseases are still a leading cause of death and, with the emergence of drug resistance, pose a great threat to human health. New drugs and strategies are thus urgently needed to improve treatment efficacy and limit drug-associated side effects. Nanotechnology-based drug delivery systems are promising approaches, offering hope in the fight against drug resistant bacteria. However, how nanocarriers influence the Response of innate immune cells to bacterial infection is mostly unknown. Results: Here, we used Mycobacterium tuberculosis as a model of bacterial infection to examine the impact of man-nose functionalization of chitosan nanocarriers (CS-NCs) on the human Macrophage Response. Both ungrafted and grafted CS-NCs were similarly internalized by Macrophages, via an actin cytoskeleton-dependent process. Although tri-mannose ligands did not modify the capacity of CS-NCs to escape lysosomal degradation, they profoundly remod-eled the Response of M. tuberculosis-infected Macrophages. mRNA sequencing showed nearly 900 genes to be differentially expressed due to tri-mannose grafting. Unexpectedly, the set of modulated genes was enriched for pathways involved in cell metabolism, particularly oxidative phosphorylation and sugar metabolism. Conclusions: The ability to modulate cell metabolism by grafting ligands at the surface of nanoparticles may thus be a promising strategy to reprogram immune cells and improve the efficacy of encapsulated drugs.

  • Tri-mannose grafting of chitosan nanocarriers remodels the Macrophage Response to bacterial infection.
    Journal of nanobiotechnology, 2019
    Co-Authors: Juan Manuel Coya, Laura De Matteis, Alexandre Giraud-gatineau, Anne Biton, Inés Serrano-sevilla, Anne Danckaert, Marie-agnès Dillies, Brigitte Gicquel, Jesús M. De La Fuente, Ludovic Tailleux
    Abstract:

    Infectious diseases are still a leading cause of death and, with the emergence of drug resistance, pose a great threat to human health. New drugs and strategies are thus urgently needed to improve treatment efficacy and limit drug-associated side effects. Nanotechnology-based drug delivery systems are promising approaches, offering hope in the fight against drug resistant bacteria. However, how nanocarriers influence the Response of innate immune cells to bacterial infection is mostly unknown. Here, we used Mycobacterium tuberculosis as a model of bacterial infection to examine the impact of mannose functionalization of chitosan nanocarriers (CS-NCs) on the human Macrophage Response. Both ungrafted and grafted CS-NCs were similarly internalized by Macrophages, via an actin cytoskeleton-dependent process. Although tri-mannose ligands did not modify the capacity of CS-NCs to escape lysosomal degradation, they profoundly remodeled the Response of M. tuberculosis-infected Macrophages. mRNA sequencing showed nearly 900 genes to be differentially expressed due to tri-mannose grafting. Unexpectedly, the set of modulated genes was enriched for pathways involved in cell metabolism, particularly oxidative phosphorylation and sugar metabolism. The ability to modulate cell metabolism by grafting ligands at the surface of nanoparticles may thus be a promising strategy to reprogram immune cells and improve the efficacy of encapsulated drugs.

  • MOESM6 of Tri-mannose grafting of chitosan nanocarriers remodels the Macrophage Response to bacterial infection
    2019
    Co-Authors: Juan Manuel Coya, Laura De Matteis, Alexandre Giraud-gatineau, Anne Biton, Inés Serrano-sevilla, Anne Danckaert, Marie-agnès Dillies, Brigitte Gicquel, Jesus De La Fuente, Ludovic Tailleux
    Abstract:

    Additional file 6: Fig. S3. Cellular uptake of tri-mannose-grafted chitosan NCs. a 100 µg/ml of Nile-Red-labelled CS-NCs-tri were incubated for 4 h with M $$\upphi$$ ϕ s, A549 epithelial cells, or HepG2 hepatocytes. NP uptake was analyzed by FACS as mentioned above. b M $$\upphi$$ ϕ s were incubated with 100 µg/ml fluorescent NCs for 2 h with or without nystatin, colchicine, cytochalasin D, or chlorpromazine. NC uptake was analyzed by FACS

  • Purinergic Signaling: A Common Path in the Macrophage Response against Mycobacterium tuberculosis and Toxoplasma gondii.
    Frontiers in Cellular and Infection Microbiology, 2017
    Co-Authors: Laetitia Petit-jentreau, Ludovic Tailleux, Janine L Coombes
    Abstract:

    Immune Responses are essential for the protection of the host against external dangers or infections and are normally efficient in the clearance of invading microbes. However, some intracellular pathogens have developed strategies to replicate and survive within host cells resulting in latent infection associated with strong inflammation. This excessive Response can cause cell and tissue damage and lead to the release of the intracellular content, in particular the nucleotide pool, into the extracellular space. Over the last decade, new studies have implicated metabolites from the purinergic pathway in shaping the host immune Response against intracellular pathogens and proved their importance in the outcome of the infection. This review aims to summarize how the immune system employs the purinergic system either to fight the pathogen, or to control collateral tissue damage. This will be achieved by focusing on the Macrophage Response against two intracellular pathogens, the human etiologic agent of tuberculosis, Mycobacterium tuberculosis and the protozoan parasite, Toxoplasma gondii.

Philippe Holzmuller - One of the best experts on this subject based on the ideXlab platform.

  • The transcriptomic analytical level determines the human monocyte-derived Macrophage Response toward either the infectious agent or the host.
    Infection Genetics and Evolution, 2016
    Co-Authors: Philippe Holzmuller, Frédéric Vezilier, Philippe Nirdé, Paul Chuchana
    Abstract:

    Macrophages exhibit multifunctional activity and play a central role in the Response to infectious agents. It is commonly accepted that the plasticity of the Response of Macrophages depends on the type of stimuli. Here we re-evaluate whether the Macrophage Response is only dependent on the stimulus. We analyzed the transcriptomic profile of monocyte-derived Macrophages (MDMs) that were activated with several pathogens and multiple in vitro-stimulations. The transcriptomic data were normalized using matched-pair analysis. Further analysis showed a clustering association with (i) specific signatures of the infectious agent and its strategy as well as (ii) a preponderance of MDM overall Responses related to individuals. Currently, the null hypothesis H0 is that the innate MDM Response is globally associated with the pathogen. Our results reveal that the global innate MDM Response is intrinsically and predominantly associated with the individual. Thus, the hypothesis is supported or negated depending on the transcriptomic analytical level. Author summary In modern medicine, diagnosis is based on objective criteria. Scientists are focused on the common denominators indicative of an infection. Analytical studies are based on this oriented approach, which defines the null hypothesis H0: the host immune Response depends on the stimulus. We observe that the Macrophage Response to a given pathogen represents

  • The transcriptomic analytical level determines the human monocyte-derived Macrophage Response toward either the infectious agent or the host
    Infection Genetics and Evolution, 2016
    Co-Authors: Philippe Holzmuller, Frédéric Vezilier, Philippe Nirdé, Paul Chuchana
    Abstract:

    Macrophages exhibit multifunctional activity and play a central role in the Response to infectious agents. It is commonly accepted that the plasticity of the Response of Macrophages depends on the type of stimuli. Here we re-evaluate whether the Macrophage Response is only dependent on the stimulus. We analyzed the transcriptomic profile of monocyte-derived Macrophages (MDMs) that were activated with several pathogens and multiple in vitrostimulations. The transcriptomic data were normalized using matched-pair analysis. Further analysis showed a clustering association with (i) specific signatures of the infectious agent and its strategy as well as (ii) a preponderance of MDM overall Responses related to individuals. Currently, the null hypothesis H0 is that the innate MDM Response is globally associated with the pathogen. Our results reveal that the global innate MDM Response is intrinsically and predominantly associated with the individual. Thus, the hypothesis is supported or negated depending on the transcriptomic analytical level.