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  1. Article ; Online: Effects of the nerve growth factor and its carrier protein on the inflammatory response from human monocytes.

    Verres, Yann / Bodin, Aude / Chevret, Sarah / Victoni, Tatiana / Gicquel, Thomas / Barreto, Emiliano / Freund-Michel, Véronique / Lagente, Vincent

    Fundamental & clinical pharmacology

    2024  

    Abstract: Background: The nerve growth factor (NGF) has been previously shown to be involved in cellular proliferation, differentiation, survival, or wound healing. This factor displays a variety of biological effects that yet remain to be explored. Previous data ...

    Abstract Background: The nerve growth factor (NGF) has been previously shown to be involved in cellular proliferation, differentiation, survival, or wound healing. This factor displays a variety of biological effects that yet remain to be explored. Previous data on cell lines show a pro-inflammatory role of NGF on monocytes.
    Objectives: The objective of the study was to investigate the pro-inflammatory effect of NGF, using a model of fresh human monocytes.
    Methods: Monocytes obtained from PBMC were exposed to NGF at various concentrations. Alternatively, monocytes were exposed to BSA, the NGF carrier protein without the NGF. Gene expression and cytokine release in the supernatant were monitored.
    Results: We found that NGF increased the expression of pro-inflammatory, chemotactic, and remodeling genes such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and C-X-C motif ligand (CXCL)8. The protein levels of CXCL8 and matrix metalloproteinase (MMP)-9 were also increased in the cell supernatants following NGF exposure. BSA alone was found to drive part of this response, bringing nuance to the inflammatory potential of the NGF.
    Conclusion: These data suggest that NGF is able to enhance monocyte inflammatory responses once cells are stimulated with another signal but is possibly not able to directly activate it. This could have implications for example in patients with bacterial infections, where NGF could worsen the local inflammation by over-activating immune cells.
    Language English
    Publishing date 2024-05-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 639134-5
    ISSN 1472-8206 ; 0767-3981
    ISSN (online) 1472-8206
    ISSN 0767-3981
    DOI 10.1111/fcp.13006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Oxidative Imbalance as a Crucial Factor in Inflammatory Lung Diseases: Could Antioxidant Treatment Constitute a New Therapeutic Strategy?

    Victoni, Tatiana / Barreto, Emiliano / Lagente, Vincent / Carvalho, Vinicius F

    Oxidative medicine and cellular longevity

    2021  Volume 2021, Page(s) 6646923

    Abstract: Inflammatory lung disease results in a high global burden of death and disability. There are no effective treatments for the most severe forms of many inflammatory lung diseases, such as chronic obstructive pulmonary disease, emphysema, corticosteroid- ... ...

    Abstract Inflammatory lung disease results in a high global burden of death and disability. There are no effective treatments for the most severe forms of many inflammatory lung diseases, such as chronic obstructive pulmonary disease, emphysema, corticosteroid-resistant asthma, and coronavirus disease 2019; hence, new treatment options are required. Here, we review the role of oxidative imbalance in the development of difficult-to-treat inflammatory lung diseases. The inflammation-induced overproduction of reactive oxygen species (ROS) means that endogenous antioxidants may not be sufficient to prevent oxidative damage, resulting in an oxidative imbalance in the lung. In turn, intracellular signaling events trigger the production of proinflammatory mediators that perpetuate and aggravate the inflammatory response and may lead to tissue damage. The production of high levels of ROS in inflammatory lung diseases can induce the phosphorylation of mitogen-activated protein kinases, the inactivation of phosphoinositide 3-kinase (PI3K) signaling and histone deacetylase 2, a decrease in glucocorticoid binding to its receptor, and thus resistance to glucocorticoid treatment. Hence, antioxidant treatment might be a therapeutic option for inflammatory lung diseases. Preclinical studies have shown that antioxidants (alone or combined with anti-inflammatory drugs) are effective in the treatment of inflammatory lung diseases, although the clinical evidence of efficacy is weaker. Despite the high level of evidence for the efficacy of antioxidants in the treatment of inflammatory lung diseases, the discovery and clinical investigation of safer, more efficacious compounds are now a priority.
    MeSH term(s) Animals ; Antioxidants/therapeutic use ; Humans ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/metabolism ; Lung/drug effects ; Lung/metabolism ; Lung Diseases/drug therapy ; Lung Diseases/immunology ; Lung Diseases/metabolism ; Oxidation-Reduction/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Antioxidants ; Reactive Oxygen Species
    Language English
    Publishing date 2021-02-09
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2021/6646923
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A multimodal tissue perfusion measurement approach for the evaluation of the effect of pimobendan, an inodilator, in a porcine sepsis model.

    Magnin, Mathieu / Gavet, Morgane / Ngo, Thien-Tam / Louzier, Vanessa / Victoni, Tatiana / Ayoub, Jean Yves / Allaouchiche, Bernard / Bonnet-Garin, Jeanne-Marie / Junot, Stéphane

    Microvascular research

    2024  Volume 154, Page(s) 104687

    Abstract: Sepsis is associated with hypoperfusion and organ failure. The aims of the study were: 1) to assess the effect of pimobendan on macrocirculation and perfusion and 2) to describe a multimodal approach to the assessment of perfusion in sepsis and compare ... ...

    Abstract Sepsis is associated with hypoperfusion and organ failure. The aims of the study were: 1) to assess the effect of pimobendan on macrocirculation and perfusion and 2) to describe a multimodal approach to the assessment of perfusion in sepsis and compare the evolution of the perfusion parameters. Eighteen anaesthetized female piglets were equipped for macrocirculation monitoring. Sepsis was induced by an infusion of Pseudomonas aeruginosa. After the occurrence of hypotension, animals were resuscitated. Nine pigs received pimobendan at the start of resuscitation maneuvers, the others received saline. Tissue perfusion was assessed using temperature gradients measured with infrared thermography (TG = core temperature - tarsus temperature), urethral perfusion index (uPI) derived from photoplethysmography and sublingual microcirculation (Sidestream dark field imaging device): De Backer score (DBs), proportion of perfused vessels (PPV), microvascular flow index (MFI) and heterogeneity index (HI). Arterial lactate and ScvO
    Language English
    Publishing date 2024-04-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80307-8
    ISSN 1095-9319 ; 0026-2862
    ISSN (online) 1095-9319
    ISSN 0026-2862
    DOI 10.1016/j.mvr.2024.104687
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Adiponectin Inhibits the Production of TNF-α, IL-6 and Chemokines by Human Lung Macrophages.

    Salvator, Hélène / Grassin-Delyle, Stanislas / Brollo, Marion / Couderc, Louis-Jean / Abrial, Charlotte / Victoni, Tatiana / Naline, Emmanuel / Devillier, Philippe

    Frontiers in pharmacology

    2021  Volume 12, Page(s) 718929

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2021-08-23
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2021.718929
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Impact of JAK/STAT inhibitors on human monocyte-derived-macrophages stimulated by cigarette smoke extract and lipopolysaccharide.

    Verres, Yann / da Silva, Camila Oliveira / Aljebawi, Bachar / Bodin, Aude / Barreto, Emiliano / Lagente, Vincent / Victoni, Tatiana

    Clinical and experimental pharmacology & physiology

    2022  Volume 49, Issue 11, Page(s) 1187–1196

    Abstract: The main risk factor for chronic obstructive pulmonary disease (COPD) is cigarette smoke (CS). It can alter many immune cells functions such as phagocytosis, efferocytosis and cytokine production. Cytokines play a role in the orchestration of ... ...

    Abstract The main risk factor for chronic obstructive pulmonary disease (COPD) is cigarette smoke (CS). It can alter many immune cells functions such as phagocytosis, efferocytosis and cytokine production. Cytokines play a role in the orchestration of inflammation in COPD. The JAK/STAT pathways are among the most important signalling components of cytokines. The objective of this work was to investigate the role of the JAK/STAT pathway with regard to cytokine release and microsphere uptake capacity (to minimize the non-specific scavenging) in human monocyte-derived-macrophages (MDMs). The MDMs were stimulated by cigarette smoke extract (CSE) alone or in combination with lipopolysaccharide (LPS). CSE alone was not associated with significant changes in the cytokine, with the exception of IL-8/CXCL8 production. However, CSE disturbed cytokine production in LPS-stimulated MDMs. CSE increase CXCL-8 and CCL2 release in LPS-stimulated monocyte-derived macrophages and suppressed the production of IL-6 and CXCL1 in these cells. CSE also decreased microsphere uptake capacity by MDMs. Then, CSE + LPS-stimulated MDMs were treated with two different JAK inhibitors. AG490 (specific inhibitor of JAK2) and ruxolitinib (inhibitor of JAK1 and JAK2). JAK/STAT inhibitors, particularly ruxolitinib, attenuated in cytokine production without completely inhibiting when compared with dexamethasone. On the other hand, the cells exposed to dexamethasone are nearly unable to capture the microspheres, while both JAK inhibitors do not affect the uptake capacity. In summary, our results showed the versatility of ruxolitinib which might bring a better balance disturbance of cytokine release and uptake capacity. The information regarding the distinctive effect of JAK/STAT inhibitors may be useful in the development of novel treatments for COPD.
    MeSH term(s) Cigarette Smoking/adverse effects ; Cytokines/metabolism ; Dexamethasone/pharmacology ; Humans ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Janus Kinase Inhibitors/metabolism ; Janus Kinase Inhibitors/pharmacology ; Janus Kinases/metabolism ; Janus Kinases/pharmacology ; Lipopolysaccharides/pharmacology ; Macrophages ; Monocytes/metabolism ; Nitriles ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pyrazoles ; Pyrimidines ; STAT Transcription Factors/metabolism ; STAT Transcription Factors/pharmacology ; Signal Transduction/physiology ; Nicotiana/adverse effects ; Nicotiana/metabolism
    Chemical Substances Cytokines ; Interleukin-6 ; Interleukin-8 ; Janus Kinase Inhibitors ; Lipopolysaccharides ; Nitriles ; Pyrazoles ; Pyrimidines ; STAT Transcription Factors ; Dexamethasone (7S5I7G3JQL) ; ruxolitinib (82S8X8XX8H) ; Janus Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2022-08-08
    Publishing country Australia
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189277-0
    ISSN 1440-1681 ; 0305-1870 ; 0143-9294
    ISSN (online) 1440-1681
    ISSN 0305-1870 ; 0143-9294
    DOI 10.1111/1440-1681.13705
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: COPD Patients Exhibit Distinct Gene Expression, Accelerated Cellular Aging, and Bias to M2 Macrophages.

    da Silva, Camila Oliveira / de Souza Nogueira, Jeane / do Nascimento, Adriana Paulino / Victoni, Tatiana / Bártholo, Thiago Prudente / da Costa, Cláudia Henrique / Costa, Andrea Monte Alto / Valença, Samuel Dos Santos / Schmidt, Martina / Porto, Luís Cristóvão

    International journal of molecular sciences

    2023  Volume 24, Issue 12

    Abstract: COPD, one of world's leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease ... ...

    Abstract COPD, one of world's leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease severity can be classified as mild, moderate, severe, and very severe. The molecular basis of inflammatory amplification, cellular aging, and immune response are critical to COPD pathogenesis. Our aim was to investigate EP300 (histone acetylase, HAT), HDAC 2 (histone deacetylase), HDAC3, and HDAC4 gene expression, telomere length, and differentiation ability to M1/M2 macrophages. For this investigation, 105 COPD patients, 42 smokers, and 73 non-smoker controls were evaluated. We identified a reduced HDAC2 expression in patients with mild, moderate, and severe severity; a reduced HDAC3 expression in patients with moderate and severe severity; an increased HDAC4 expression in patients with mild severity; and a reduced EP300 expression in patients with severe severity. Additionally, HDAC2 expression was reduced in patients with emphysema and exacerbator, along with a reduced HDAC3 expression in patients with emphysema. Surprisingly, smokers and all COPD patients showed telomere shortening. COPD patients showed a higher tendency toward M2 markers. Our data implicate genetic changes in COPD phenotypes and severity, in addition to M2 prevalence, that might influence future treatments and personalized therapies.
    MeSH term(s) Humans ; Pulmonary Disease, Chronic Obstructive ; Pulmonary Emphysema ; Macrophages ; Cellular Senescence/genetics ; Gene Expression ; Emphysema
    Language English
    Publishing date 2023-06-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24129913
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Clinical Relevance of the Anti-inflammatory Effects of Roflumilast on Human Bronchus: Potentiation by a Long-Acting Beta-2-Agonist.

    Salvator, Hélène / Buenestado, Amparo / Brollo, Marion / Naline, Emmanuel / Victoni, Tatiana / Longchamp, Elisabeth / Tenor, Hermann / Grassin-Delyle, Stanislas / Devillier, Philippe

    Frontiers in pharmacology

    2020  Volume 11, Page(s) 598702

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2020-12-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2020.598702
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: L'inflammasome NLRP3 : physiopathologie et application thérapeutique.

    Gicquel, Thomas / Robert, Sacha / Victoni, Tatiana / Lagente, Vincent

    Presse medicale (Paris, France : 1983)

    2016  Volume 45, Issue 4 Pt 1, Page(s) 438–446

    Abstract: The innate immune system constitutes the first line of host defense against pathogens. "Nonself", such as exogenous particles or pathogens, triggers an inflammatory response. Inflammasomes are molecular platforms activated upon cellular infection or ... ...

    Title translation The NLRP3 inflammasome: Physiopathology and therapeutic application.
    Abstract The innate immune system constitutes the first line of host defense against pathogens. "Nonself", such as exogenous particles or pathogens, triggers an inflammatory response. Inflammasomes are molecular platforms activated upon cellular infection or stress that trigger the maturation of proinflammatory cytokines such as IL-1β. Activation of the NLRP3 inflammasome pathway, the most extensively studied, appears to be the corner stone of many inflammatory diseases, including Crohn's disease, rheumatoid arthritis and gout. Cryopyrine-associated periodic syndromes (CAPS) are NLRP3 inflammasome-associated diseases. Canakinumab (Ilaris(®)) is the only drug approved for CAPS treatment in France. Targeted therapy against NLRP3 inflammasome and IL-1β might be the new anti-inflammatory drugs.
    MeSH term(s) Cryopyrin-Associated Periodic Syndromes/chemically induced ; Cryopyrin-Associated Periodic Syndromes/drug therapy ; Humans ; Inflammasomes/adverse effects ; Inflammasomes/therapeutic use ; NLR Family, Pyrin Domain-Containing 3 Protein/adverse effects
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human
    Language French
    Publishing date 2016-04
    Publishing country France
    Document type Journal Article
    ZDB-ID 120943-7
    ISSN 2213-0276 ; 0032-7867 ; 0755-4982 ; 0301-1518
    ISSN (online) 2213-0276
    ISSN 0032-7867 ; 0755-4982 ; 0301-1518
    DOI 10.1016/j.lpm.2016.01.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Alteration of immunophenotype of human macrophages and monocytes after exposure to cigarette smoke.

    da Silva, Camila Oliveira / Gicquel, Thomas / Daniel, Yoann / Bártholo, Thiago / Vène, Elise / Loyer, Pascal / Pôrto, Luís Cristóvão / Lagente, Vincent / Victoni, Tatiana

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 12796

    Abstract: Cigarette smoke exposure (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). Macrophages have an important role in COPD because they release pro-inflammatory and anti-inflammatory cytokines. The present study's we investigate ... ...

    Abstract Cigarette smoke exposure (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). Macrophages have an important role in COPD because they release pro-inflammatory and anti-inflammatory cytokines. The present study's we investigate the functional changes in macrophages and monocytes exposed to cigarette smoke extract (CSE). Herein, using human monocyte-derived macrophages (MDMs) from healthy donors and we found that CSE was not associated with significant changes in the production of pro inflammatory cytokines by MDMs. In contrast, exposure to CSE suppressed the production of IL-6 and Gro-a/CXCL1 by LPS-stimulated-MDMs, but had an additive effect on the release of IL-8/CXCL8 and MCP1/CCL2. However, CSE exposure was associated with greater production, TARC/CCL-17 and CCL22/MDC. Moreover, MDMs displayed a lower uptake capacity after CSE exposure. We identify, for what is to our knowledge the first time that monocytes from patients with COPD produced less IL-8/CXCL8 and Gro-α/CXCL1 after LPS stimulation and produced higher levels of TARC/CCL17 and MDC/CCL-22 after IL-4 stimulation. Our present results highlighted a skewed immune response, with an imbalance in M1 vs. M2 cytokine production. In conclusion, exposure to CS has contrasting, multifaceted effects on macrophages and monocytes. Our data may provide a better understanding of the mechanisms underlying COPD.
    MeSH term(s) Aged ; Aged, 80 and over ; Cigarette Smoking/adverse effects ; Cytokines/metabolism ; Female ; Humans ; Inflammation Mediators/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Middle Aged ; Monocytes/immunology ; Monocytes/metabolism ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/metabolism ; Risk Factors ; Smoke/adverse effects ; Nicotiana/adverse effects
    Chemical Substances Cytokines ; Inflammation Mediators ; Smoke
    Language English
    Publishing date 2020-07-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-68753-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: COPD Patients Exhibit Distinct Gene Expression, Accelerated Cellular Aging, and Bias to M2 Macrophages

    Camila Oliveira da Silva / Jeane de Souza Nogueira / Adriana Paulino do Nascimento / Tatiana Victoni / Thiago Prudente Bártholo / Cláudia Henrique da Costa / Andrea Monte Alto Costa / Samuel dos Santos Valença / Martina Schmidt / Luís Cristóvão Porto

    International Journal of Molecular Sciences, Vol 24, Iss 9913, p

    2023  Volume 9913

    Abstract: COPD, one of world’s leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease ... ...

    Abstract COPD, one of world’s leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease severity can be classified as mild, moderate, severe, and very severe. The molecular basis of inflammatory amplification, cellular aging, and immune response are critical to COPD pathogenesis. Our aim was to investigate EP300 (histone acetylase, HAT), HDAC 2 (histone deacetylase), HDAC3, and HDAC4 gene expression, telomere length, and differentiation ability to M1/M2 macrophages. For this investigation, 105 COPD patients, 42 smokers, and 73 non-smoker controls were evaluated. We identified a reduced HDAC2 expression in patients with mild, moderate, and severe severity; a reduced HDAC3 expression in patients with moderate and severe severity; an increased HDAC4 expression in patients with mild severity; and a reduced EP300 expression in patients with severe severity. Additionally, HDAC2 expression was reduced in patients with emphysema and exacerbator, along with a reduced HDAC3 expression in patients with emphysema. Surprisingly, smokers and all COPD patients showed telomere shortening. COPD patients showed a higher tendency toward M2 markers. Our data implicate genetic changes in COPD phenotypes and severity, in addition to M2 prevalence, that might influence future treatments and personalized therapies.
    Keywords COPD ; HDAC ; telomere ; macrophage ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610 ; 616
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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