11 research outputs found

    Skills Labs - Deliverable 2.1.a: Casusidee Estuarine systems: the Scheldt

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    Tysmans, D., Lansu, A., Löhr, A., Landsman, N., Huiskes, A., & Verkruysse, B. (2008). Skills Labs - Deliverable 2.1.a: Casusidee Estuarine systems: the Scheldt.Volgens de Emergo-methode uitgewerkt casusidee van casus Estuarine systems: the Scheldt binnen het project Skills Labs.SURFFoundatio

    Monocytes Control Second-Phase Neutrophil Emigration in Established Lipopolysaccharide-induced Murine Lung Injury

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    Rationale: Acute lung injury (ALI) is an important cause of morbidity and mortality, with no currently effective pharmacological therapies. Neutrophils have been specifically implicated in the pathogenesis of ALI, and there has been significant research into the mechanisms of early neutrophil recruitment, but those controlling the later phases of neutrophil emigration that characterize disease are poorly understood. Objectives: To determine the influence of peripheral blood monocytes (PBMs) in established ALI. Methods: In a murine model of LPS-induced ALI, three separate models of conditional monocyte ablation were used: systemic liposomal clodronate (sLC), inducible depletion using CD11b diphtheria toxin receptor (CD11b DTR) transgenic mice, and antibody-dependent ablation of CCR2(hi) monocytes. Measurements and Main Results: PBMs play a critical role in regulating neutrophil emigration in established murine LPS-induced lung injury. Gr1(hi) and Gr1(lo) PBM subpopulations contribute to this process. PBM depletion is associated with a significant reduction in measures of lung injury. The specificity of PBM depletion was demonstrated by replenishment studies in which the effects were reversed by systemic PBM infusion but not by systemic or local pulmonary infusion of mature macrophages or lymphocytes. Conclusions: These results suggest that PBMs, or the mechanisms by which they influence pulmonary neutrophil emigration, could represent therapeutic targets in established ALI

    Knowledge co‐production: A pathway to effective fisheries management, conservation, and governance

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    Although it is assumed that the outcomes from scientific research inform management and policy, the so-called knowledge–action gap (i.e., the disconnect between scientific knowledge and its application) is a recognition that there are many reasons why new knowledge is not always embraced by knowledge users. The concept of knowledge co-production has gained popularity within the environmental and conservation research communities as a mechanism of bridging the gap between knowledge and action, but has yet to be fully embraced in fisheries research. Here we describe what co-production is, outline its benefits (relative to other approaches to research) and challenges, and provide practical guidance on how to embrace and enact knowledge co-production within fisheries research. Because co-production is an iterative and context-dependent process, there is no single way to do it, but there are best practices that can facilitate the generation of actionable research through respectful and inclusive partnerships. We present several brief case studies where we describe examples of where co-production has worked in practice and the benefits it has accrued. As more members of the fisheries science and management community effectively engage in co-production, it will be important to reflect on the processes and share lessons with others. We submit that co-production has manifold benefits for applied science and should lead to meaningful improvements in fisheries management, conservation, and governance

    Tissue-resident macrophages self-maintain locally throughout adult life with minimal contribution from circulating monocytes

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    Despite accumulating evidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remains that tissue macrophages derive from monocytes. Using parabiosis and fate-mapping approaches, we confirmed that monocytes do not show significant contribution to tissue macrophages in the steady state. Similarly, we found that after depletion of lung macrophages, the majority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-stimulating factor (M-Csf)- and granulocyte macrophage (GM)-CSF-dependent manner but independently of interleukin-4. We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised. Expansion of host macrophages was functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors. Collectively, these results indicate that tissue-resident macrophages and circulating monocytes should be classified as mononuclear phagocyte lineages that are independently maintained in the steady state
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