47 research outputs found

    Identifying cost-competitive greenhouse gas mitigation potential of French agriculture

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    The agriculture, forestry and other land use sector are responsible for 24% (10–12 Pg CO2e per year) of anthropogenic greenhouse gas (GHG) emissions worldwide, with concomitant opportunities for mitigation. A scientific panel used deliberative methods to identify ten technical measures comprising 26 sub-measures to reduce GHG emissions from agriculture in France. Their abatement potential and cost are compared. The proposed measures concern nitrogen (N) management, management practices that increase carbon stocks in soils and biomass, livestock diets, and energy production and consumption on farms. Results show that the total abatement potential can be divided into three parts. One third of the cumulated abatement potential corresponds to sub-measures that can be implemented at a negative technical cost. These sub-measures focus on increased efficiency in input use including N fertilisers, animal feed and energy. The second third are sub-measures with moderate cost (€25 per metric Mg of avoided CO2e). These require investment with no direct financial return, the purchase of particular inputs, dedicated labour time or involve production losses. Assuming additivity, the cumulated abatement is 32.3 Tg CO2e per year in 2030, but only 10 Tg (i.e. 10% of current agricultural emissions) when calculated under current inventory rules. This study confirms that a significant abatement potential exists in the agricultural sector, with two thirds of this potential at low or even negative cost. This is likely to be an underestimated as it is based on a status quo of the current agricultural system. Results also emphasise the need to upgrade inventory rules so that efforts to reduce emissions can be accounted for

    Validation of the candidacy of toll-like receptor 5 (Tlr5) as a Salmonella susceptibility gene

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    The extreme susceptibility to infection with Salmonella Typhimurium of wild-derived MOLF/Ei has been linked to one chromosomal region (Ity3). Toll-like receptor 5 (Tlr5) is located within the Ity3 interval and its candidacy as a Salmonella-susceptibility gene was evaluated in vitro and in vivo by comparing the Tlr5 C57BL/6J and MOLF/Ei alleles (85). In vitro studies using NF-kappaB-dependent reporter genes showed that sequence variants found within the coding region of MOLF/Ei Tlr5 did not affect the response of Tlr5 to flagellin compared to C57BL/6J. MOLF/Ei promoter had a slightly stronger basal activity than the C57BL/6J allele. In vivo study using Ity3 congenic mice showed that mice homozygous for MOLF/Ei allele at Ity3 had a stronger response to flagellin as measured by IL-6 secretion in the serum. Finally, we can conclude that Tlr5 is involved in the disease phenotype underlying Ity3 however, it is not clear if the impact of Tlr5 is primary or secondary

    Organo-Mineral Interactions Are More Important for Organic Matter Retention in Subsoil Than Topsoil

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    International audienceDecomposing crop residues contribute to soil organic matter (SOM) accrual; however, the factors driving the fate of carbon (C) and nitrogen (N) in soil fractions is still largely unknown, especially the influence of soil mineralogy and autochthonous organic matter concentration. The objectives of this work were (1) to evaluate the retention of C and N from crop residue in the form of occluded and mineral-associated SOM in topsoil (0-20 cm) and subsoil (30-70 cm) previously incubated for 51 days with 13 C-15 N-labelled corn residues, and (2) to explore if specific minerals preferentially control the retention of residue-derived C and N in topsoil and subsoil. We used topsoil and subsoil having similar texture and mineralogy as proxies for soils being rich (i.e., topsoil) and poor (i.e., subsoil) in autochthonous organic matter. We performed a sequential density fractionation procedure and measured residue-derived C and N in occluded and mineral-associated SOM fractions, and used X-ray diffraction analysis of soil density fractions to investigate their mineralogy. In accordance with our hypothesis, the retention of C and N from crop residue through organo-mineral interactions was greater in subsoil than topsoil. The same minerals were involved in the retention of residue-derived organic matter in topsoil and subsoil, but the residue-derived organic matter was associated with a denser fraction in the subsoil (i.e., 2.5-2.6. g cm −3) than in the topsoil (i.e., 2.3-2.5 g cm −3). In soils and soil horizons with high clay content and reactive minerals, we find that a low SOM concentration leads to the rapid stabilization of C and N from newly added crop residues

    Unc93b1 -Dependent Endosomal Toll-Like Receptor Signaling Regulates Inflammation and Mortality during Coxsackievirus B3 Infection.

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    Coxsackievirus strain B serotype 3 (CVB3)-induced myocarditis is an important human disease that causes permanent tissue damage and can lead to death from acute infection or long-term morbidity caused by chronic inflammation. The timing and magnitude of immune activation following CVB3 infection can mediate a positive host outcome or increase tissue pathology. To better elucidate the role of endosomal Toll-like receptor (TLR) signaling in acute CVB3 infection, we studied mice with a loss-of-function mutation, known as Letr for 'loss of endosomal TLR response', in Unc93b1, which is a chaperone protein for TLR3, TLR7 and TLR9. Using Unc93b1(Letr/)(Letr) mice, we determined that Unc93b1-dependent TLR activation was essential for the survival of acute CVB3-induced myocarditis. We also determined that a lack of endosomal TLR signaling was associated with a higher viral load in target organs and that it increased inflammation, necrosis and fibrosis in cardiac tissue. Loss of Unc93b1 function was also associated with increased cardiac expression of Ifn-b and markers of tissue injury and fibrosis including Lcn2 and Serpina3n early after CVB3 infection. These observations establish a significant role for Unc93b1 in the regulation of the host inflammatory response to CVB3 infection and also reveal potential mediators of host tissue damage that merit further investigation in acute viral myocarditis

    Contribution of IL-1RI Signaling to Protection against Cryptococcus neoformans 52D in a Mouse Model of Infection

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    Interleukin-1 alpha (IL-1α) and interleukin-1 beta (IL-1β) are pro-inflammatory cytokines that are induced after Cryptococcus neoformans infection and activate the interleukin-1 receptor type I (IL-1RI). To establish the role of IL-1RI signaling in protection against cryptococcal infection, we analyzed wild-type (WT) and IL-1RI-deficient (IL-1RI−/−) mice on the BALB/c background. IL-1RI−/− mice had significantly reduced survival compared to WT mice after intratracheal challenge with C. neoformans 52D. Microbiological analysis showed a significant increase in the lung and brain fungal burden of IL-1RI−/− compared to WT mice beginning at weeks 1 and 4 postinfection, respectively. Histopathology showed that IL-1RI−/− mice exhibit greater airway epithelial mucus secretion and prominent eosinophilic crystals that were absent in WT mice. Susceptibility of IL-1RI−/− mice was associated with significant induction of a Th2-biased immune response characterized by pulmonary eosinophilia, M2 macrophage polarization, and recruitment of CD4+ IL-13+ T cells. Expression of pro-inflammatory [IL-1α, IL-1β, TNFα, and monocyte chemoattractant protein 1 (MCP-1)], Th1-associated (IFNγ), and Th17-associated (IL-17A) cytokines was significantly reduced in IL-1RI−/− lungs compared to WT. WT mice also had higher expression of KC/CXCL1 and sustained neutrophil recruitment to the lung; however, antibody-mediated depletion of these cells showed that they were dispensable for lung fungal clearance. In conclusion, our data indicate that IL-1RI signaling is required to activate a complex series of innate and adaptive immune responses that collectively enhance host defense and survival after C. neoformans 52D infection in BALB/c mice
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