28 research outputs found

    Food-web structure in relation to environmental gradients and predator-prey ratios in tank-bromeliad ecosystems

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    Little is known of how linkage patterns between species change along environmental gradients. The small, spatially discrete food webs inhabiting tank-bromeliads provide an excellent opportunity to analyse patterns of community diversity and food-web topology (connectance, linkage density, nestedness) in relation to key environmental variables (habitat size, detrital resource, incident radiation) and predators: prey ratios. We sampled 365 bromeliads in a wide range of understorey environments in French Guiana and used gut contents of invertebrates to draw the corresponding 365 connectance webs. At the bromeliad scale, habitat size (water volume) determined the number of species that constitute food-web nodes, the proportion of predators, and food-web topology. The number of species as well as the proportion of predators within bromeliads declined from open to forested habitats, where the volume of water collected by bromeliads was generally lower because of rainfall interception by the canopy. A core group of microorganisms and generalist detritivores remained relatively constant across environments. This suggests that (i) a highly-connected core ensures food-web stability and key ecosystem functions across environments, and (ii) larger deviations in food-web structures can be expected following disturbance if detritivores share traits that determine responses to environmental changes. While linkage density and nestedness were lower in bromeliads in the forest than in open areas, experiments are needed to confirm a trend for lower food-web stability in the understorey of primary forests

    Nitric oxide short-circuits interleukin-12-mediated tumor regression

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    Interleukin-12 (IL-12) can promote tumor regression via activation of multiple lymphocytic and myelocytic eVectors. Whereas the cytotoxic mechanisms employed by T/NK/NKT cells in IL-12-mediated tumor kill are well deWned, the antitumor role of macrophage-produced cytotoxic metabolites has been more controversial. To this end, we investigated the speciWc role of nitric oxide (NO), a major macrophage eVector molecule, in post-IL-12 tumor regression. Analysis of tumors following a single intratumoral injection of slow-release IL-12 microspheres showed an IFN-dependent sevenfold increase in inducible nitric oxide synthase (iNOS) expression within 48 h. Flow cytometric analysis of tumor-resident leukocytes and in vivo depletion studies identiWed CD11b+ F4/80+ Gr1lo macrophages as the primary source of iNOS. Blocking of post-therapy iNOS activity with N-nitro-L-arginine methyl ester (L-NAME)dramatically enhanced tumor suppression revealing the inhibitory eVect of NO on IL-12-driven antitumor immunity. Superior tumor regression in mice receiving combination treatment was associated with enhanced survival and proliferation of activated tumor-resident CD8+ T-eVector/memory cells (Tem). These Wndings demonstrate that macrophageproduced NO negatively regulates the antitumor activity of IL-12 via its detrimental eVects on CD8+ T cells and identify L-NAME as a potent adjuvant in IL-12 therapy of cancer
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