Rheagogies: modelling non-trophic effects in food webs

In a food web, nutrients flow via trophic links. For this reason, trophic interactions have a fundamental character due to the principle of mass conservation. To further comply with this principle, we consider a food web model that includes nutrient cycling. Non-trophic effects amongst species of the food web are modelled as interaction modifications, i.e., a functional change in the trophic interaction between two species caused by a third species (a three-party interaction that we call ‘‘rheagogy’’).We also consider that the ecological communities modelled by the food webs result from an assembly process that involves colonisations and extinctions. We find that two distinct classes of ecological communities must be distinguished: (a) ‘‘superefficient’’ communities, in which almost all available nutrients are incorporated into the biomass and (b) ‘‘sub-efficient’’ ones, in which a large proportion of nutrients is not fixed by living organisms. We show that rheagogies (that model non-trophic interactions) are crucial: the larger the effects of rheagogies, the easier the construction of super-efficient communities. These communities are characterized by positive rheagogies, meaning that a certain proportion of mutualistic interactions is necessary. Systems with few or weak rheagogies are less likely to use available abiotic resources efficiently. Although richness (i.e., number of species) is also positively related to efficient nutrient use, its importance is much smaller than that of rheagogies

Spatially mixed crops to control the stratified dispersal of airborne fungal diseases

Intraspecific crop diversification is thought to be a possible solution to the disease susceptibility of monocultured crops. We modelled the stratified dispersal of an airborne pathogen population in order to identify the spatial patterns of cultivar mixtures that could slow epidemic spread driven by dual dispersal mechanisms acting over both short and long distances. We developed a model to simulate the propagation of a fungal disease in a 2D field, including a reaction-diffusion model for short-distance disease dispersal, and a stochastic model for long-distance dispersal. The model was fitted to data for the spatio-temporal spread of faba bean rust (caused by Uromyces viciae-fabae) through a discontinuous field. The model was used to compare the effectiveness of eight different planting patterns of cultivar mixtures against a disease spread by short-distance and stratified dispersal. Our combined modelling approach provides a reasonably good fit with the observed data for the spread of faba bean rust. Similar predictive power could be expected for the management of resource-mediated invasions by other airborne fungi. If a disease spreads by short-distance dispersal, random mixtures can be used to slow the epidemic spread, since their spatial irregularity creates a natural barrier to the progression of a smooth epidemic wave. In the context of stratified dispersal, heterogeneous patterns should be used that include a minimum distance between susceptible units, which decreases the probability of infection by long-distance spore dispersal. We provide a simple framework for modelling the stratified dispersal of disease in a diversified crop. The model suggests that the spatial arrangement of components in cultivar mixtures has to accord with the dispersal characteristics of the pathogen in order to increase the efficiency of diversification strategies in agro-ecosystems and forestry. It can be applied in low input agriculture to manage pathogen invasion by intercropping and cultivar mixtures, and to design sustainable systems of land use

Global Production Increased by Spatial Heterogeneity in a Population Dynamics Model

Spatial and temporal heterogeneity are often described as important factors having a strong impact on biodiversity. The effect of heterogeneity is in most cases analyzed by the response of biotic interactions such as competition of predation. It may also modify intrinsic population properties such as growth rate. Most of the studies are theoretic since it is often difficult to manipulate spatial heterogeneity in practice. Despite the large number of studies dealing with this topics, it is still difficult to understand how the heterogeneity affects populations dynamics. On the basis of a very simple model, this paper aims to explicitly provide a simple mechanism which can explain why spatial heterogeneity may be a favorable factor for production.We consider a two patch model and a logistic growth is assumed on each patch. A general condition on the migration rates and the local subpopulation growth rates is provided under which the total carrying capacity is higher than the sum of the local carrying capacities, which is not intuitive. As we illustrate, this result is robust under stochastic perturbations

Loss of testosterone impairs anti-tumor neutrophil function.

In men, the incidence of melanoma rises rapidly after age 50, and nearly two thirds of melanoma deaths are male. The immune system is known to play a key role in controlling the growth and spread of malignancies, but whether age- and sex-dependent changes in immune cell function account for this effect remains unknown. Here, we show that in castrated male mice, neutrophil maturation and function are impaired, leading to elevated metastatic burden in two models of melanoma. Replacement of testosterone effectively normalized the tumor burden in castrated male mice. Further, the aberrant neutrophil phenotype was also observed in prostate cancer patients receiving androgen deprivation therapy, highlighting the evolutionary conservation and clinical relevance of the phenotype. Taken together, these results provide a better understanding of the role of androgen signaling in neutrophil function and the impact of this biology on immune control of malignancies

IL-2 Suppression of IL-12p70 by a Recombinant HSV-1 Expressing IL-2 Induces T-Cell Auto-Reactivity and CNS Demyelination

To evaluate the role of cellular infiltrates in CNS demyelination in immunocompetent mice, we have used a model of multiple sclerosis (MS) in which different strains of mice are infected with a recombinant HSV-1 expressing IL-2. Histologic examination of the mice infected with HSV-IL-2 demonstrates that natural killer cells, dendritic cells, B cells, and CD25 (IL-2rα) do not play any role in the HSV-IL-2-induced demyelination. T cell depletion, T cell knockout and T cell adoptive transfer experiments suggest that both CD8+ and CD4+ T cells contribute to HSV-IL-2-induced CNS demyelination with CD8+ T cells being the primary inducers. In the adoptive transfer studies, all of the transferred T cells irrespective of their CD25 status at the time of transfer were positive for expression of FoxP3 and depletion of FoxP3 blocked CNS demyelination by HSV-IL-2. The expression levels of IL-12p35 relative to IL-12p40 differed in BM-derived macrophages infected with HSV-IL-2 from those infected with wild-type HSV-1. HSV-IL-2-induced demyelination was blocked by injecting HSV-IL-2-infected mice with IL-12p70 DNA. This study demonstrates that suppression of the IL-12p70 function of macrophages by IL-2 causes T cells to become auto-aggressive. Interruption of this immunoregulatory axis results in demyelination of the optic nerve, the spinal cord and the brain by autoreactive T cells in the HSV-IL-2 mouse model of MS

Caspase-1 Dependent IL-1β Secretion Is Critical for Host Defense in a Mouse Model of Chlamydia pneumoniae Lung Infection

Chlamydia pneumoniae (CP) is an important human pathogen that causes atypical pneumonia and is associated with various chronic inflammatory disorders. Caspase-1 is a key component of the ‘inflammasome’, and is required to cleave pro-IL-1β to bioactive IL-1β. Here we demonstrate for the first time a critical requirement for IL-1β in response to CP infection. Caspase-1−/− mice exhibit delayed cytokine production, defective clearance of pulmonary bacteria and higher mortality in response to CP infection. Alveolar macrophages harbored increased bacterial numbers due to reduced iNOS levels in Caspase-1−/− mice. Pharmacological blockade of the IL-1 receptor in CP infected wild-type mice phenocopies Caspase-1-deficient mice, and administration of recombinant IL-1β rescues CP infected Caspase-1−/− mice from mortality, indicating that IL-1β secretion is crucial for host immune defense against CP lung infection. In vitro investigation reveals that CP-induced IL-1β secretion by macrophages requires TLR2/MyD88 and NLRP3/ASC/Caspase-1 signaling. Entry into the cell by CP and new protein synthesis by CP are required for inflammasome activation. Neither ROS nor cathepsin was required for CP infection induced inflammasome activation. Interestingly, Caspase-1 activation during CP infection occurs with mitochondrial dysfunction indicating a possible mechanism involving the mitochondria for CP-induced inflammasome activation

Deficiency of CCAAT/enhancer binding protein-epsilon reduces atherosclerotic lesions in LDLR-/- Mice

10.1371/journal.pone.0085341PLoS ONE91-POLN