Environmental Costs of Government-Sponsored Agrarian Settlements in Brazilian Amazonia

Brazil has presided over the most comprehensive agrarian reform frontier colonization program on Earth, in which ~1.2 million settlers have been translocated by successive governments since the 1970's, mostly into forested hinterlands of Brazilian Amazonia. These settlements encompass 5.3% of this ~5 million km2 region, but have contributed with 13.5% of all land conversion into agropastoral land uses. The Brazilian Federal Agrarian Agency (INCRA) has repeatedly claimed that deforestation in these areas largely predates the sanctioned arrival of new settlers. Here, we quantify rates of natural vegetation conversion across 1911 agrarian settlements allocated to 568 Amazonian counties and compare fire incidence and deforestation rates before and after the official occupation of settlements by migrant farmers. The timing and spatial distribution of deforestation and fires in our analysis provides irrefutable chronological and spatially explicit evidence of agropastoral conversion both inside and immediately outside agrarian settlements over the last decade. Deforestation rates are strongly related to local human population density and road access to regional markets. Agrarian settlements consistently accelerated rates of deforestation and fires, compared to neighboring areas outside settlements, but within the same counties. Relocated smallholders allocated to forest areas undoubtedly operate as pivotal agents of deforestation, and most of the forest clearance occurs in the aftermath of government-induced migration

Evidence for rangewide panmixia despite multiple barriers to dispersal in a marine mussel

Oceanographic features shape the distributional and genetic patterns of marine species by interrupting or promoting connections among populations. Although general patterns commonly arise, distributional ranges and genetic structure are species-specific and do not always comply with the expected trends. By applying a multimarker genetic approach combined with Lagrangian particle simulations (LPS) we tested the hypothesis that oceanographic features along northeastern Atlantic and Mediterranean shores influence dispersal potential and genetic structure of the intertidal mussel Perna perna. Additionally, by performing environmental niche modelling we assessed the potential and realized niche of P. perna along its entire native distributional range and the environmental factors that best explain its realized distribution. Perna perna showed evidence of panmixia across > 4,000 km despite several oceanographic breaking points detected by LPS. This is probably the result of a combination of life history traits, continuous habitat availability and stepping-stone dynamics. Moreover, the niche modelling framework depicted minimum sea surface temperatures (SST) as the major factor shaping P. perna distributional range limits along its native areas. Forthcoming warming SST is expected to further change these limits and allow the species to expand its range polewards though this may be accompanied by retreat from warmer areas.Fundacao para a Ciencia e Tecnologia (FCT-MEC, Portugal) [UID/Multi/04326/2013, IF/01413/2014/CP1217/CT0004]; South African Research Chairs Initiative (SARChI) of the Department of Science and Technology; National Research Foundation; South African National Research Foundation (NRF); Portuguese Fundacao para a Ciencia e Tecnologia (FCT) [SFRH/BPD/85040/2012, SFRH/BPD/111003/2015]info:eu-repo/semantics/publishedVersio

Profile of Central and Effector Memory T Cells in the Progression of Chronic Human Chagas Disease

Chagas disease is a parasitic infection caused by protozoan Trypanosoma cruzi that affects approximately 11 million people in Latin America. The involvement of the host's immune response on the development of severe forms of Chagas disease has not been fully elucidated. Studies on the immune response against T. cruzi infection show that the immunoregulatory mechanisms are necessary to prevent the deleterious effect of excessive immune response stimulation and consequently the fatal outcome of the disease. A recall response against parasite antigens observed in in vitro peripheral blood cell culture clearly demonstrates that memory response is generated during infection. Memory T cells are heterogeneous and differ in both the ability to migrate and exert their effector function. This heterogeneity is reflected in the definition of central (TCM) and effector memory (TEM) T cells. Our results suggest that a balance between regulatory and effectors T cells may be important for the progression and development of the disease. Furthermore, the high percentage of central memory CD4+ T cells in indeterminate patients after stimulation suggests that these cells may modulate host's inflammatory response by controlling cell migration to tissues and their effector role during chronic phase of the disease

Coinfection with Different Trypanosoma cruzi Strains Interferes with the Host Immune Response to Infection

A century after the discovery of Trypanosoma cruzi in a child living in Lassance, Minas Gerais, Brazil in 1909, many uncertainties remain with respect to factors determining the pathogenesis of Chagas disease (CD). Herein, we simultaneously investigate the contribution of both host and parasite factors during acute phase of infection in BALB/c mice infected with the JG and/or CL Brener T. cruzi strains. JG single infected mice presented reduced parasitemia and heart parasitism, no mortality, levels of pro-inflammatory mediators (TNF-α, CCL2, IL-6 and IFN-γ) similar to those found among naïve animals and no clinical manifestations of disease. On the other hand, CL Brener single infected mice presented higher parasitemia and heart parasitism, as well as an increased systemic release of pro-inflammatory mediators and higher mortality probably due to a toxic shock-like systemic inflammatory response. Interestingly, coinfection with JG and CL Brener strains resulted in intermediate parasitemia, heart parasitism and mortality. This was accompanied by an increase in the systemic release of IL-10 with a parallel increase in the number of MAC-3+ and CD4+ T spleen cells expressing IL-10. Therefore, the endogenous production of IL-10 elicited by coinfection seems to be crucial to counterregulate the potentially lethal effects triggered by systemic release of pro-inflammatory mediators induced by CL Brener single infection. In conclusion, our results suggest that the composition of the infecting parasite population plays a role in the host response to T. cruzi in determining the severity of the disease in experimentally infected BALB/c mice. The combination of JG and CL Brener was able to trigger both protective inflammatory immunity and regulatory immune mechanisms that attenuate damage caused by inflammation and disease severity in BALB/c mice