Arctic soil methane sink increases with drier conditions and higher ecosystem respiration.

Arctic wetlands are known methane (CH4) emitters but recent studies suggest that the Arctic CH4 sink strength may be underestimated. Here we explore the capacity of well-drained Arctic soils to consume atmospheric CH4 using >40,000 hourly flux observations and spatially distributed flux measurements from 4 sites and 14 surface types. While consumption of atmospheric CH4 occurred at all sites at rates of 0.092 ± 0.011 mgCH4 m-2 h-1 (mean ± s.e.), CH4 uptake displayed distinct diel and seasonal patterns reflecting ecosystem respiration. Combining in situ flux data with laboratory investigations and a machine learning approach, we find biotic drivers to be highly important. Soil moisture outweighed temperature as an abiotic control and higher CH4 uptake was linked to increased availability of labile carbon. Our findings imply that soil drying and enhanced nutrient supply will promote CH4 uptake by Arctic soils, providing a negative feedback to global climate change.

Heavy metals in the Arctic: Distribution and enrichment of five metals in Alaskan soils.

Metal contamination of food and water resources is a known public health issue in Arctic and sub-Arctic communities due to the proximity of many communities to mining and drilling sites. In addition, permafrost thaw may release heavy metals sequestered in previously frozen soils, potentially contaminating food and water resources by increasing the concentration of metals in freshwater, plants, and wildlife. Here we assess the enrichment of selected heavy metals in Alaskan soils by synthesizing publicly available data of soil metal concentrations. We analyzed data of soil concentrations of arsenic, chromium, mercury, nickel, and lead from over 1,000 samples available through the USGS Alaskan Geochemical Database to evaluate 1) the spatial distribution of sampling locations for soil metal analysis, 2) metal concentrations in soils from different land cover types and depths, and 3) the occurrence of soils in Alaska with elevated metal concentrations relative to other soils. We found substantial clustering of sample sites in the southwestern portion of Alaska in discontinuous and sporadic permafrost, while the continuous permafrost zone in Northern Alaska and the more populous Interior are severely understudied. Metal concentration varied by land cover type but lacked consistent patterns. Concentrations of chromium, mercury, and lead were higher in soils below 10 cm depth, however these deeper soils are under-sampled. Arsenic, chromium, mercury, nickel and lead concentrations exceeded average values for US soils by one standard deviation or more in 3.7% to 18.7% of the samples in this dataset. Our analysis highlights critical gaps that impede understanding of how heavy metals in thawing permafrost soils may become mobilized and increase exposure risk for Arctic communities.

Tryptophan hydroxylase-1 regulates immune tolerance and inflammation.

Nutrient deprivation based on the loss of essential amino acids by catabolic enzymes in the microenvironment is a critical means to control inflammatory responses and immune tolerance. Here we report the novel finding that Tph-1 (tryptophan hydroxylase-1), a synthase which catalyses the conversion of tryptophan to serotonin and exhausts tryptophan, is a potent regulator of immunity. In models of skin allograft tolerance, tumor growth, and experimental autoimmune encephalomyelitis, Tph-1 deficiency breaks allograft tolerance, induces tumor remission, and intensifies neuroinflammation, respectively. All of these effects of Tph-1 deficiency are independent of its downstream product serotonin. Because mast cells (MCs) appear to be the major source of Tph-1 and restoration of Tph-1 in the MC compartment in vivo compensates for the defect, these experiments introduce a fundamentally new mechanism of MC-mediated immune suppression that broadly impacts multiple arms of immunity.

A retinoic acid-dependent checkpoint in the development of CD4+ T cell-mediated immunity.

It is known that vitamin A and its metabolite, retinoic acid (RA), are essential for host defense. However, the mechanisms for how RA controls inflammation are incompletely understood. The findings presented in this study show that RA signaling occurs concurrent with the development of inflammation. In models of vaccination and allogeneic graft rejection, whole body imaging reveals that RA signaling is temporally and spatially restricted to the site of inflammation. Conditional ablation of RA signaling in T cells significantly interferes with CD4(+) T cell effector function, migration, and polarity. These findings provide a new perspective of the role of RA as a mediator directly controlling CD4(+) T cell differentiation and immunity.

Transplantation survival is maintained by granzyme B+ regulatory cells and adaptive regulatory T cells.

Granzyme B (GZB) has been implicated as an effector mechanism in regulatory T cells (T(reg)) suppression. In a model of T(reg)-dependent graft tolerance, it is shown that GZB- deficient mice are unable to establish long-term tolerance. Moreover, mice overexpressing the inhibitor of GZB, serine protease inhibitor 6, are also resistant to tolerization to alloantigen. Graft survival was shorter in bone marrow-mixed chimeras reconstituted with GZB-deficient T(reg) as compared with wild-type T(reg). Whereas there was no difference in graft survival in mixed chimeras reconstituted with wild-type, perforin-deficient, or Fas ligand-deficient T(reg). Finally, data also show that if alloreactive effectors cannot express FoxP3 and be induced to convert in the presence of competent T(reg), then graft tolerance is lost. Our data are the first in vivo data to implicate GZB expression by T(reg) in sustaining long-lived graft survival.