Geothermally warmed soils reveal persistent increases in the respiratory costs of soil microbes contributing to substantial C losses

Increasing temperatures can accelerate soil organic matter decomposition and release large amounts of CO₂ to the atmosphere, potentially inducing positive warming feedbacks. Alterations to the temperature sensitivity and physiological functioning of soil microorganisms may play a key role in these carbon (C) losses. Geothermally active areas in Iceland provide stable and continuous soil temperature gradients to test this hypothesis, encompassing the full range of warming scenarios projected by the Intergovernmental Panel on Climate Change for the northern region. We took soils from these geothermal sites 7 years after the onset of warming and incubated them at varying temperatures and substrate availability conditions to detect persistent alterations of microbial physiology to long-term warming. Seven years of continuous warming ranging from 1.8 to 15.9 °C triggered a 8.6–58.0% decrease on the C concentrations in the topsoil (0–10 cm) of these sub-arctic silt-loam Andosols. The sensitivity of microbial respiration to temperature (Q₁₀) was not altered. However, soil microbes showed a persistent increase in their microbial metabolic quotients (microbial respiration per unit of microbial biomass) and a subsequent diminished C retention in biomass. After an initial depletion of labile soil C upon soil warming, increasing energy costs of metabolic maintenance and resource acquisition led to a weaker capacity of C stabilization in the microbial biomass of warmer soils. This mechanism contributes to our understanding of the acclimated response of soil respiration to in situ soil warming at the ecosystem level, despite a lack of acclimation at the physiological level. Persistent increases in the respiratory costs of soil microbes in response to warming constitute a fundamental process that should be incorporated into climate change-C cycling models.     

Modulation of Higher-Order Olfaction Components on Executive Functions in Humans

The prefrontal (PFC) and orbitofrontal cortex (OFC) appear to be associated with both executive functions and olfaction. However, there is little data relating olfactory processing and executive functions in humans. The present study aimed at exploring the role of olfaction on executive functioning, making a distinction between primary and more cognitive aspects of olfaction. Three executive tasks of similar difficulty were used. One was used to assess hot executive functions (Iowa Gambling Task-IGT), and two as a measure of cold executive functioning (Stroop Colour and Word Test-SCWT and Wisconsin Card Sorting Test-WCST). Sixty two healthy participants were included: 31 with normosmia and 31 with hyposmia. Olfactory abilities were assessed using the ‘‘Sniffin’ Sticks’’ test and the olfactory threshold, odour discrimination and odour identification measures were obtained. All participants were female, aged between 18 and 60. Results showed that participants with hyposmia displayed worse performance in decision making (IGT; Cohen’s-d = 0.91) and cognitive flexibility (WCST; Cohen’s-d between 0.54 and 0.68) compared to those with normosmia. Multiple regression adjusted by the covariates participants’ age and education level showed a positive association between odour identification and the cognitive inhibition response (SCWT-interference; Beta = 0.29; p = .034). The odour discrimination capacity was not a predictor of the cognitive executive performance. Our results suggest that both hot and cold executive functions seem to be associated with higher-order olfactory functioning in humans. These results robustly support the hypothesis that olfaction and executive measures have a common neural substrate in PFC and OFC, and suggest that olfaction might be a reliable cognitive marker in psychiatric and neurologic disorders.     

Effect of serum concentration on the cytotoxicity of clay particles

Nanoparticle cytotoxicity testing based on in vitro methods frequently lack consistency. Even the inclusion of the commonly employed growth supplement, FCS (fetal calf serum), generates variable results. Thus, our object was to investigate the effect of FCS concentration on the cytotoxic behaviour of the unmodified nanoclay, Cloisite® Na⁺. Human monocytic U937 cells in medium supplemented with 5% FCS, 2.5% FCS or serum‐free medium were treated with 1 mg/ml Cloisite Na⁺. Cell growth in 2.5% FCS was significantly inhibited by Cloisite Na⁺ within 48 h, whereas little effect was seen with a supplement of 5% FCS. Without serum, cell growth was inhibited and Cloisite Na⁺ had a detrimental effect on these cells. In media supplemented with FCS, the nanoclays agglomerated together to form large bundles, whereas they were evenly dispersed throughout the medium in the absence of serum. Clay particles, therefore, have cytotoxic properties that may be linked to their dispersion pattern. These adverse effects seem to be masked by 5% FCS. Serum supplementation is an important consideration in the toxicological assessments of nanomaterials on cells, which needs to be addressed in the standardization of in vitro testing methods.     

Statistical analysis of the Bacterial Carbohydrate Structure Data Base (BCSDB): Characteristics and diversity of bacterial carbohydrates in comparison with mammalian glycans

Background  

There are considerable differences between bacterial and mammalian glycans. In contrast to most eukaryotic carbohydrates, bacterial glycans are often composed of repeating units with diverse functions ranging from structural reinforcement to adhesion, colonization and camouflage. Since bacterial glycans are typically displayed at the cell surface, they can interact with the environment and, therefore, have significant biomedical importance.     

Rural and urban distribution of wild and domestic carnivore stools in the context of Echinococcus multilocularis environmental exposure

In zoonotic infections, the relationships between animals and humans lead to parasitic disease with severity that ranges from mild symptoms to life-threatening conditions. In cities and their surrounding areas, this statement is truer with the overcrowding of the protagonists of the parasites’ life cycle. The present study aims to investigate the distribution of a parasite, Echinococcus multilocularis, which is the causative agent of alveolar echinococcosis, using copro-sampling in historically endemic rural settlements of the eastern part of France and in newly endemic areas including urban parks and settlements surrounding Paris. Based on 2741 morphologically identified and geolocalized copro-samples, the density of fox faeces was generally higher in the surrounding settlements, except for one rural area where the faeces were at larger density downtown in the winter. Fox faeces are rare but present in urban parks. Dog faeces are concentrated in the park entrances and in the centre of the settlements. DNA was extracted for 1530 samples that were collected and identified from fox, dog, cat, stone marten and badger carnivore hosts. Echinococcus multilocularis diagnosis and host faecal tests were performed using real-time PCR. We failed to detect the parasite in the surroundings of Paris, but the parasite was found in the foxes, dogs and cats in the rural settlements and their surroundings in the historically endemic area. A spatial structuring of the carnivore stool distribution was highlighted in the present study with high densities of carnivore stools among human occupied areas within some potentially high-risk locations.     

Mechanisms of TNF induction by heat-killed Staphylococcus aureus differ upon the origin of mononuclear phagocytes

Mononuclear phagocytes are among the first immune cells activated after pathogens invasion. Although they all derive from the same progenitor in the bone marrow, their characteristics differ on the compartment from which they are derived. In this work, we investigated the contribution of phagocytosis for tumor necrosis factor (TNF) production by murine mononuclear phagocytes (monocytes, peritoneal and alveolar macrophages) in response to heat-killed Staphylococcus aureus (HKSA). Mononuclear phagocytes behaved differently, depending on their compartment of residence. Indeed, when bacterial uptake or phagosome maturation was blocked, activation through membrane receptors was sufficient for a maximal production of TNF and interleukin-10 by peritoneal macrophages. In contrast, monocytes, and to a lesser extent alveolar macrophages, required phagocytosis for optimal cytokine production. While investigating the different actors of signalization, we found that p38 kinase and phosphatidylinositol 3-kinase were playing an important role in HKSA phagocytosis and TNF production. Furthermore, blocking the α(5)β(1)-integrin significantly decreased TNF production in response to HKSA in all three cell types. Finally, using mononuclear phagocytes from NOD2 knockout mice, we observed that TNF production in response to HKSA was dependent on NOD2 for monocytes and peritoneal macrophages. In conclusion, we demonstrate that the mechanisms of activation leading to TNF production in response to HKSA are specific for each mononuclear phagocyte population and involve different recognition processes and signaling pathways. The influence of the compartments on cell properties and behavior should be taken into account, to better understand cell physiology and host-pathogen interaction, and to define efficient strategies to fight infection.     

Crystallographic studies of the Escherichia coli quinol-fumarate reductase with inhibitors bound to the quinol-binding site

The quinol-fumarate reductase (QFR) respiratory complex of Escherichia coli is a four-subunit integral-membrane complex that catalyzes the final step of anaerobic respiration when fumarate is the terminal electron acceptor. The membrane-soluble redox-active molecule menaquinol (MQH(2)) transfers electrons to QFR by binding directly to the membrane-spanning region. The crystal structure of QFR contains two quinone species, presumably MQH(2), bound to the transmembrane-spanning region. The binding sites for the two quinone molecules are termed Q(P) and Q(D), indicating their positions proximal (Q(P)) or distal (Q(D)) to the site of fumarate reduction in the hydrophilic flavoprotein and iron-sulfur protein subunits. It has not been established whether both of these sites are mechanistically significant. Co-crystallization studies of the E. coli QFR with the known quinol-binding site inhibitors 2-heptyl-4-hydroxyquinoline-N-oxide and 2-[1-(p-chlorophenyl)ethyl] 4,6-dinitrophenol establish that both inhibitors block the binding of MQH(2) at the Q(P) site. In the structures with the inhibitor bound at Q(P), no density is observed at Q(D), which suggests that the occupancy of this site can vary and argues against a structurally obligatory role for quinol binding to Q(D). A comparison of the Q(P) site of the E. coli enzyme with quinone-binding sites in other respiratory enzymes shows that an acidic residue is structurally conserved. This acidic residue, Glu-C29, in the E. coli enzyme may act as a proton shuttle from the quinol during enzyme turnover.