Identification and analysis of seven effector protein families with different adaptive and evolutionary histories in plant-associated members of the Xanthomonadaceae.

The Xanthomonadaceae family consists of species of non-pathogenic and pathogenic γ-proteobacteria that infect different hosts, including humans and plants. In this study, we performed a comparative analysis using 69 fully sequenced genomes belonging to this family, with a focus on identifying proteins enriched in phytopathogens that could explain the lifestyle and the ability to infect plants. Using a computational approach, we identified seven phytopathogen-enriched protein families putatively secreted by type II secretory system: PheA (CM-sec), LipA/LesA, VirK, and four families involved in N-glycan degradation, NixE, NixF, NixL, and FucA1. In silico and phylogenetic analyses of these protein families revealed they all have orthologs in other phytopathogenic or symbiotic bacteria, and are involved in the modulation and evasion of the immune system. As a proof of concept, we performed a biochemical characterization of LipA from Xac306 and verified that the mutant strain lost most of its lipase and esterase activities and displayed reduced virulence in citrus. Since this study includes closely related organisms with distinct lifestyles and highlights proteins directly related to adaptation inside plant tissues, novel approaches might use these proteins as biotechnological targets for disease control, and contribute to our understanding of the coevolution of plant-associated bacteria

Sized-based indicators show depth-dependent change over time in the deep sea

Size-based indicators are well established as a management tool in shelf seas as they respond to changes in fishing pressure and describe important aspects of community function. In the deep sea, however, vital rates are much slower and body size relationships vary with depth, making it less clear how size-based indicators can be applied and whether they are appropriate for detecting changes through time. The deep-sea fish stocks of the North Atlantic underwent a period of exploitation followed by management and conservation action that relieved this pressure. We used data from a deep-water bottom trawl survey in the Rockall Trough, at depths of 300–2000 m, to test whether size-based indicators changed over a 16-year period, during which fishing pressure decreased. We applied four indicators to these data: mean body length, mean maximum length, large fish indicator (LFI) and the slope of the biomass spectrum. Patterns were analysed within four different depth bands. The LFI and slope of the biomass spectrum showed positive change over time, suggesting recovery from fishing pressure. This response was generally most apparent in the shallowest depth band, where most fishing activity has been distributed. Values of the LFI were much higher overall than in shelf seas, so the same reference points cannot be applied to all marine ecosystems. These findings imply that size-based indicators can be usefully applied to the deep sea and that they potentially track changes in fishing pressure in the medium term

Prothrombotic state and impaired fibrinolysis in bullous pemphigoid, the most frequent autoimmune blistering disease

Bullous pemphigoid (BP) is a potentially life-threatening autoimmune blistering disease that is burdened with an increased risk of cardiovascular events. In BP, there is an interplay between inflammation and coagulation both locally, which contributes to skin damage, and systemically, which leads to a prothrombotic state. Fibrinolysis is an important defence mechanism against thrombosis, but has only been studied locally in BP and no systemic data are available. The aim of this observational study was to evaluate systemic fibrinolysis and coagulation activation in patients with BP. We measured parameters of fibrinolysis and coagulation by immunoenzymatic methods in plasma from 20 patients with BP in an active phase and during remission after corticosteroid treatment. The controls were 20 age- and sex-matched healthy subjects. Plasma levels of plasminogen activator inhibitor type 1 (PAI-1) antigen, PAI-1 activity and tissue plasminogen activator (t-PA) antigen were significantly higher in the BP patients with active disease than in healthy controls (P=0\ub70001 for all), as were the plasma levels of the fibrin fragment d-dimer and prothrombin fragment F1+2 (P=0\ub70001 for both). During remission after treatment, levels of PAI-1 antigen and PAI-1 activity decreased significantly (P=0\ub7008 and P=0\ub7006, respectively), and there was also a significant decrease in plasma levels of d-dimer (P=0\ub70001) and F1+2 (P=0\ub70001). Fibrinolysis is inhibited in patients with active BP, due mainly to an increase in plasma levels of PAI-1. Corticosteroids not only induce the regression of BP lesions, but also reduce the inhibition of fibrinolysis, which may contribute to decreasing thrombotic risk. \ua9 2012 British Society for Immunology

Interactions between Inflammation and Coagulation in Autoimmune and Immune-Mediated Skin Diseases

Inflammation and coagulation systems are simultaneously activated in autoimmune and immune-mediated skin disorders, and the cross-talk that amplifies and maintains their activation seems to have both local and systemic implications. This interplay occurs in bullous pemphigoid (BP), the prototype autoimmune blistering disease in which eosinophil recruitment and thrombin generation locally contribute to the formation of bullae and inflammatory tissue damage. Moreover, the systemic activation of coagulation may explain the increased thrombotic risk observed in BP patients. Atopic dermatitis (AD), a chronically relapsing immune-mediated inflammatory skin disease, also involves the local and systemic activation of coagulation, which means that a prothrombotic state could theoretically develop, although the incidence of thrombosis is not increased in AD patients probably because of their young age. In psoriasis, a erythematous-squamous inflammatory immune-mediated skin disorder, the activation of coagulation seems to be mainly systemic and related to systemic inflammation, thus potentially contributing to the disease-related increase in cardiovascular risk in this disease. The activation of coagulation has also been suggested an additional pathomechanism in dermatitis herpetiformis (DH), a chronic-relapsing autoimmune skin disease associated with gluten sensitivity and celiac disease, but its precise role has not yet been defined. Taken together, these data provide the rationale for controlled clinical trials aimed at evaluating the usefulness of anticoagulant treatment in autoimmune skin disorders to counteract the local and systemic effects of coagulation activatio