Wild phage evolution: Bacteria possess a diversity of highly specific phage defense mechanisms that evolve rapidly and that account for a large proportion of bacterial genomes. These dynamics must be understood if phage therapy is to be seriously considered for clinical use. Hussain et al . studied a set of nearly clonal wild-caught Vibrio lentus hosts and their phage and found that the hosts segregated into two groups infected by different viruses (see the Perspective by Meaden and Fineran). Puzzlingly, both host groups have the same surface phage receptors. This apparent paradox was resolved by sequencing of the hosts, which revealed distinct suites of endogenous but mobile phage defense elements (PDEs) in the two host phenotypes. Indeed, the PDEs constitute a large fraction of the flexible noncore genome of the bacteria. This means the PDEs can evolve and transfer from cell to cell without interfering with metabolic processes required to synthesize essential cell surface molecules. —CA

Irritable bowel syndrome (IBS), one of the most frequent digestive disorders, is characterized by chronic and recurrent abdominal pain and altered bowel habit. The origin seems to be multifactorial and is still not well defined for the different subtypes. Genetic, epigenetic and sex-related modifications of the functioning of the nervous and immune-endocrine supersystems and regulation of brain-gut physiology and bile acid production and absorption are certainly involved. Acquired predisposition may act in conjunction with infectious, toxic, dietary and life event-related factors to enhance epithelial permeability and elicit mucosal microinflammation, immune activation and dysbiosis. Notably, strong evidence supports the role of bacterial, viral and parasitic infections in triggering IBS, and targeting microbiota seems promising in view of the positive response to microbiota-related therapies in some patients. However, the lack of highly predictive diagnostic biomarkers and the complexity and heterogeneity of IBS patients make management difficult and unsatisfactory in many cases, reducing patient health-related quality of life and increasing the sanitary burden. This article reviews specific alterations and interventions targeting the gut microbiota in IBS, including prebiotics, probiotics, synbiotics, non-absorbable antibiotics, diets, fecal transplantation and other potential future approaches useful for the diagnosis, prevention and treatment of IBS.

Significance: Emergence of the pathogen Klebsiella pneumoniae (particularly of carbapenem-resistant strains) is considered a dire threat to public health. Resistance and virulence determinants may favor the emergence of untreatable infections. Understanding the mechanisms involved in the pathogenesis and epidemicity of K. pneumoniae is essential for managing outbreaks and developing treatments. Here we identify a CUP system (Kpi) and infer the epidemiology of Kpi ⁺ K. pneumoniae in Europe. We demonstrate a direct link between Kpi presence and K . pneumoniae persistence in the hospital environment. Adherence of the bacterium to different cell types enables host colonization, favoring nosocomial outbreaks and spread of infection. Kpi appears to play a key role in the host–pathogen interaction and is associated with the worldwide-disseminated ST-15 clone.

Eosinophils are innate immune granulocytes actively involved in defensive responses and in local and systemic inflammatory processes. Beyond these effector roles, eosinophils are fundamental to maintaining homeostasis in the tissues they reside. Gastrointestinal eosinophils modulate barrier function and mucosal immunity and promote tissue development through their direct communication with almost every cellular component. This is possible thanks to the variety of receptors they express and the bioactive molecules they store and release, including cytotoxic proteins, cytokines, growth factors, and neuropeptides and neurotrophines. A growing body of evidence points to the eosinophil as a key neuro-immune player in the regulation of gastrointestinal function, with potential implications in pathophysiological processes. Eosinophil–neuron interactions are facilitated by chemotaxis and adhesion molecules, and the mediators released may have excitatory or inhibitory effects on each cell type, with physiological consequences dependent on the type of innervation involved. Of special interest are the disorders of the brain–gut interaction (DBGIs), mainly functional dyspepsia (FD) and irritable bowel syndrome (IBS), in which mucosal eosinophilia and eosinophil activation have been identified. In this review, we summarize the main roles of gastrointestinal eosinophils in supporting gut homeostasis and the evidence available on eosinophil–neuron interactions to bring new insights that support the fundamental role of this neuro-immune crosstalk in maintaining gut health and contributing to the pathophysiology of DBGIs.

Background: Since post-infarction heart failure (HF) determines a great morbidity and mortality, and given the physiopathology implications of advanced glycation end products (AGE) in the genesis of myocardial dysfunction, it was intended to analyze the prognostic value of these molecules in order to predict post-infarction HF development. Methods: A prospective clinical study in patients after first acute coronary syndrome was conducted. The follow-up period was consisted in 1 year. In 194 patients consecutively admitted in the coronary unit for myocardial infarct fluorescent AGE levels were measured. The association between glycaemic parameters and the development of post-infarction HF were analyzed in those patients. Finally, we identified the variables with independent predictor value by performing a multivariate analysis of Hazard ratio for Cox regression. Results: Eleven out of 194 patients (5.6%) developed HF during follow-up (median: 1.0 years [0.8 - 1.5 years]). Even though basal glucose, fructosamine and glycated haemoglobin were significant predictive factors in the univariate analysis, after being adjusted by confounding variables and AGE they lost their statistical signification. Only AGE (Hazard Ratio 1.016, IC 95%: 1.006-1.026; p<0,001), together with NT-proBNP and the infarct extension were predictors for post-infarction HF development, where AGE levels over the median value 5-fold increased the risk of HF development during follow-up. Conclusions: AGE are an independent marker of post-infarction HF development risk.