Heme Oxygenase-1 and Autophagy Linked for Cytoprotection.

BACKGROUND: Heme-oxygenase (HO) catalyzes the main enzymatic step of heme degradation and generates anti-inflammatory end products with protective roles in physiological and pathological situations. The importance of HO in pathological conditions is evidenced by its pharmacological inhibition or genetic blockage in different models of stress such as infection, inflammation and oxidative stress. Under these situations, another well-known protective process triggered is autophagy. Autophagy is a homeostatic process that eliminates defective cytosolic components and organelles, allowing cells and tissues to recover through recycling of functional blocks for anabolic reactions. Recently, studies have demonstrated a link between HO activity and autophagy activation. OBJECTIVE: In this review, we focus on the interplay between HO and autophagy, and highlight its importance in homeostasis maintenance under stress conditions.

Nod-like proteins in inflammation and disease.

The field of innate immunity has undergone an enormous upheaval during the last decade. The discovery of different groups of proteins, called pattern recognition molecules (PRMs), which detect microbial components, so-called pathogen-associated molecular patterns (PAMPs) and trigger protective responses, had a huge impact on the understanding of innate immune responses. Among the PRMs, the intracellular Nod-like receptors (NLRs) have recently been identified as key mediators of inflammatory and immune responses. The NLR family is divided into subfamilies on the basis of their different signal transduction domains, and recent studies have highlighted the role of certain NLRs, including Nod1, Nod2, Nalp3, Ipaf and Naip5, in the detection of intracellular microbes and possibly 'danger signals'. In this review, we summarize the current knowledge on the function of these proteins in immunity and inflammation, with a focus on their participation in different disease pathologies.

Phenotypic properties, drug susceptibility and genetic relatedness of Stenotrophomonas maltophilia clinical strains from seven hospitals in Rio de Janeiro, Brazil.

AIMS: To investigate phenotypic aspects including biotyping, drug susceptibility and production of extracellular enzymes and genetic diversity of Stenotrophomonas maltophilia clinical strains obtained from seven hospitals in Rio de Janeiro, Brazil. METHODS AND RESULTS: Thirty-nine S. maltophilia strains were investigated by biotying, susceptibility testing, extracellular enzymes detection and by randomly amplified polymorphic DNA (RAPD)-PCR. Biotyping distinguished 13 biotypes among 39, and one of them was prevalent. The majority of the strains produced DNase, gelatinase and haemolysin. Protease, lipases and phospholipase C activities were observed in highly variable amounts. None of the strains was elastase producer. The percentage of full susceptibility, by agar dilution, was 100, 94.8, 81.6 and 26.3% for trimethoprim/sulphametoxazole, ticarcillin/clavulanate, ciprofloxacin and ceftazidime, respectively. Thirty-three RAPD-PCR profiles were obtained suggesting multiple sources of acquisition. CONCLUSIONS: The results pointed out the necessity of monitoring S. maltophilia especially in critical hospital wards, to assure effective control measures. SIGNIFICANCE AND IMPACT OF THE STUDY: Despite of the genetic diversity among the strains, in two situations it was observed indistinguishable RAPD-PCR profiles among strains isolated from different patients who had been hospitalized in the same hospital ward, suggesting the possibility of nosocomial transmission that until now has been rarely related.