Identification of Adipose Tissue as a Reservoir of Macrophages after Acute Myocardial Infarction

Medullary and extra-medullary hematopoiesis has been shown to govern inflammatory cell infiltration and subsequently cardiac remodeling and function after acute myocardial infarction (MI). Emerging evidence positions adipose tissue (AT) as an alternative source of immune cell production. We, therefore, hypothesized that AT could act as a reservoir of inflammatory cells that participate in cardiac homeostasis after MI. To reveal the distinct role of inflammatory cells derived from AT or bone marrow (BM), chimeric mice were generated using standard repopulation assays. We showed that AMI increased the number of AT-derived macrophages in the cardiac tissue. These macrophages exhibit pro-inflammatory characteristics and their specific depletion improved cardiac function as well as decreased infarct size and interstitial fibrosis. We then reasoned that the alteration of AT-immune compartment in type 2 diabetes could, thus, contribute to defects in cardiac remodeling. However, in these conditions, myeloid cells recruited in the infarcted heart mainly originate from the BM, and AT was no longer used as a myeloid cell reservoir. Altogether, we showed here that a subpopulation of cardiac inflammatory macrophages emerges from myeloid cells of AT origin and plays a detrimental role in cardiac remodeling and function after MI. Diabetes abrogates the ability of AT-derived myeloid cells to populate the infarcted heart.     

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Wireless Personal Communications - Ever since the branching of the sustainable and circular literature on business models of the late 2000s and early 2010´s, academia´s, businesses and...     

Analysis of the Phospholipid Profile of the Collection Strain PAO1 and Clinical Isolates of Pseudomonas aeruginosa in Relation to Their Attachment Capacity

Bacteria form multicellular and resistant structures named biofilms. Biofilm formation starts with the attachment phase, and the molecular actors involved in this phase, except adhesins, are poorly characterized. There is growing evidence that phospholipids are more than simple structural bricks. They are involved in bacterial adaptive physiology, but little is known about their role in biofilm formation. Here, we report a mass spectrometry analysis of the phospholipid (PL) profile of several strains of Pseudomonas aeruginosa isolated from cystic fibrosis patients. The aim of our study was to evaluate a possible link between the PL profile of a strain and its attachment phenotype. Our results showed that PL profile is strongly strain-dependent. The PL profile of P. aeruginosa PAO1, a collection strain, was different from those of 10 clinical isolates characterized either by a very low or a very high attachment capacity. We observed also that the clinical strain’s PL profiles varied even more importantly between isolates. By comparing groups of strains having similar attachment capacities, we identified one PL, PE 18:1-18:1, as a potential molecular actor involved in attachment, the first step in biofilm formation. This PL represents a possible target in the fight against biofilms.     

Use of honey bees (Apis mellifera L.) to detect the presence of Mediterranean fruit fly (Ceratitis capitata Wiedemann) larvae in Valencia oranges

BACKGROUND: When fruit deteriorates a characteristic profile of volatile chemicals is produced that is different from that produced by healthy fruits. The identification of such chemicals allows the possibility of monitoring the fruit for early signs of deterioration with biological sensors. The use of honey bees and other insects as biological sensors is well known. This study aimed to identify the volatiles produced by oranges infested with larvae of the Mediterranean fruit fly and to test the ability of honey bees, conditioned to this volatile chemical profile, to detect such oranges. RESULTS: Seventeen compounds that were present in higher concentrations in the volatile profiles of infested oranges than in those of insect‐free fruits were mixed at the same relative concentrations as those in the collected volatiles of infested oranges. The synthetic mixture was used to train honey bees by classical Pavlovian conditioning and subsequent tests showed that they were then able to discriminate between medfly‐infested and uninfested oranges. CONCLUSION: This study demonstrates an innovative way of detecting, at an early stage, the symptoms of damage to oranges by the Mediterranean fruit fly. Copyright © 2012 Society of Chemical Industry     

Biocontrol of Biofilm Formation: Jamming of Sessile-Associated Rhizobial Communication by Rhodococcal Quorum-Quenching

Biofilms are complex structures formed by a community of microbes adhering to a surface and/or to each other through the secretion of an adhesive and protective matrix. The establishment of these structures requires a coordination of action between microorganisms through powerful communication systems such as quorum-sensing. Therefore, auxiliary bacteria capable of interfering with these means of communication could be used to prevent biofilm formation and development. The phytopathogen Rhizobium rhizogenes, which causes hairy root disease and forms large biofilms in hydroponic crops, and the biocontrol agent Rhodococcus erythropolis R138 were used for this study. Changes in biofilm biovolume and structure, as well as interactions between rhizobia and rhodococci, were monitored by confocal laser scanning microscopy with appropriate fluorescent biosensors. We obtained direct visual evidence of an exchange of signals between rhizobia and the jamming of this communication by Rhodococcus within the biofilm. Signaling molecules were characterized as long chain (C₁₄) N-acyl-homoserine lactones. The role of the Qsd quorum-quenching pathway in biofilm alteration was confirmed with an R. erythropolis mutant unable to produce the QsdA lactonase, and by expression of the qsdA gene in a heterologous host, Escherichia coli. Finally, Rhizobium biofilm formation was similarly inhibited by a purified extract of QsdA enzyme.     

Np(V) and Pu(v) ion exchange and surface-mediated reduction mechanisms on montmorillonite

Due to their ubiquity and chemical reactivity, aluminosilicate clays play an important role in actinide retardation and colloid-facilitated transport in the environment. In this work, Pu(V) and Np(V) sorption to Na-montmorillonite was examined as a function of ionic strength, pH, and time. Np(V) sorption equilibrium was reached within 2 h. Sorption was relatively weak and showed a pH and ionic strength dependence. An approximate NpO(2)(+) → Na(+) Vanselow ion exchange coefficient (Kv) was determined on the basis of Np(V) sorption in 0.01 and 1.0 M NaCl solutions at pH < 5 (Kv ~ 0.3). In contrast to Np(V), Pu(V) sorption equilibrium was not achieved on the time-scale of weeks. Pu(V) sorption was much stronger than Np(V), and sorption rates exhibited both a pH and ionic strength dependence. Differences in Np(V) and Pu(V) sorption behavior are indicative of surface-mediated transformation of Pu(V) to Pu(IV) which has been reported for a number of redox-active and redox-inactive minerals. A model of the pH and ionic strength dependence of Pu(V) sorption rates suggests that H(+) exchangeable cations facilitate Pu(V) reduction. While surface complexation may play a dominant role in Pu sorption and colloid-facilitated transport under alkaline conditions, results from this study suggest that Pu(V) ion exchange and surface-mediated reduction to Pu(IV) can immobilize Pu or enhance its colloid-facilitated transport in the environment at neutral to mildly acidic pHs.     

Fault Analysis and Evaluation of a True Random Number Generator Embedded in a Processor

True Random Number Generators have many uses, in particular they play a key role in security applications and cryptographic algorithms. Our interest lies in the quality of their generated random numbers. More specifically, for such utilizations, a slight deviation of the numbers from a “perfect” behavior can have disastrous consequences. It is then necessary to devise schemes for the testing of these generators in order to detect non-random properties of their numbers. Moreover, one should consider them from an attacker point of view and use any means to try to perturbate their good functionnality. In this article we describe such experiments and several standard statistical tools for the generators testing. We also present experimental results obtained through the study of a generator embedded in a processor in order to illustrate our methodology. We show that its pertubation leads to the apparition of dangerous deviations in its numbers distribution.     

Acute exposure to silica nanoparticles enhances mortality and increases lung permeability in a mouse model of Pseudomonas aeruginosa pneumonia

Background

The lung epithelium constitutes the first barrier against invading pathogens and also a major surface potentially exposed to nanoparticles. In order to ensure and preserve lung epithelial barrier function, the alveolar compartment possesses local defence mechanisms that are able to control bacterial infection. For instance, alveolar macrophages are professional phagocytic cells that engulf bacteria and environmental contaminants (including nanoparticles) and secrete pro-inflammatory cytokines to effectively eliminate the invading bacteria/contaminants. The consequences of nanoparticle exposure in the context of lung infection have not been studied in detail. Previous reports have shown that sequential lung exposure to nanoparticles and bacteria may impair bacterial clearance resulting in increased lung bacterial loads, associated with a reduction in the phagocytic capacity of alveolar macrophages.

Results

Here we have studied the consequences of SiO₂ nanoparticle exposure on Pseudomonas aeruginosa clearance, Pseudomonas aeruginosa-induced inflammation and lung injury in a mouse model of acute pneumonia. We observed that pre-exposure to SiO₂ nanoparticles increased mice susceptibility to lethal pneumonia but did not modify lung clearance of a bioluminescent Pseudomonas aeruginosa strain. Furthermore, internalisation of SiO₂ nanoparticles by primary alveolar macrophages did not reduce the capacity of the cells to clear Pseudomonas aeruginosa. In our murine model, SiO₂ nanoparticle pre-exposure preferentially enhanced Pseudomonas aeruginosa-induced lung permeability (the latter assessed by the measurement of alveolar albumin and IgM concentrations) rather than contributing to Pseudomonas aeruginosa-induced lung inflammation (as measured by leukocyte recruitment and cytokine concentration in the alveolar compartment).

Conclusions

We show that pre-exposure to SiO₂ nanoparticles increases mice susceptibility to lethal pneumonia but independently of macrophage phagocytic function. The deleterious effects of SiO₂ nanoparticle exposure during Pseudomonas aeruginosa-induced pneumonia are related to alterations of the alveolar-capillary barrier rather than to modulation of the inflammatory responses.

Electronic supplementary material

The online version of this article (doi:10.1186/s12989-014-0078-9) contains supplementary material, which is available to authorized users.