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Skin wound infections are a significant health problem, and antibiotic resistance is on the rise. Mast cells (MCs) have been shown to contribute to host–defense responses in certain bacterial infections, but their role in skin wound superinfection is unknown. We subjected 2 MC-deficient mouse strains to Pseudomonas aeruginosa skin wound infection and found significantly delayed wound closure in infected skin wounds. This delay was associated with impaired bacterial clearance in the absence of MCs. Engraftment of MCs restored both bacterial clearance and wound closure. Bacterial killing was dependent on IL-6 released from MCs, and engraftment with IL-6–deficient MCs failed to control wound infection. Treatment with recombinant IL-6 enhanced bacterial killing and resulted in the control of wound infection and normal wound healing in vivo. Taken together, our results demonstrate a defense mechanism for boosting host innate immune responses, namely effects of MC-derived IL-6 on antimicrobial functions of keratinocytes.

Mast cells (MCs) are cells of hematopoietic origin that normally reside in mucosal tissues, often near epithelial cells, glands, smooth muscle cells, and nerves. Best known for their contributions to pathology during IgE-associated disorders such as food allergy, asthma, and anaphylaxis, MCs are also thought to mediate IgE-associated effector functions during certain parasite infections. However, various MC populations also can be activated to express functional programs—such as secreting preformed and/or newly synthesized biologically active products—in response to encounters with products derived from diverse pathogens, other host cells (including leukocytes and structural cells), damaged tissue, or the activation of the complement or coagulation systems, as well as by signals derived from the external environment (including animal toxins, plant products, and physical agents). In this review, we will discuss evidence suggesting that MCs can perform diverse effector and immunoregulatory roles that contribute to homeostasis or pathology in mucosal tissues.

SummaryMagnesium has a key role in osteoporosis and could enhance implant osseointegration in osteoporotic patients. Titanium implants impregnated with Mg ions were installed in the tibia of ovariectomized rats. The release of Mg induced a significant increase of bone formation and the expression of anabolic markers in the peri-implant bone.IntroductionThe success of endosseous implants is highly predictable in patients possessing normal bone status, but it may be impaired in patients with osteoporosis. Thus, the application of strategies that adjuvate implant healing in compromized sites is of great interest. Magnesium has a key role in osteoporosis prevention and it is an interesting candidate for this purpose. In this study, the cellular and molecular effects of magnesium release from implants were investigated at the early healing stages of implant integration.MethodsOsteoporosis was induced in 24 female rats by means of ovariectomy and low-calcium diet. Titanium mini-screws were coated with mesoporous titania films and were loaded with magnesium (test group) or left as native (control group). The implants were inserted in the tibia and femur of the rats. One, 2 and 7 days after implantation, the implants were retrieved and histologically examined. In addition, expression of genes was evaluated in the peri-implant bone tissue at day 7 by means of quantitative polymerase chain reactions with pathway-oriented arrays.ResultsThe histological evaluation revealed that new bone formation started already during the first week of healing for both groups. However, around the test implants, new bone was significantly more abundant and spread along a larger surface of the implants. In addition, the release of magnesium induced a significantly higher expression of BMP6.ConclusionsThese results provide evidence that the release of magnesium promoted rapid bone formation and the activation of osteogenic signals in the vicinity of implants placed in osteoporotic bone.

Thanks to their ability to build three-dimensional bioconstructions, Sabellaria worms strongly regulate community structure and ecosystem functioning in coastal ecosystems. Such reefs and the degree of connectivity between them are crucial for identifying population units that are relevant in conservation strategy and management. To help bridge the gap in connectivity information about the Sabellaria alveolata reefs, this study is focused on the genetic characterization of some populations along the Italian coast to compare them with other Mediterranean and Atlantic reefs; explore the correlation between genetic and geographical distances; and infer the extent of connectivity between these populations. Ten reefs were investigated: seven in the Mediterranean and three in the Atlantic. A region of 608 nucleotides in mtCOI was sequenced in six reefs from Tyrrhenian Sea (Latium, Italy) and in a reef from the Atlantic French coast. Sequences from two Portuguese and one Sicily populations were obtained from the Barcode of Life Data (BOLD) Systems database for comparison. The spatial comparative analysis revealed the smallest genetic differences within the Atlantic populations and the greatest differences between the Atlantic and the Mediterranean populations, thus demonstrating a general decrease in genetic similarity with increasing geographical distance, as the genetic distance regression on geographic distance, clustering and ordination analyses supported. A striking genetic distance emerged between the populations of Latium and that of Sicily, showing, in particular, a considerably higher number of differences with Sicily than the Atlantic populations. Our results are in line with the surface circulation entering from Gibraltar, the internal hydrodynamic regime of the Mediterranean and with the concept of cells of ecosystem functioning, that support, on one hand, the internal connectivity between the Tyrrhenian reefs and, on the other hand, a barrier to connectivity between the Sicilian and Tyrrhenian reefs.

▪ Abstract  This review focuses on recent progress in our understanding of how mast cells can contribute to the initiation, development, expression, and regulation of acquired immune responses, both those associated with IgE and those that are apparently expressed independently of this class of Ig. We emphasize findings derived from in vivo studies in mice, particularly those employing genetic approaches to influence mast cell numbers and/or to alter or delete components of pathways that can regulate mast cell development, signaling, or function. We advance the hypothesis that mast cells not only can function as proinflammatory effector cells and drivers of tissue remodeling in established acquired immune responses, but also may contribute to the initiation and regulation of such responses. That is, we propose that mast cells can also function as immunoregulatory cells. Finally, we show that the notion that mast cells have primarily two functional configurations, off (or resting) or on (or activated for extensive mediator release), markedly oversimplifies reality. Instead, we propose that mast cells are “tunable,” by both genetic and environmental factors, such that, depending on the circumstances, the cell can be positioned phenotypically to express a wide spectrum of variation in the types, kinetics, and/or magnitude of its secretory functions.

Key Points Mast cells and basophils are important sources of effector function in IgE-associated immune responses and are also potential sources of immunoregulatory function. The best-understood mechanism for eliciting IgE-dependent effector function in mast cells and basophils is aggregation of FcɛRI, for example, by the crosslinking of FcɛRI-bound IgE with multivalent antigen. Protein-tyrosine kinase (PTK)-mediated activation mechanisms are triggered by FcɛRI aggregation. Several adaptor proteins and enzymes are involved in the activation of crucial signalling pathways, which lead to degranulation, lipid-mediator release, and cytokine and chemokine production and secretion. Inhibitory receptors, such as FcγRIIB, gp49B1, paired immunoglobulin-like receptor B (PIRB) and mast-cell function-associated antigen (MAFA) inhibit cell activation by using their immunoreceptor tyrosine-based inhibitory motifs (ITIMs) to recruit the SH2-domain-containing protein tyrosine phosphatases SHP1 and SHP2, or SH2-domain-containing inositol polyphosphate 5′ phosphatase 1 (SHIP1) and SHIP2. Binding of monomeric IgE to FcɛRI enhances the surface expression of FcɛRI, which is associated with increased sensitivity to antigen challenge and the increased production of mediators and cytokines after FcɛRI aggregation. Binding of monomeric IgE to FcɛRI can also enhance mast-cell survival, although the mechanism(s) that underlies this effect is not fully understood. Mast-cell development and growth are crucially regulated by the survival and developmental factor c-KIT ligand (stem-cell factor, SCF). However, many other cytokines can positively (for example, IL-3, IL-4 and IL-6) or negatively (for example, transforming growth factor-β) affect the survival and/or proliferation of various mast-cell populations. IL-3 is an important basophil survival and developmental factor, and it promotes basophilia in mice in vivo . However, IL-3 is not required for baseline levels of basophil production in mice. Depending on the circumstances, FcɛRI aggregation can enhance mast-cell survival and/or proliferation, promote apoptosis or have neutral effects on survival. Life-versus-death decisions in mast cells are influenced by many endogenous and exogenous factors. Endogenous factors include mast-cell-derived cytokines, cytokine receptors, adhesion molecules, death receptors, caspases, BCL-2-family proteins, intracellular signalling molecules (lipids and proteins) and transcription factors. The effects of IgE on FcɛRI surface expression and survival of mast cells and basophils are additional potential targets for anti-IgE therapy of allergic diseases. Mast cells and basophils are important effector cells in T helper 2 (T H 2)-cell-dependent, immunoglobulin-E-associated allergic disorders and immune responses to parasites. The crosslinking of IgE that is bound to the high-affinity receptor FcɛRI with multivalent antigen results in the aggregation of FcɛRI and the secretion of products that can have effector, immunoregulatory or autocrine effects. This response can be enhanced markedly in cells that have been exposed to high levels of IgE, which results in the increased surface expression of FcɛRI. Moreover, recent work indicates that monomeric IgE (in the absence of crosslinking) can render mast cells resistant to apoptosis induced by growth-factor deprivation in vitro and, under certain circumstances, can induce the release of cytokines. So, the binding of IgE to FcɛRI might influence mast-cell and basophil survival directly or indirectly, and can also regulate cellular function.

This paper focuses on the archaeological and architectural analysis of the Late Roman settlement of Umm al-Dabadib (Kharga Oasis, Egypt). The available information on the archaeological remains of this site includes on-site hand-made sketches, photographs, 3D surveys. The final aim of this specific research is the interpretation and reconstruction of the historical context of this site by combining sources of different nature. This paper presents the methodology employed to elaborate the 3D data in order to achieve a digital restitution of the archaeological map of the entire settlement, which covers an area of about one hectare. The starting point was the elaboration of the close-range photogrammetric survey of the Fortified Settlement that allowed the creation of a 3D point cloud of the whole area, based on the elaboration of over 5,000 photographs, from which a complete and detailed metric model was derived. This 3D model played a key role to extract metric information and to reconstruct the geometrical structure of the settlement, but this result could only be achieved thanks to the successful combination of the digital data with the hand-made sketches and the pictures taken in situ in the recent past. This paper represents an outcome of the project LIFE (Living In a Fringe Environment), funded by the ERC CoGrant 681673.

Purpose The Needs Evaluation Questionnaire (NEQ) is a self-administered instrument with 23 dichotomous items that is used both in oncology clinical practice and in research. It was originally developed for use in setting of hospitalization. The aim of the present study was to assess the factor structure of the NEQ in an outpatient oncology sample and to compare the unmet needs of inpatients and outpatients in the Italian context. Methods In 6 Italian oncology departments, 783 patients completed the NEQ. Patients included in the study had different primary tumor sites and were in different phases of the disease and care process. There were 195 inpatients and 588 outpatients total. Results Confirmatory factor analysis (CFA) showed that, with outpatients, the NEQ retained the distribution of the items in five main areas previously described with inpatients. Cancer outpatients expressed high percentages of unmet needs primarily concerning “material needs” and “needs for psycho-emotional support.” Our survey also suggested that, in addition to the 23 original items, four new items could be tested for specific use with outpatients. Conclusions Our findings highlight the importance of establishing routine assessment of unmet needs also in clinical oncology settings different from wards—such as day hospitals, ambulatory rehabilitation, or follow-up ambulatory care—where, at least in the Italian context, the rate of unmet needs is currently considerably high. The NEQ could be an effective tool for this assessment.

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