Increased geographical distribution and richness of non-native freshwater fish species in Argentina: evidence from a literature review

The present study is a full review of the non-native freshwater fish species introduced into Argentina and their relationship to the main environmental features and introduction vectors of each freshwater ecoregion. The total number of non-native freshwater fish species was compiled through a literature survey; information on spatial–temporal patterns of species records and invasion vectors was retrieved for all ten freshwater ecoregions of Argentina. Our survey revealed that 18–22 non-native fish species had been recorded up to 1999, and a total of 40 introduced fish species, of which 18 are invasive and five potentially invasive, had been registered in seven Argentinean ecoregions as of May 2020. According to georeferenced records, the rainbow trout Oncorhynchus mykiss and common carp Cyprinus carpio were the non-native fish species with the greatest number of records and largest invaded areas, probably due to their species-specific ecological traits. Invasive fish species differed clearly between the Patagonia, Lower Paraná, and Lower Uruguay ecoregions, probably because of a combination of the environmental conditions, structure of native assemblages, and invasion pathways in each ecoregion. Except for the recognized impact of non-native salmonids, the adverse effects of introduced fish species have been little studied, indicating the need for further research to clarify the role of ecological shifts triggered by the introduction and establishment of non-native fish species in Argentina. In contrast to the high diversity of aquatic species and freshwater environments, the spread and impact of invasive fish species in Argentina is little known, particularly compared with other South American countries.Fil: Espínola, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Rabuffetti, Ana Pia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Carrara, Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Abrial, Elie. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Ferlay, Elise Mathilde Charlotte. Polytechnic School Of The University Of Tours; FranciaFil: Yoya, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Blettler, Martin Cesar Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto Nacional de Limnología. Universidad Nacional del Litoral. Instituto Nacional de Limnología; ArgentinaFil: Baigún, Claudio Rafael M.. Universidad Nacional de San Martín. Instituto de Investigación e Ingeniería Ambiental. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigación e Ingeniería Ambiental; ArgentinaFil: Wantzen, Karl Matthias. Centre National de la Recherche Scientifique; FranciaFil: Neves dos Santos, Luciano. Universidade Federal do Estado do Rio de Janeiro; Brasi

Caractérisation de la polarisation des macrophages pulmonaires humains et voies de régulation

In pulmonary diseases such as asthma and chronic obstructive pulmonary disease, macrophages orchestrate inflammatory reactions. In response to environmental signals, macrophages exhibit a phenotypic polarization that mirrors the Th1/Th2 polarization. Upon exposure to bacterial lipopolysaccharide (LPS), macrophages undergo M1 polarization. In contrast, interleukin (IL)-4/IL-13 induce M2 polarization.In our first study, we characterized the phenotypic differentiation of human lung macrophages (LM) using a whole-transcriptome approach. Cytokines, lipid metabolism and membrane markers were among the most affected genes. LPS-induced M1 polarization was associated with an increase in the production of cytokines (TNF-α, IL-1β, CCL2, 3, 4, 5, CXCL1, 8, 10), in PGE2 signalling and in the expression of CD38 and CD197. IL-4/IL-13-induced M2 macrophages increased expression of cytokines (CCL13, 17, 22, 26), 15-lipoxygenase (15-LOX) and CD206. In the second study, we investigated the expression of 15-LOX-1 and 15-LOX-2 and their roles in regulating the polarization of human LM. LPS increased the expression of 15-LOX-2 whereas IL-4/IL-13 induced the expression of 15-LOX-1. Inhibition of the 15-LOX pathways decreased the production of both M1 and M2 cytokines. The third study investigated the expression of α7 nicotinic receptors (α7nAChR) and their regulating roles in the polarization of LM. Expression of α7nAChR was found in unstimulated LM. Specific α7nAChR agonists decreased the in vitro production of both M1 and M2 cytokines. Our work adds new insights in the macrophage polarization and some of the regulatory pathways that may be involved in pulmonary diseasesLes macrophages jouent un rôle dans l'inflammation de certaines pathologies pulmonaires comme l'asthme et la broncho pneumopathie chronique obstructive. Selon la dichotomie Th1 et Th2, les macrophages s'activent en phénotype M1/M2 en fonction du microenvironnement. Sous l'influence du lipopolysaccharide (LPS) les macrophages s'activent en phénotype M1. A l'inverse, l'exposition aux cytokines Th2 (interleukine (IL)-4/IL-13) induit un phénotype M2 des macrophages. Nous avons réalisé une étude transcriptomique des marqueurs de la polarisation M1/M2 des macrophages pulmonaires humains. La polarisation M1 induite par le LPS augmente la production des cytokines (TNF-α, IL-1β, CCL2, 3, 4, 5, CXCL1, 8, 10), de la PGE2 et l'expression du CD38 et CD197. La polarisation M2 induite par l'IL-4/IL-13 augmente l'expression des cytokines (CCL13, 17, 22, 26), de la 15-lipoxygénase (15-LOX) et du CD206. Nous avons évalué l'expression des 15-LOX-1 et 15-LOX-2 et leur rôle dans la régulation de la polarisation des macrophages pulmonaires. Le LPS augmente l'expression de la 15-LOX-2 alors que l'IL-4/IL-13 augmente l'expression de la 15-LOX-1. L'inhibition des 15-lipoxygénases diminue la production des cytokines M1/M2. Enfin, nous avons étudié l'expression et le rôle du récepteur nicotinique α7 dans la polarisation des macrophages pulmonaires humains. Ces derniers expriment les récepteurs nicotiniques α7 dont la stimulation par des agonistes nicotiniques α7 diminue la production des cytokines M1/M2. Ce travail apporte de nouvelles connaissances sur la polarisation des macrophages, dont certaines voies de régulation peuvent être impliquées dans les pathologies inflammatoire pulmonaire

Phenotypic characterization of polarized in vitro human lung macrophages and regulatory pathways

Les macrophages jouent un rôle dans l'inflammation de certaines pathologies pulmonaires comme l'asthme et la broncho pneumopathie chronique obstructive. Selon la dichotomie Th1 et Th2, les macrophages s'activent en phénotype M1/M2 en fonction du microenvironnement. Sous l'influence du lipopolysaccharide (LPS) les macrophages s'activent en phénotype M1. A l'inverse, l'exposition aux cytokines Th2 (interleukine (IL)-4/IL-13) induit un phénotype M2 des macrophages. Nous avons réalisé une étude transcriptomique des marqueurs de la polarisation M1/M2 des macrophages pulmonaires humains. La polarisation M1 induite par le LPS augmente la production des cytokines (TNF-α, IL-1β, CCL2, 3, 4, 5, CXCL1, 8, 10), de la PGE2 et l'expression du CD38 et CD197. La polarisation M2 induite par l'IL-4/IL-13 augmente l'expression des cytokines (CCL13, 17, 22, 26), de la 15-lipoxygénase (15-LOX) et du CD206. Nous avons évalué l'expression des 15-LOX-1 et 15-LOX-2 et leur rôle dans la régulation de la polarisation des macrophages pulmonaires. Le LPS augmente l'expression de la 15-LOX-2 alors que l'IL-4/IL-13 augmente l'expression de la 15-LOX-1. L'inhibition des 15-lipoxygénases diminue la production des cytokines M1/M2. Enfin, nous avons étudié l'expression et le rôle du récepteur nicotinique α7 dans la polarisation des macrophages pulmonaires humains. Ces derniers expriment les récepteurs nicotiniques α7 dont la stimulation par des agonistes nicotiniques α7 diminue la production des cytokines M1/M2. Ce travail apporte de nouvelles connaissances sur la polarisation des macrophages, dont certaines voies de régulation peuvent être impliquées dans les pathologies inflammatoire pulmonairesIn pulmonary diseases such as asthma and chronic obstructive pulmonary disease, macrophages orchestrate inflammatory reactions. In response to environmental signals, macrophages exhibit a phenotypic polarization that mirrors the Th1/Th2 polarization. Upon exposure to bacterial lipopolysaccharide (LPS), macrophages undergo M1 polarization. In contrast, interleukin (IL)-4/IL-13 induce M2 polarization.In our first study, we characterized the phenotypic differentiation of human lung macrophages (LM) using a whole-transcriptome approach. Cytokines, lipid metabolism and membrane markers were among the most affected genes. LPS-induced M1 polarization was associated with an increase in the production of cytokines (TNF-α, IL-1β, CCL2, 3, 4, 5, CXCL1, 8, 10), in PGE2 signalling and in the expression of CD38 and CD197. IL-4/IL-13-induced M2 macrophages increased expression of cytokines (CCL13, 17, 22, 26), 15-lipoxygenase (15-LOX) and CD206. In the second study, we investigated the expression of 15-LOX-1 and 15-LOX-2 and their roles in regulating the polarization of human LM. LPS increased the expression of 15-LOX-2 whereas IL-4/IL-13 induced the expression of 15-LOX-1. Inhibition of the 15-LOX pathways decreased the production of both M1 and M2 cytokines. The third study investigated the expression of α7 nicotinic receptors (α7nAChR) and their regulating roles in the polarization of LM. Expression of α7nAChR was found in unstimulated LM. Specific α7nAChR agonists decreased the in vitro production of both M1 and M2 cytokines. Our work adds new insights in the macrophage polarization and some of the regulatory pathways that may be involved in pulmonary disease

The Role of Toll-Like Receptors in the Production of Cytokines by Human Lung Macrophages

International audienceBackground: The Toll-like receptor (TLR) family is involved in the recognition of and response to microbial infections. These receptors are expressed in leukocytes. TLR stimulation induces the production of proinflammatory cytokines and chemokines. Given that human lung macrophages (LMs) constitute the first line of defense against inhaled pathogens, the objective of this study was to investigate the expression and function of TLR subtypes in this cell population. Methods: Human primary LMs were obtained from patients undergoing surgical resection. The RNA and protein expression levels of TLRs, chemokines, and cytokines were assessed after incubation with subtype-selective agonists. Results: In human LMs, the TLR expression level varied from one subtype to another. Stimulation with subtype-selective agonists induced an intense, concentration- and time-dependent increase in the production of chemokines and cytokines. TLR4 stimulation induced the strongest effect, whereas TLR9 stimulation induced a much weaker response. Conclusions: The stimulation of TLRs in human LMs induces intense cytokine and chemokine production, a characteristic of the proinflammatory M1 macrophage phenotype. © 2018 The Author(s). Published by S. Karger AG, Basel

Comparison of the in vitro pharmacological profiles of long-acting muscarinic antagonists in human bronchus

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Adiponectin Inhibits the Production of TNF-α, IL-6 and Chemokines by Human Lung Macrophages

International audienceBackground: Obesity is associated with an elevated risk of severe respiratory infections and inflammatory lung diseases. The objectives were to investigate 1) the production of adiponectin by human lung explants, 2) the expression of the adiponectin receptors AdipoR1 and AdipoR2 by human lung macrophages (LMs), and 3) the impact of recombinant human adiponectin and a small-molecule APN receptor agonist (AdipoRon) on LMs activation. Material and methods: Human parenchyma explants and LMs were isolated from patients operated for carcinoma. The LMs were cultured with recombinant adiponectin or AdipoRon and stimulated with lipopolysaccharide (10 ng ml −1 ), poly (I:C) (10 µg ml −1 ) or interleukin (IL)-4 (10 ng ml −1 ) for 24 h. Cytokines or adiponectin, released by explants or LMs, were measured using ELISAs. The mRNA levels of AdipoR1 and AdipoR2 were determined using real-time quantitative PCR. AdipoRs expression was also assessed with confocal microscopy. Results: Adiponectin was released by lung explants at a level negatively correlated with the donor’s body mass index. AdipoR1 and AdipoR2 were both expressed in LMs. Adiponectin (3–30 µg ml −1 ) and AdipoRon (25–50 μM) markedly inhibited the LPS- and poly (I:C)-induced release of Tumor Necrosis Factor-α, IL-6 and chemokines (CCL3, CCL4, CCL5, CXCL1, CXCL8, CXCL10) and the IL-4-induced release of chemokines (CCL13, CCL17, CCL22) in a concentration-dependent manner. Recombinant adiponectin produced in mammalian cells (lacking low molecular weight isoforms) had no effects on LMs. Conclusion and implications: The low-molecular-weight isoforms of adiponectin and AdipoRon have an anti-inflammatory activity in the lung environment. Targeting adiponectin receptors may constitute a new means of controlling airways inflammation

Laligation native simplifie l’étude de l’activité etdu mécanismed’action des peptides antimicrobiens à multiples domaines :cas des Big défensines d’huître.

International audienceLesBigdéfensinesd'invertébrésmarinssontdespetitesprotéinesantimicrobiennesdontlastructureparticulièrementoriginaleassocieundomaineN-terminalglobulaireàundomaineC-terminalsemblableauxβ-défensinesdevertébrés.LapremièreBigdéfensineaétédécritechez un chélicérate ancestral, la Limule. Depuis, ces molécules ont été identifiées dansdiverses espèces de mollusques bivalves, notamment les huitres chez lesquelles plusieursformes ont été décrites. Certaines de ces formes, comme la Cg-BigDef1, voient leurexpressiontrèsfortementinduiteenréponseàl'infectionmicrobienne,laissantsupposerunrôle majeur dans la défense antimicrobienne des huitres. Nous avons ici entrepris decaractériserl’activitéantimicrobiennedelaCg-BigDef1etdesesdeuxdomainesstructurauxisolés. Pour cela nous avons synthétisé les deux domaines et la molécule entière parsynthèse en phase solide et ligation native (NCL) en s’appuyant sur une méthodologierécemment développée pour la synthèse du partenaire thioester. Les résultats obtenusmontrent que la Cg-BigDef1 est microbicide sur un large spectre de bactéries et dechampignons filamenteux, incluant des pathogènes des huitres du genre Vibrio. NousobservonségalementdepuissantesactivitésantimicrobiennessurdessouchescliniquesdeStaphylocoques isolées de patients mucoviscidosiques et posant des problèmes demultirésistance aux antibiotiques (MRSA). Ces activités sont stables à salinité élevée.L’activitédesdeuxdomainesséparésestglobalement très faiblepar rapportàlamoléculeentièreetcesdeuxdomainesdéploientdesactivitéssynergiques.Enfin,auxconcentrationsminimales inhibitrices, laCg-BigDef1 induit seulement la perméabilisation desmembranesdesbactériesàGramnégatifalorsquesondomaineglobulaireN-terminalseulperméabiliselesmembranesdesbactériesàGrampositifetdesbactériesà Gramnégatif

Hippocampal expression of a virus-derived protein impairs memory in mice

International audienceThe analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the natural property of a viral protein identified as a major effector of behavioral disorders during infection. We used the phosphoprotein (P) of Borna disease virus, which acts as a decoy substrate for protein kinase C (PKC) when expressed in neurons and disrupts synaptic plasticity. By a lentiviral-based strategy, we directed the singled-out expression of P in the dentate gyrus of the hippocampus and we examined its impact on mouse behavior. Mice expressing the P protein displayed increased anxiety and impaired long-term memory in contextual and spatial memory tasks. Interestingly, these effects were dependent on P protein phosphorylation by PKC, as expression of a mutant form of P devoid of its PKC phosphorylation sites had no effect on these behaviors. We also revealed features of behavioral impairment induced by P protein expression but that were independent of its phosphorylation by PKC. Altogether, our findings provide insight into the behavioral correlates of viral infection , as well as into the impact of virus-mediated alterations of the PKC pathway on behavioral functions. dentate gyrus | hippocampus | virus | memory | protein kinase