| 1. |
- Barouki, Robert, et al.
(författare)
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The COVID-19 pandemic and global environmental change : Emerging research needs
- 2021
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Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 146
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Tidskriftsartikel (refereegranskat)abstract
- The outbreak of COVID-19 raised numerous questions on the interactions between the occurrence of new infections, the environment, climate and health. The European Union requested the H2020 HERA project which aims at setting priorities in research on environment, climate and health, to identify relevant research needs regarding Covid-19. The emergence and spread of SARS-CoV-2 appears to be related to urbanization, habitat destruction, live animal trade, intensive livestock farming and global travel. The contribution of climate and air pollution requires additional studies. Importantly, the severity of COVID-19 depends on the interactions between the viral infection, ageing and chronic diseases such as metabolic, respiratory and cardiovascular diseases and obesity which are themselves influenced by environmental stressors. The mechanisms of these interactions deserve additional scrutiny. Both the pandemic and the social response to the disease have elicited an array of behavioural and societal changes that may remain long after the pandemic and that may have long term health effects including on mental health. Recovery plans are currently being discussed or implemented and the environmental and health impacts of those plans are not clearly foreseen. Clearly, COVID-19 will have a longlasting impact on the environmental health field and will open new research perspectives and policy needs.
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| 2. |
- Destoumieux-Garzón, Delphine, et al.
(författare)
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Resistance to antimicrobial peptides in vibrios
- 2010
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Ingår i: Antibiotics. - : MDPI. - 0066-4774 .- 2079-6382. ; 3:4, s. 540-563
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Forskningsöversikt (refereegranskat)abstract
- Vibrios are associated with a broad diversity of hosts that produce antimicrobial peptides (AMPs) as part of their defense against microbial infections. In particular, vibrios colonize epithelia, which function as protective barriers and express AMPs as a first line of chemical defense against pathogens. Recent studies have shown they can also colonize phagocytes, key components of the animal immune system. Phagocytes infiltrate infected tissues and use AMPs to kill the phagocytosed microorganisms intracellularly, or deliver their antimicrobial content extracellularly to circumvent tissue infection. We review here the mechanisms by which vibrios have evolved the capacity to evade or resist the potent antimicrobial defenses of the immune cells or tissues they colonize. Among their strategies to resist killing by AMPs, primarily vibrios use membrane remodeling mechanisms. In particular, some highly resistant strains substitute hexaacylated Lipid A with a diglycine residue to reduce their negative surface charge, thereby lowering their electrostatic interactions with cationic AMPs. As a response to envelope stress, which can be induced by membrane-active agents including AMPs, vibrios also release outer membrane vesicles to create a protective membranous shield that traps extracellular AMPs and prevents interaction of the peptides with their own membranes. Finally, once AMPs have breached the bacterial membrane barriers, vibrios use RND efflux pumps, similar to those of other species, to transport AMPs out of their cytoplasmic space.
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| 3. |
- LeRoux, Frederique, et al.
(författare)
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The emergence of Vibrio pathogens in Europe : ecology, evolution, and pathogenesis (Paris, 11-12th March 2015)
- 2015
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Ingår i: Frontiers in Microbiology. - : Frontiers Media SA. - 1664-302X. ; 6
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Tidskriftsartikel (refereegranskat)abstract
- Global change has caused a worldwide increase in reports of Vibrio-associated diseases with ecosystem-wide impacts on humans and marine animals. In Europe, higher prevalence of human infections followed regional climatic trends with outbreaks occurring during episodes of unusually warm weather. Similar patterns were also observed in Vibrio-associated diseases affecting marine organisms such as fish, bivalves and corals. Basic knowledge is still lacking on the ecology and evolutionary biology of these bacteria as well as on their virulence mechanisms. Current limitations in experimental systems to study infection and the lack of diagnostic tools still prevent a better understanding of Vibrio emergence. A major challenge is to foster cooperation between fundamental and applied research in order to investigate the consequences of pathogen emergence in natural Vibrio populations and answer federative questions that meet societal needs. Here we report the proceedings of the first European workshop dedicated to these specific goals of the Vibrio research community by connecting current knowledge to societal issues related to ocean health and food security.
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| 4. |
- Schmitt, Paulina, et al.
(författare)
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Immune responses in the Pacific oyster Crassostrea gigas : an overview with focus on summer mortalities
- 2012
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Ingår i: Oysters. - : Nova Science Publishers, Inc.. - 9781621005186 - 1621005186 - 9781621005575 ; , s. 227-273
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Bokkapitel (refereegranskat)abstract
- The Pacific oyster Crassostrea gigas is an important cultured species whose production has suffered from recurrent summer mortality events worldwide over the past two decades. In France, these mortality outbreaks have become devastating for the production of juvenile stages since 2008, and have resulted in great economic losses that currently threaten this activity. Studies on oyster immunity have been performed to better understand its response to pathogens, in particular to bacteria of the Vibrio genus and Herpes viruses, both found in moribund oysters. The immune response of C. gigas relies entirely on the innate immune system, in which hemocytes, the oyster circulating blood cells, are the main cellular mediators of the defense system. Activated when pathogen-associated molecular patterns are recognized by plasma soluble or cell surface pattern recognition receptors, hemocytes operate in a coordinated manner with soluble factors in the hemolymph to circumvent the infection. Over the past years, research efforts have substantially increased the knowledge of the molecular bases of oyster immunity, from non-self recognition proteins, to cytokines, signaling pathways and defense effectors including protease inhibitors, hydrolytic enzymes and antimicrobial peptides/proteins. This review describes the present state of our knowledge on the cellular and molecular effectors of oyster immunity, and describes the oyster responses to pathogenic Vibrio and Herpes species.
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| 5. |
- Vanhove, Audrey Sophie, et al.
(författare)
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Outer membrane vesicles are vehicles for the delivery of Vibrio tasmaniensis virulence factors to oyster immune cells
- 2015
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Ingår i: Environmental Microbiology. - : Wiley. - 1462-2912 .- 1462-2920. ; 17:4, s. 1152-1165
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Tidskriftsartikel (refereegranskat)abstract
- VibriotasmaniensisLGP32, a facultative intracellular pathogen of oyster haemocytes, was shown here to release outer membrane vesicles (OMVs) both in the extracellular milieu and inside haemocytes. Intracellular release of OMVs occurred inside phagosomes of intact haemocytes having phagocytosed few vibrios as well as in damaged haemocytes containing large vacuoles heavily loaded with LGP32. The OMV proteome of LGP32 was shown to be rich in hydrolases (25%) including potential virulence factors such as proteases, lipases, phospholipases, haemolysins and nucleases. One major caseinase/gelatinase named Vsp for vesicular serine protease was found to be specifically secreted through OMVs in which it is enclosed. Vsp was shown to participate in the virulence phenotype of LGP32 in oyster experimental infections. Finally, OMVs were highly protective against antimicrobial peptides, increasing the minimal inhibitory concentration of polymyxin B by 16-fold. Protection was conferred by OMV titration of polymyxin B but did not depend on the activity of Vsp or another OMV-associated protease. Altogether, our results show that OMVs contribute to the pathogenesis of LGP32, being able to deliver virulence factors to host immune cells and conferring protection against antimicrobial peptides.
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