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RISS 인기검색어
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- 저자 : Aucouturier, (검색결과 3 건)
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Allergic Sensitization Driving Immune Phenotyping and Disease Severity in a Mouse Model of Asthma
Dijoux Eléonore,Klein Martin,Misme-Aucouturier Barbara,Cheminant Marie-Aude,de Carvalho Marion,Collin Louise,Hassoun Dorian,Delage Erwan,Gourdel Mathilde,Loirand Gervaise,Sauzeau Vincent,Magnan Antoin 대한천식알레르기학회 2023 Allergy, Asthma & Immunology Research Vol.15 No.2
Purpose: Asthma is a frequent chronic inflammatory bronchial disease affecting more than 300 million patients worldwide, 70% of whom are secondary to allergy. The diversity of asthmatic endotypes contributes to their complexity. The inter-relationship between allergen and other exposure and the airway microbiome adds to the phenotypic diversity and defines the natural course of asthma. Here, we compared the mouse models of house dust mite (HDM)-induced allergic asthma. Allergic sensitization was performed via various routes and associated with outcomes. Methods: Mice were sensitized with HDM via the oral, nasal or percutaneous routes. Lung function, barrier integrity, immune response and microbiota composition were analyzed. Results: Severe impairment of respiratory function was observed in the mice sensitized by the nasal and cutaneous paths. It was associated with epithelial dysfunction characterized by an increased permeability secondary to junction protein disruption. Such sensitization paths induced a mixed eosinophilic and neutrophilic inflammatory response with high interleukin (IL)-17 airway secretion. In contrast, orally sensitized mice showed a mild impairment of respiratory function. Epithelial dysfunction was mild with increased mucus production, but preserved epithelial junctions. Regarding lung microbiota, sensitization provoked a significant loss of diversity. At the genus level, Cutibacterium, Acinetobacter, Streptococcus and Lactobacillus were found to be modulated according to the sensitization pathway. An increase in theanti-inflammatory microbiota metabolites was observed in the oral-sensitization group. Conclusions: Our study highlights the strong impact of the sensitization route on the pathophysiology and the critical phenotypic diversity of allergic asthma in a mouse model.
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Conformation as a Therapeutic Target in the Prionoses and other Neurodegenerative Conditions
Wisniewski, Thomas,Sigurdsson, Einar M.,Aucouturier, Pierre,Frangione, B. 한림대학교 환경·생명과학연구소 2000 국제학술회의 Vol.2000 No.-
Abnormal protein conformation is increasingly being recognized as part of the pathogenesis of numerous neurodegenerative conditions. The common theme in all these diseases is the conversion of a normal cellular and/or circulating protein into an insoluble, aggregated, β-sheet rich form which is deposited in the brain. The aggregated proteins can accumulate extracellularly, often in the form of amyloid, or intracellularly producing inclusion bodies. These deposits are toxic and produce neuronal dysfunction and death. A unique category of the conformational conditions are prion related diseases(or prionoses), where the etiology is thought to be related to conversion of the normal prion protein, PrP□ ,into an infectious and pathogenic form, PrP□. However, the most common of these disorders is Alzheimer's disease(AD) where the central events is thought to be the conversion of normal soluble amyloid(sAβ) into fibrillar Aβin the form of neuritic plaques and congophilic angiopathy. Our growing understanding of the mechanisms involved in this category of disease, raises the possibility of therapeutic approaches based directly on the prevention and reversal of pathologic protein conformations. Possible approaches include synthetic β-sheet breaker peptides, which our preliminary data suggest may be useful for both AD and the prionoses, as well as immunological approaches where an antibody and/or cell mediated response is triggered against the aggregating abnormal protein.
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Conformation as a Therapeutic Target in the Prionoses and other Neurodegenerative Conditions
Wisniewski, Thomas,Sigurdsson, Einar M.,Aucouturier, Pierre,Frangione, B. 한림대학교 환경·생명과학연구소 2000 [일송 국제심포지엄] 노화와 만성퇴행성 신경질환 Vol.- No.3
Abnormal protein conformation is increasingly being recognized as part of the pathogenesis of numerous neurodegenerative conditions. The common theme in all these diseases is the conversion of a normal cellular and/or circulation protein into an insoluble, aggregated, β-sheet rich form which is deposited in the brain. The aggregated proteins can accumulate extracellularly, often in the form of amyloid, or intracellularly producing inclusion bodies. These deposits are toxic and produce neuronal dysfunction and death. A unique category of the conformational conditions are prion related diseases (or prionoses), where the etiology is thought to be related to conversion of the normal prion protein, PrP^c, into an infectious and pathogenic form, PrP^Sc. However, the most common of these disorders is Alzheimer's disease (AD) where the central event is thought to be the conversion of normal soluble amyloid (sAβ) into fibrillar Aβ in the form of neuritic plaques and congophilic angiopathy. Our growing understanding of the mechanisms involved in this category of disease, raises the pathologic protein conformations. Possible approaches include synthetic β-sheet breaker peptides, which our preliminary data suggest may be useful for both AD and the prionoses, as well as immunological approaches where an antibody and/or cell mediated response is triggered against the aggregation abnormal protein.
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