Your browser doesn't support javascript.
loading
Chronic Leptin Deficiency Improves Tolerance of Physiological Damage and Host-Pathogen Cooperation during Yersinia pseudotuberculosis Infection.
Sanchez, Karina K; Troha, Katia; Mu, Andre; Redford, Samuel E; McCarville, Justin L; Insenga, Arianna; Stengel, Sarah; Lee, Yujung Michelle; Ayres, Janelle S.
Afiliación
  • Sanchez KK; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Troha K; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Mu A; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Redford SE; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • McCarville JL; Division of Biological Sciences, University of California, San Diego, La Jolla, California, USA.
  • Insenga A; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Stengel S; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Lee YM; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
  • Ayres JS; Molecular and Systems Physiology Lab, Gene Expression Lab, Nomis Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studiesgrid.250671.7, La Jolla, California, USA.
Infect Immun ; 90(9): e0024222, 2022 09 15.
Article en En | MEDLINE | ID: mdl-35924898
To combat infections, hosts employ a combination of antagonistic and cooperative defense strategies. The former refers to pathogen killing mediated by resistance mechanisms, while the latter refers to physiological defense mechanisms that promote host health during infection independent of pathogen killing, leading to an apparent cooperation between the host and the pathogen. Previous work has shown that Leptin, a pleiotropic hormone that plays a central role in regulating appetite and energy metabolism, is indispensable for resistance mechanisms, while a role for Leptin signaling in cooperative host-pathogen interactions remains unknown. Using a mouse model of Yersinia pseudotuberculosis (Yptb) infection, an emerging pathogen that causes fever, diarrhea, and mesenteric lymphadenitis in humans, we found that the physiological effects of chronic Leptin-signaling deficiency conferred protection from Yptb infection due to increased host-pathogen cooperation rather than greater resistance defenses. The protection against Yptb infection was independent of differences in food consumption, lipolysis, or fat mass. Instead, we found that the chronic absence of Leptin signaling protects from a shift to lipid utilization during infection that contributes to Yptb lethality. Furthermore, we found that the survival advantage conferred by Leptin deficiency was associated with increased liver and kidney damage. Our work reveals an additional level of complexity for the role of Leptin in infection defense and demonstrates that in some contexts, in addition to tolerating the pathogen, tolerating organ damage is more beneficial for survival than preventing the damage.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Yersinia pseudotuberculosis / Infecciones por Yersinia pseudotuberculosis Límite: Humans Idioma: En Revista: Infect Immun Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Yersinia pseudotuberculosis / Infecciones por Yersinia pseudotuberculosis Límite: Humans Idioma: En Revista: Infect Immun Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos