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Inflammaging phenotype in rhesus macaques is associated with a decline in epithelial barrier-protective functions and increased pro-inflammatory function in CD161-expressing cells.
Walker, Edith M; Slisarenko, Nadia; Gerrets, Giovanni L; Kissinger, Patricia J; Didier, Elizabeth S; Kuroda, Marcelo J; Veazey, Ronald S; Jazwinski, S Michal; Rout, Namita.
Afiliación
  • Walker EM; Division of Microbiology, Tulane National Primate Research Center, Covington, LA, USA.
  • Slisarenko N; Division of Microbiology, Tulane National Primate Research Center, Covington, LA, USA.
  • Gerrets GL; Division of Microbiology, Tulane National Primate Research Center, Covington, LA, USA.
  • Kissinger PJ; School of Public Health & Tropical Medicine, Tulane University, New Orleans, LA, USA.
  • Didier ES; Center for Comparative Medicine and California National Primate Research Center, University of California Davis, Davis, CA, USA.
  • Kuroda MJ; Center for Comparative Medicine and California National Primate Research Center, University of California Davis, Davis, CA, USA.
  • Veazey RS; Division of Comparative Pathology, Tulane National Primate Research Center, Covington, LA, USA.
  • Jazwinski SM; Tulane Center for Aging, Tulane University, New Orleans, LA, USA.
  • Rout N; Division of Microbiology, Tulane National Primate Research Center, Covington, LA, USA. nrout@tulane.edu.
Geroscience ; 41(6): 739-757, 2019 12.
Article en En | MEDLINE | ID: mdl-31713098
The development of chronic inflammation, called inflammaging, contributes to the pathogenesis of age-related diseases. Although it is known that both B and T lymphocyte compartments of the adaptive immune system deteriorate with advancing age, the impact of aging on immune functions of Th17-type CD161-expressing innate immune cells and their role in inflammaging remain incompletely understood. Here, utilizing the nonhuman primate model of rhesus macaques, we report that a dysregulated Th17-type effector function of CD161+ immune cells is associated with leaky gut and inflammatory phenotype of aging. Higher plasma levels of inflammatory cytokines IL-6, TNF-α, IL-1ß, GM-CSF, IL-12, and Eotaxin correlated with elevated markers of gut permeability including LPS-binding protein (LBP), intestinal fatty acid binding protein (I-FABP), and sCD14 in aging macaques. Further, older macaques displayed significantly lower frequencies of circulating Th17-type immune cells comprised of CD161+ T cell subsets, NK cells, and innate lymphoid cells. Corresponding with the increased markers of gut permeability, production of the type-17 cytokines IL-17 and IL-22 was impaired in CD161+ T cell subsets and NK cells, along with a skewing towards IFN-γ cytokine production. These findings suggest that reduced frequencies of CD161+ immune cells along with a specific loss in Th17-type effector functions contribute to impaired gut barrier integrity and systemic inflammation in aging macaques. Modulating type-17 immune cell functions via cytokine therapy or dietary interventions towards reducing chronic inflammation in inflammaging individuals may have the potential to prevent or delay age-related chronic diseases and improve immune responses in the elderly population.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Envejecimiento / Epitelio / Subfamilia B de Receptores Similares a Lectina de Células NK / Células Th17 / Inmunidad Innata / Inflamación Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Geroscience Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
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XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Envejecimiento / Epitelio / Subfamilia B de Receptores Similares a Lectina de Células NK / Células Th17 / Inmunidad Innata / Inflamación Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: Geroscience Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza