Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid. / Lunding, Bjørg Skjøth; Bassi, Maria Rossaria; Christensen, Jan Pravsgaard; Thomsen, Allan Randrup; Sørensen, Torben Lykke; Vorum, Henrik; Honoré, Bent; Nissen, Mogens Holst; Steffensen, Maria Abildgaard.

In: Experimental Eye Research, Vol. 245, 109984, 2024.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Lunding, BS, Bassi, MR, Christensen, JP, Thomsen, AR, Sørensen, TL, Vorum, H, Honoré, B, Nissen, MH & Steffensen, MA 2024, 'Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid', Experimental Eye Research, vol. 245, 109984. https://doi.org/10.1016/j.exer.2024.109984

APA

Lunding, B. S., Bassi, M. R., Christensen, J. P., Thomsen, A. R., Sørensen, T. L., Vorum, H., Honoré, B., Nissen, M. H., & Steffensen, M. A. (2024). Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid. Experimental Eye Research, 245, [109984]. https://doi.org/10.1016/j.exer.2024.109984

Vancouver

Lunding BS, Bassi MR, Christensen JP, Thomsen AR, Sørensen TL, Vorum H et al. Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid. Experimental Eye Research. 2024;245. 109984. https://doi.org/10.1016/j.exer.2024.109984

Author

Lunding, Bjørg Skjøth ; Bassi, Maria Rossaria ; Christensen, Jan Pravsgaard ; Thomsen, Allan Randrup ; Sørensen, Torben Lykke ; Vorum, Henrik ; Honoré, Bent ; Nissen, Mogens Holst ; Steffensen, Maria Abildgaard. / Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid. In: Experimental Eye Research. 2024 ; Vol. 245.

Bibtex

@article{73703903ff434c63ad827d44a7e97273,

title = "Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid",

abstract = "Aging changes the responsiveness of our immune defense, and this decline in immune reactivity plays an important role in the increased susceptibility to infections that marks progressing age. Aging is also the most pronounced risk factor for development of age-related macular degeneration (AMD), a disease that is characterized by dysfunctional retinal pigment epithelial (RPE) cells and loss of central vision. We have previously shown that acute systemic viral infection has a large impact on the retina in young mice, leading to upregulation of chemokines in the RPE/choroid (RPE/c) and influx of CD8 T cells in the neuroretina. In this study, we sought to investigate the impact of systemic infection on the RPE/c in aged mice to evaluate whether infection in old age could play a role in the pathogenesis of AMD. We found that systemic infection in mice led to upregulation of genes from the crystallin family in the RPE/c from aged mice, but not in the RPE/c from young mice. Crystallin alpha A (CRYAA) was the most upregulated gene, and increased amounts of CRYAA protein were also detected in the aged RPE/c. Increased CRYAA gene and protein expression has previously been found in drusen and choroid from AMD patients, and this protein has also been linked to neovascularization. Since both drusen and neovascularization are important hallmarks of advanced AMD, it is interesting to speculate if upregulation of crystallins in response to infection in old age could be relevant for the pathogenesis of AMD.",

author = "Lunding, {Bj{\o}rg Skj{\o}th} and Bassi, {Maria Rossaria} and Christensen, {Jan Pravsgaard} and Thomsen, {Allan Randrup} and S{\o}rensen, {Torben Lykke} and Henrik Vorum and Bent Honor{\'e} and Nissen, {Mogens Holst} and Steffensen, {Maria Abildgaard}",

note = "Copyright {\textcopyright} 2024. Published by Elsevier Ltd.",

year = "2024",

doi = "10.1016/j.exer.2024.109984",

language = "English",

volume = "245",

journal = "Experimental Eye Research",

issn = "0014-4835",

publisher = "Academic Press",

}

RIS

TY - JOUR

T1 - Systemic infection in aged mice causes upregulation of crystallin alpha A in the RPE/choroid

AU - Lunding, Bjørg Skjøth

AU - Bassi, Maria Rossaria

AU - Christensen, Jan Pravsgaard

AU - Thomsen, Allan Randrup

AU - Sørensen, Torben Lykke

AU - Vorum, Henrik

AU - Honoré, Bent

AU - Nissen, Mogens Holst

AU - Steffensen, Maria Abildgaard

PY - 2024

Y1 - 2024

N2 - Aging changes the responsiveness of our immune defense, and this decline in immune reactivity plays an important role in the increased susceptibility to infections that marks progressing age. Aging is also the most pronounced risk factor for development of age-related macular degeneration (AMD), a disease that is characterized by dysfunctional retinal pigment epithelial (RPE) cells and loss of central vision. We have previously shown that acute systemic viral infection has a large impact on the retina in young mice, leading to upregulation of chemokines in the RPE/choroid (RPE/c) and influx of CD8 T cells in the neuroretina. In this study, we sought to investigate the impact of systemic infection on the RPE/c in aged mice to evaluate whether infection in old age could play a role in the pathogenesis of AMD. We found that systemic infection in mice led to upregulation of genes from the crystallin family in the RPE/c from aged mice, but not in the RPE/c from young mice. Crystallin alpha A (CRYAA) was the most upregulated gene, and increased amounts of CRYAA protein were also detected in the aged RPE/c. Increased CRYAA gene and protein expression has previously been found in drusen and choroid from AMD patients, and this protein has also been linked to neovascularization. Since both drusen and neovascularization are important hallmarks of advanced AMD, it is interesting to speculate if upregulation of crystallins in response to infection in old age could be relevant for the pathogenesis of AMD.

AB - Aging changes the responsiveness of our immune defense, and this decline in immune reactivity plays an important role in the increased susceptibility to infections that marks progressing age. Aging is also the most pronounced risk factor for development of age-related macular degeneration (AMD), a disease that is characterized by dysfunctional retinal pigment epithelial (RPE) cells and loss of central vision. We have previously shown that acute systemic viral infection has a large impact on the retina in young mice, leading to upregulation of chemokines in the RPE/choroid (RPE/c) and influx of CD8 T cells in the neuroretina. In this study, we sought to investigate the impact of systemic infection on the RPE/c in aged mice to evaluate whether infection in old age could play a role in the pathogenesis of AMD. We found that systemic infection in mice led to upregulation of genes from the crystallin family in the RPE/c from aged mice, but not in the RPE/c from young mice. Crystallin alpha A (CRYAA) was the most upregulated gene, and increased amounts of CRYAA protein were also detected in the aged RPE/c. Increased CRYAA gene and protein expression has previously been found in drusen and choroid from AMD patients, and this protein has also been linked to neovascularization. Since both drusen and neovascularization are important hallmarks of advanced AMD, it is interesting to speculate if upregulation of crystallins in response to infection in old age could be relevant for the pathogenesis of AMD.

U2 - 10.1016/j.exer.2024.109984

DO - 10.1016/j.exer.2024.109984

M3 - Journal article

C2 - 38945517

VL - 245

JO - Experimental Eye Research

JF - Experimental Eye Research

SN - 0014-4835

M1 - 109984

ER -

ID: 396846311