Human cytomegalovirus infection triggers a paracrine senescence loop in renal epithelial cells.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
08 Mar 2024
Historique:
received: 09 07 2023
accepted: 22 02 2024
medline: 9 3 2024
pubmed: 9 3 2024
entrez: 8 3 2024
Statut: epublish

Résumé

Human cytomegalovirus (HCMV) is an opportunistic pathogen causing severe diseases in immunosuppressed individuals. To replicate its double-stranded DNA genome, HCMV induces profound changes in cellular homeostasis that may resemble senescence. However, it remains to be determined whether HCMV-induced senescence contributes to organ-specific pathogenesis. Here, we show a direct cytopathic effect of HCMV on primary renal proximal tubular epithelial cells (RPTECs), a natural setting of HCMV disease. We find that RPTECs are fully permissive for HCMV replication, which endows them with an inflammatory gene signature resembling the senescence-associated secretory phenotype (SASP), as confirmed by the presence of the recently established SenMayo gene set, which is not observed in retina-derived epithelial (ARPE-19) cells. Although HCMV-induced senescence is not cell-type specific, as it can be observed in both RPTECs and human fibroblasts (HFFs), only infected RPTECs show downregulation of LAMINB1 and KI67 mRNAs, and enhanced secretion of IL-6 and IL-8, which are well-established hallmarks of senescence. Finally, HCMV-infected RPTECs have the ability to trigger a senescence/inflammatory loop in an IL-6-dependent manner, leading to the development of a similar senescence/inflammatory phenotype in neighboring uninfected cells. Overall, our findings raise the intriguing possibility that this unique inflammatory loop contributes to HCMV-related pathogenesis in the kidney.

Identifiants

pubmed: 38459109
doi: 10.1038/s42003-024-05957-5
pii: 10.1038/s42003-024-05957-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

292

Subventions

Organisme : Università degli Studi di Torino (University of Turin)
ID : PoC - TOINPROVE/2020

Informations de copyright

© 2024. The Author(s).

Références

Griffiths, P. & Reeves, M. Pathogenesis of human cytomegalovirus in the immunocompromised host. Nat. Rev. Microbiol. 19, 759–773 (2021).
pubmed: 34168328 pmcid: 8223196 doi: 10.1038/s41579-021-00582-z
Kabani, N. & Ross, S. A. Congenital Cytomegalovirus Infection. J. Infect. Dis. 221, S9–S14 (2020).
pubmed: 32134480 pmcid: 8453618 doi: 10.1093/infdis/jiz446
Atabani, S. F. et al. Cytomegalovirus replication kinetics in solid organ transplant recipients managed by preemptive therapy. Am. J. Transplant. 12, 2457–2464 (2012).
pubmed: 22594993 pmcid: 3510308 doi: 10.1111/j.1600-6143.2012.04087.x
Deayton, J. R. et al. Importance of cytomegalovirus viraemia in risk of disease progression and death in HIV-infected patients receiving highly active antiretroviral therapy. Lancet 363, 2116–2121 (2004).
pubmed: 15220032 doi: 10.1016/S0140-6736(04)16500-8
Streblow, D. N., Orloff, S. L. & Nelson, J. A. Acceleration of allograft failure by cytomegalovirus. Curr. Opin. Immunol. 19, 577–582 (2007).
pubmed: 17716883 pmcid: 3509935 doi: 10.1016/j.coi.2007.07.012
Fields, B. N., Knipe, D. M. & Howley, P. M. Fields virology. (Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013).
Bughio, F., Elliott, D. A. & Goodrum, F. An endothelial cell-specific requirement for the UL133-UL138 locus of human cytomegalovirus for efficient virus maturation. J. Virol. 87, 3062–3075 (2013).
pubmed: 23283945 pmcid: 3592143 doi: 10.1128/JVI.02510-12
Bogdanow, B., Phan, Q. V. & Wiebusch, L. Emerging Mechanisms of G1/S Cell Cycle Control by Human and Mouse Cytomegaloviruses. mBio 12, e0293421 (2021).
pubmed: 34903047 doi: 10.1128/mBio.02934-21
Paladino, P., Marcon, E., Greenblatt, J. & Frappier, L. Identification of herpesvirus proteins that contribute to G1/S arrest. J. Virol. 88, 4480–4492 (2014).
pubmed: 24501404 pmcid: 3993752 doi: 10.1128/JVI.00059-14
Sanchez, V. & Spector, D. H. Subversion of cell cycle regulatory pathways. Curr. Top Microbiol. Immunol. 325, 243–262 (2008).
pubmed: 18637510
Spector, D. H. Human cytomegalovirus riding the cell cycle. Med. Microbiol. Immunol. 204, 409–419 (2015).
pubmed: 25776080 doi: 10.1007/s00430-015-0396-z
Xiaofei, E. & Kowalik, T. F. The DNA damage response induced by infection with human cytomegalovirus and other viruses. Viruses 6, 2155–2185 (2014).
pubmed: 24859341 doi: 10.3390/v6052155
E, X. et al. An E2F1-mediated DNA damage response contributes to the replication of human cytomegalovirus. PLoS Pathog 7, e1001342 (2011).
pubmed: 21589897 pmcid: 3093362 doi: 10.1371/journal.ppat.1001342
Gaspar, M. & Shenk, T. Human cytomegalovirus inhibits a DNA damage response by mislocalizing checkpoint proteins. Proc. Natl. Acad. Sci. USA 103, 2821–2826 (2006).
pubmed: 16477038 pmcid: 1413835 doi: 10.1073/pnas.0511148103
Merchut-Maya, J. M. et al. Human cytomegalovirus hijacks host stress response fueling replication stress and genome instability. Cell Death Differ. 29, 1639–1653 (2022).
pubmed: 35194187 pmcid: 9346009 doi: 10.1038/s41418-022-00953-w
Alwine, J. C. Modulation of host cell stress responses by human cytomegalovirus. Curr. Top Microbiol. Immunol. 325, 263–279 (2008).
pubmed: 18637511
Castillo, J. P. & Kowalik, T. F. HCMV infection: modulating the cell cycle and cell death. Int. Rev. Immunol. 23, 113–139 (2004).
pubmed: 14690857 doi: 10.1080/08830180490265565
Kalejta, R. F. & Shenk, T. Manipulation of the cell cycle by human cytomegalovirus. Front. Biosci. 7, d295–d306 (2002).
pubmed: 11779699 doi: 10.2741/kalejta
Calcinotto, A. et al. Cellular Senescence: Aging, Cancer, and Injury. Physiol. Rev. 99, 1047–1078 (2019).
pubmed: 30648461 doi: 10.1152/physrev.00020.2018
Herranz, N. & Gil, J. Mechanisms and functions of cellular senescence. J. Clin. Invest. 128, 1238–1246 (2018).
pubmed: 29608137 pmcid: 5873888 doi: 10.1172/JCI95148
Gorgoulis, V. et al. Cellular Senescence: Defining a Path Forward. Cell 179, 813–827 (2019).
pubmed: 31675495 doi: 10.1016/j.cell.2019.10.005
Docherty, M.-H., O’Sullivan, E. D., Bonventre, J. V. & Ferenbach, D. A. Cellular Senescence in the Kidney. J. Am. Soc. Nephrol. 30, 726–736 (2019).
pubmed: 31000567 pmcid: 6493983 doi: 10.1681/ASN.2018121251
Gonzalez-Meljem, J. M., Apps, J. R., Fraser, H. C. & Martinez-Barbera, J. P. Paracrine roles of cellular senescence in promoting tumourigenesis. Br. J. Cancer 118, 1283–1288 (2018).
pubmed: 29670296 pmcid: 5959857 doi: 10.1038/s41416-018-0066-1
Ferreira-Gonzalez, S. et al. Paracrine cellular senescence exacerbates biliary injury and impairs regeneration. Nat. Commun. 9, 1020 (2018).
pubmed: 29523787 pmcid: 5844882 doi: 10.1038/s41467-018-03299-5
Kohli, J., Veenstra, I. & Demaria, M. The struggle of a good friend getting old: cellular senescence in viral responses and therapy. EMBO Rep. 22, e52243 (2021).
pubmed: 33734564 pmcid: 8024996 doi: 10.15252/embr.202052243
Tsuji, S. et al. SARS-CoV-2 infection triggers paracrine senescence and leads to a sustained senescence-associated inflammatory response. Nat. Aging 2, 115–124 (2022).
pubmed: 37117754 pmcid: 10154207 doi: 10.1038/s43587-022-00170-7
Lee, S. et al. Virus-induced senescence is a driver and therapeutic target in COVID-19. Nature 599, 283–289 (2021).
pubmed: 34517409 doi: 10.1038/s41586-021-03995-1
Tripathi, U. et al. SARS-CoV-2 causes senescence in human cells and exacerbates the senescence-associated secretory phenotype through TLR-3. Aging (Albany NY) 13, 21838–21854 (2021).
pubmed: 34531331 doi: 10.18632/aging.203560
Noris, E. et al. Cell cycle arrest by human cytomegalovirus 86-kDa IE2 protein resembles premature senescence. J. Virol. 76, 12135–12148 (2002).
pubmed: 12414954 pmcid: 136868 doi: 10.1128/JVI.76.23.12135-12148.2002
Zannetti, C. et al. The expression of p16INK4a tumor suppressor is upregulated by human cytomegalovirus infection and required for optimal viral replication. Virology 349, 79–86 (2006).
pubmed: 16504234 doi: 10.1016/j.virol.2006.01.042
Fortunato, E. A. Using Diploid Human Fibroblasts as a Model System to Culture, Grow, and Study Human Cytomegalovirus Infection. Methods Mol. Biol. 2244, 39–50 (2021).
pubmed: 33555581 doi: 10.1007/978-1-0716-1111-1_3
Plachter, B., Sinzger, C. & Jahn, G. Cell types involved in replication and distribution of human cytomegalovirus. Adv. Virus Res. 46, 195–261 (1996).
pubmed: 8824701 doi: 10.1016/S0065-3527(08)60073-1
Wilkerson, I., Laban, J., Mitchell, J. M., Sheibani, N. & Alcendor, D. J. Retinal pericytes and cytomegalovirus infectivity: implications for HCMV-induced retinopathy and congenital ocular disease. J. Neuroinflamm. 12, 2 (2015).
doi: 10.1186/s12974-014-0219-y
Popik, W., Correa, H., Khatua, A., Aronoff, D. M. & Alcendor, D. J. Mesangial cells, specialized renal pericytes and cytomegalovirus infectivity: Implications for HCMV pathology in the glomerular vascular unit and post-transplant renal disease. J. Transl. Sci. 5, 1–12 (2019).
de Magalhães, J. P., Chainiaux, F., Remacle, J. & Toussaint, O. Stress-induced premature senescence in BJ and hTERT-BJ1 human foreskin fibroblasts. FEBS Lett. 523, 157–162 (2002).
pubmed: 12123824 doi: 10.1016/S0014-5793(02)02973-3
Wieser, M. et al. hTERT alone immortalizes epithelial cells of renal proximal tubules without changing their functional characteristics. Am. J. Physiol. Renal. Physiol. 295, F1365–F1375 (2008).
pubmed: 18715936 doi: 10.1152/ajprenal.90405.2008
Murphy, E., Rigoutsos, I., Shibuya, T. & Shenk, T. E. Reevaluation of human cytomegalovirus coding potential. Proc. Natl. Acad. Sci. USA 100, 13585–13590 (2003).
pubmed: 14593199 pmcid: 263857 doi: 10.1073/pnas.1735466100
Wang, D., Yu, Q.-C., Schröer, J., Murphy, E. & Shenk, T. Human cytomegalovirus uses two distinct pathways to enter retinal pigmented epithelial cells. PNAS 104, 20037–20042 (2007).
pubmed: 18077432 pmcid: 2148418 doi: 10.1073/pnas.0709704104
Nogalski, M. T. et al. A tumor-specific endogenous repetitive element is induced by herpesviruses. Nat. Commun. 10, 90 (2019).
pubmed: 30626867 pmcid: 6327058 doi: 10.1038/s41467-018-07944-x
Matz, M. et al. Early post-transplant urinary IP-10 expression after kidney transplantation is predictive of short- and long-term graft function. Kidney Int. 69, 1683–1690 (2006).
pubmed: 16572110 doi: 10.1038/sj.ki.5000343
Bolignano, D. et al. Neutrophil Gelatinase–Associated Lipocalin (NGAL) as a Marker of Kidney Damage. Ame. J. Kidney Dis. 52, 595–605 (2008).
doi: 10.1053/j.ajkd.2008.01.020
Young, A. R. J. & Narita, M. SASP reflects senescence. EMBO Rep. 10, 228–230 (2009).
pubmed: 19218920 pmcid: 2658552 doi: 10.1038/embor.2009.22
Saul, D. et al. A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues. Nat. Commun. 13, 4827 (2022).
pubmed: 35974106 pmcid: 9381717 doi: 10.1038/s41467-022-32552-1
Shimi, T. et al. The role of nuclear lamin B1 in cell proliferation and senescence. Genes Dev. 25, 2579–2593 (2011).
pubmed: 22155925 pmcid: 3248680 doi: 10.1101/gad.179515.111
Kohli, J. et al. Algorithmic assessment of cellular senescence in experimental and clinical specimens. Nat. Protoc. 16, 2471–2498 (2021).
pubmed: 33911261 pmcid: 8710232 doi: 10.1038/s41596-021-00505-5
Nagelkerke, A. & Span, P. N. Staining Against Phospho-H2AX (γ-H2AX) as a Marker for DNA Damage and Genomic Instability in Cancer Tissues and Cells. Adv. Exp. Med. Biol. 899, 1–10 (2016).
pubmed: 27325258 doi: 10.1007/978-3-319-26666-4_1
Admasu, T. D., Rae, M. & Stolzing, A. Dissecting primary and secondary senescence to enable new senotherapeutic strategies. Ageing. Res. Rev. 70, 101412 (2021).
pubmed: 34302996 doi: 10.1016/j.arr.2021.101412
Kojima, H., Inoue, T., Kunimoto, H. & Nakajima, K. IL-6-STAT3 signaling and premature senescence. JAKSTAT 2, e25763 (2013).
pubmed: 24416650 pmcid: 3876432
Monzani, A. et al. Fulminant cytomegalovirus infection in a preterm newborn. Minerva. Pediatr. 70, 408–409 (2018).
pubmed: 29943548 doi: 10.23736/S0026-4946.17.05136-2
Salmonowicz, H. & Passos, J. F. Detecting senescence: a new method for an old pigment. Aging Cell 16, 432–434 (2017).
pubmed: 28185406 pmcid: 5418201 doi: 10.1111/acel.12580
Georgakopoulou, E. A. et al. Specific lipofuscin staining as a novel biomarker to detect replicative and stress-induced senescence. A method applicable in cryo-preserved and archival tissues. Aging (Albany NY) 5, 37–50 (2013).
pubmed: 23449538 doi: 10.18632/aging.100527
Field, M. et al. The use of NGAL and IP-10 in the prediction of early acute rejection in highly sensitized patients following HLA-incompatible renal transplantation. Transpl. Int. 27, 362–370 (2014).
pubmed: 24438378 doi: 10.1111/tri.12266
Chuprin, A. et al. Cell fusion induced by ERVWE1 or measles virus causes cellular senescence. Genes Dev. 27, 2356–2366 (2013).
pubmed: 24186980 pmcid: 3828521 doi: 10.1101/gad.227512.113
Martínez, I. et al. Induction of DNA double-strand breaks and cellular senescence by human respiratory syncytial virus. Virulence 7, 427–442 (2016).
pubmed: 26809688 pmcid: 4871660 doi: 10.1080/21505594.2016.1144001
Thangaraj, A. et al. HIV TAT-mediated microglial senescence: Role of SIRT3-dependent mitochondrial oxidative stress. Redox Biol. 40, 101843 (2021).
pubmed: 33385630 doi: 10.1016/j.redox.2020.101843
Yan, Y. et al. NS1 of H7N9 Influenza A Virus Induces NO-Mediated Cellular Senescence in Neuro2a Cells. Cell Physiol. Biochem. 43, 1369–1380 (2017).
pubmed: 28992616 doi: 10.1159/000481848
Shelton, D. N., Chang, E., Whittier, P. S., Choi, D. & Funk, W. D. Microarray analysis of replicative senescence. Curr. Biol. 9, 939–945 (1999).
pubmed: 10508581 doi: 10.1016/S0960-9822(99)80420-5
Dimri, G. P. et al. A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl. Acad. Sci. USA 92, 9363–9367 (1995).
pubmed: 7568133 pmcid: 40985 doi: 10.1073/pnas.92.20.9363
Meyer, K., Patra, T., Vijayamahantesh & Ray, R. SARS-CoV-2 Spike Protein Induces Paracrine Senescence and Leukocyte Adhesion in Endothelial Cells. J. Virol. 95, e0079421 (2021).
pubmed: 34160250 doi: 10.1128/JVI.00794-21
Terman, A. & Brunk, U. T. Lipofuscin: mechanisms of formation and increase with age. APMIS 106, 265–276 (1998).
pubmed: 9531959 doi: 10.1111/j.1699-0463.1998.tb01346.x
Gariano, G. R. et al. The intracellular DNA sensor IFI16 gene acts as restriction factor for human cytomegalovirus replication. PLoS Pathog. 8, e1002498 (2012).
pubmed: 22291595 pmcid: 3266931 doi: 10.1371/journal.ppat.1002498
Biolatti, M. et al. The Viral Tegument Protein pp65 Impairs Transcriptional Upregulation of IL-1β by Human Cytomegalovirus through Inhibition of NF-kB Activity. Viruses 10, 567 (2018).
pubmed: 30332797 pmcid: 6213739 doi: 10.3390/v10100567
Dobin, A. et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics 29, 15–21 (2013).
pubmed: 23104886 doi: 10.1093/bioinformatics/bts635
Li, B. & Dewey, C. N. RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome. BMC Bioinform. 12, 323 (2011).
doi: 10.1186/1471-2105-12-323
Love, M. I., Huber, W. & Anders, S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 15, 550 (2014).
pubmed: 25516281 pmcid: 4302049 doi: 10.1186/s13059-014-0550-8
Subramanian, A. et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc. Natl. Acad. Sci. USA 102, 15545–15550 (2005).
pubmed: 16199517 pmcid: 1239896 doi: 10.1073/pnas.0506580102
Zhou, Y. et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat. Commun. 10, 1523 (2019).
pubmed: 30944313 pmcid: 6447622 doi: 10.1038/s41467-019-09234-6
Iannucci, A. et al. Toll-like receptor 4-mediated inflammation triggered by extracellular IFI16 is enhanced by lipopolysaccharide binding. PLoS Pathog. 16, e1008811 (2020).
pubmed: 32903274 pmcid: 7505474 doi: 10.1371/journal.ppat.1008811
Itahana, K., Itahana, Y. & Dimri, G. P. Colorimetric detection of senescence-associated β galactosidase. Methods Mol. Biol. 965, 143–156 (2013).
pubmed: 23296655 pmcid: 3769963 doi: 10.1007/978-1-62703-239-1_8
Zanoni, I. et al. An endogenous caspase-11 ligand elicits interleukin-1 release from living dendritic cells. Science 352, 1232–1236 (2016).
pubmed: 27103670 pmcid: 5111085 doi: 10.1126/science.aaf3036

Auteurs

Stefano Raviola (S)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Gloria Griffante (G)

Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Andrea Iannucci (A)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.
Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.

Shikha Chandel (S)

Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Irene Lo Cigno (I)

Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Davide Lacarbonara (D)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Valeria Caneparo (V)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.

Selina Pasquero (S)

Viral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, University of Turin, Medical School, Turin, Italy.

Francesco Favero (F)

Bioinformatics Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Bioinformatics Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Davide Corà (D)

Bioinformatics Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Bioinformatics Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Elena Trisolini (E)

Pathology Unit, Department of Health Sciences, University of Eastern Piedmont, Novara, Italy.

Renzo Boldorini (R)

Pathology Unit, Department of Health Sciences, University of Eastern Piedmont, Novara, Italy.

Vincenzo Cantaluppi (V)

Nephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Santo Landolfo (S)

Viral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, University of Turin, Medical School, Turin, Italy.

Marisa Gariglio (M)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy.
Molecular Virology Unit, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Marco De Andrea (M)

Intrinsic Immunity Unit, CAAD - Center for Translational Research on Autoimmune and Allergic Disease, University of Eastern Piedmont, Novara, Italy. marco.deandrea@unito.it.
Viral Pathogenesis Unit, Department of Public Health and Pediatric Sciences, University of Turin, Medical School, Turin, Italy. marco.deandrea@unito.it.

Classifications MeSH