Contribution of viral and bacterial infections to senescence and immunosenescence

Front Cell Infect Microbiol. 2023 Sep 11:13:1229098. doi: 10.3389/fcimb.2023.1229098. eCollection 2023.

Abstract

Cellular senescence is a key biological process characterized by irreversible cell cycle arrest. The accumulation of senescent cells creates a pro-inflammatory environment that can negatively affect tissue functions and may promote the development of aging-related diseases. Typical biomarkers related to senescence include senescence-associated β-galactosidase activity, histone H2A.X phosphorylation at serine139 (γH2A.X), and senescence-associated heterochromatin foci (SAHF) with heterochromatin protein 1γ (HP-1γ protein) Moreover, immune cells undergoing senescence, which is known as immunosenescence, can affect innate and adaptative immune functions and may elicit detrimental effects over the host's susceptibility to infectious diseases. Although associations between senescence and pathogens have been reported, clear links between both, and the related molecular mechanisms involved remain to be determined. Furthermore, it remains to be determined whether infections effectively induce senescence, the impact of senescence and immunosenescence over infections, or if both events coincidently share common molecular markers, such as γH2A.X and p53. Here, we review and discuss the most recent reports that describe cellular hallmarks and biomarkers related to senescence in immune and non-immune cells in the context of infections, seeking to better understand their relationships. Related literature was searched in Pubmed and Google Scholar databases with search terms related to the sections and subsections of this review.

Keywords: SASP; bacteria; chronic infections; immunosenescence; persistent infections; senescence; virus.

Publication types

  • Review

MeSH terms

  • Bacterial Infections*
  • Biomarkers
  • Cellular Senescence
  • Heterochromatin
  • Humans
  • Immunosenescence*

Substances

  • Heterochromatin
  • Biomarkers

Grants and funding

This work was funded by ANID - Millennium Science Initiative Program – ICN2021_45: Millennium Institute on Immunology and Immunotherapy (ICN2021_45, former ACE2021, ICN09_016 and P09/016-F), FONDECYT grant #1190864, FONDECYT grant #1191300, FONDECYT grant #1201039, FONDECYT grant #1211959, FONDECYT grant #1190830, FONDECYT grant #1231851 and FONDEF ID21I10335 from the Agencia Nacional de Investigación y Desarrollo (ANID). This work was also supported by the Regional Government of Antofagasta through the Innovation Fund for Competitiveness FIC-R 2017 (BIP Code: 30488811-0). Additionally, this work is supported by ANID-PCHA/Doctorado Nacional #21220694, #21210960, #21210662, ANID Postdoctoral FONDECYT #3210473, and ANID-PCHA/Gastos Operacionales proyecto de tesis Doctoral/#242220039.