Eye tissues containing senescent cells become infection hotspots through a vicious cycle mechanism. Senescent retinal pigment epithelium and corneal cells release inflammatory proteins called SASP that attract opportunistic pathogens like Streptococcus pneumoniae, while these same pathogens exploit the chronic inflammation to establish persistent infections in conditions like chronic keratitis and age-related macular degeneration.
This finding represents a significant shift in understanding age-related eye disease vulnerability. Rather than viewing aging and infection as separate processes, this research reveals they amplify each other through cellular senescence pathways. The implications extend beyond ophthalmology—if senescent cells create pathogen-friendly environments in eye tissues, similar mechanisms likely operate throughout aging bodies. The therapeutic potential appears substantial: senolytics that clear senescent cells could simultaneously reduce infection susceptibility and slow age-related eye disease progression. However, this review synthesizes existing evidence rather than presenting new clinical data, and the proposed senolytic interventions remain largely experimental. The bidirectional relationship suggests that treating either senescence or infections alone may prove insufficient—combination approaches targeting both aging mechanisms and pathogen resistance could revolutionize care for age-related eye diseases.
