Ageing lungs undergo a series of structural and cellular changes that increase vulnerability to respiratory infections such as influenza and COVID-19, according to a review of age-related pulmonary biology. These changes do not simply reduce lung capacity; they actively alter immune function and inflammatory responses in ways that can turn routine infections into life-threatening events.
As the lungs age, they lose elasticity, airway walls may thicken, and the alveoli responsible for gas exchange become less efficient. The chest wall stiffens, reducing respiratory reserve. At the cellular level, lung cells accumulate damage from repeated exposure to pollutants, smoke, and infection. Many enter a state known as cellular senescence, remaining metabolically active but no longer dividing. Senescent cells release inflammatory mediators that sustain a state of chronic, low-grade inflammation in the lungs, even in the absence of infection, a phenomenon referred to as “inflammaging.”
When a respiratory virus arrives, it encounters a system already primed with elevated inflammatory signalling. The immune response frequently overshoots, producing tissue swelling and fluid accumulation in the airways rather than a controlled, targeted defence. Oxygen exchange is impaired and, in severe cases, the inflammatory cascade itself becomes a significant driver of harm alongside the virus.
Ageing also weakens key components of adaptive immunity: pathogen recognition slows, antibody responses are reduced in magnitude, and some immune cells release disproportionately large quantities of inflammatory signals without efficiently clearing the infection. The airway epithelial barrier also weakens, facilitating viral entry. Comorbidities common in older adults, including cardiovascular disease, diabetes, and chronic obstructive pulmonary disease, compound this vulnerability further.
Source: Soliman R. How Aging Lungs Turn Respiratory Infections Into Dangerous Storms of Inflammation and Broken Immunity. Popular Science, 22 April 2026.
As the lungs age, they lose elasticity, airway walls may thicken, and the alveoli responsible for gas exchange become less efficient. The chest wall stiffens, reducing respiratory reserve. At the cellular level, lung cells accumulate damage from repeated exposure to pollutants, smoke, and infection. Many enter a state known as cellular senescence, remaining metabolically active but no longer dividing. Senescent cells release inflammatory mediators that sustain a state of chronic, low-grade inflammation in the lungs, even in the absence of infection, a phenomenon referred to as “inflammaging.”
When a respiratory virus arrives, it encounters a system already primed with elevated inflammatory signalling. The immune response frequently overshoots, producing tissue swelling and fluid accumulation in the airways rather than a controlled, targeted defence. Oxygen exchange is impaired and, in severe cases, the inflammatory cascade itself becomes a significant driver of harm alongside the virus.
Ageing also weakens key components of adaptive immunity: pathogen recognition slows, antibody responses are reduced in magnitude, and some immune cells release disproportionately large quantities of inflammatory signals without efficiently clearing the infection. The airway epithelial barrier also weakens, facilitating viral entry. Comorbidities common in older adults, including cardiovascular disease, diabetes, and chronic obstructive pulmonary disease, compound this vulnerability further.
Source: Soliman R. How Aging Lungs Turn Respiratory Infections Into Dangerous Storms of Inflammation and Broken Immunity. Popular Science, 22 April 2026.
