Influenza and respiratory viral infections are historically responsible for significant morbidity and mortality, with high infection rates found in the elderly (>65 years). It is estimated that older patients account for the most serious cases of pneumonia with the highest rate of hospitalizations, number of days hospitalized, emergency department visits, and deaths. While it has been well established that innate and adaptive immune responses to influenza are impaired with aging, the molecular mechanisms that underlie these impairments or how these responses are altered during the course of a respiratory viral infection are not fully understood.
Normal lung aging is associated with multiple structural and functional changes in the respiratory tract. Age-associated changes in intrinsic mechanisms that aid in cell regeneration and repair, such as depletion of adult stem cell reservoirs, mitochondrial dysfunction, increased oxidative stress, and telomere shortening, contribute to an inability of lung cells to maintain baseline homeostasis. In healthy aging, common cellular stresses can yield primary senescent cells that diminish tissue-repair capacity due to cell cycle arrest in progenitor cells and increase production of proinflammatory and matrix-degrading molecules. Due to increased prevalence of comorbidities in older persons as well as age-associated changes in cellular and molecular signaling pathways in the respiratory and conducting airways of the lung, there is a pressing need to understand the molecular mechanisms that underlie these impairments and develop cutting-edge therapies that specifically target and improve innate immune responses in older persons.
This Research Topic solicits manuscript submissions that evaluate different respiratory viral infections that impact older persons and examine potential therapies that might improve these responses. Examination of specific immune and non-immune cell types and the impact of aging on these cell types will also be included.
Influenza and respiratory viral infections are historically responsible for significant morbidity and mortality, with high infection rates found in the elderly (>65 years). It is estimated that older patients account for the most serious cases of pneumonia with the highest rate of hospitalizations, number of days hospitalized, emergency department visits, and deaths. While it has been well established that innate and adaptive immune responses to influenza are impaired with aging, the molecular mechanisms that underlie these impairments or how these responses are altered during the course of a respiratory viral infection are not fully understood.
Normal lung aging is associated with multiple structural and functional changes in the respiratory tract. Age-associated changes in intrinsic mechanisms that aid in cell regeneration and repair, such as depletion of adult stem cell reservoirs, mitochondrial dysfunction, increased oxidative stress, and telomere shortening, contribute to an inability of lung cells to maintain baseline homeostasis. In healthy aging, common cellular stresses can yield primary senescent cells that diminish tissue-repair capacity due to cell cycle arrest in progenitor cells and increase production of proinflammatory and matrix-degrading molecules. Due to increased prevalence of comorbidities in older persons as well as age-associated changes in cellular and molecular signaling pathways in the respiratory and conducting airways of the lung, there is a pressing need to understand the molecular mechanisms that underlie these impairments and develop cutting-edge therapies that specifically target and improve innate immune responses in older persons.
This Research Topic solicits manuscript submissions that evaluate different respiratory viral infections that impact older persons and examine potential therapies that might improve these responses. Examination of specific immune and non-immune cell types and the impact of aging on these cell types will also be included.
