About this Research Topic
Infectious and non-infectious respiratory diseases are regarded as accelerated-age conditions in which chronic inflammation, exacerbated/dysregulated immune responses, and immunological senescence cell burden coexist. Accordingly, cellular senescence and inflammaging have emerged as potential pathophysiology mechanisms of interstitial and obstructive lung diseases.
Age is also a significant risk factor for certain infectious diseases such as severe coronavirus disease 2019 (COVID-19) and influenza A(H1N1) pdm09 H1N1, yet the mechanisms behind this relationship have remained poorly understood. Older adults, especially those who are frail, had notably worse outcomes in the COVID-19 and influenza A pandemic. This disparity continues today when COVID-19 vaccination has been applied globally, largely due to a waning vaccination response with age. A key contributor to this attenuated vaccination response is immunosenescence, the age-related physiological alterations of cellular and humoral immunity and inflammaging, a state of persistent elevation of circulating pro-inflammatory proteins secondary to continuous antigenic stimulation.
Although cytokine network participation in aging-related to respiratory diseases has been implicated in various lung diseases, many questions remain to be answered. What do we know about cytokine networks with alteration in the metalloproteinases system concerning respiratory disease development and progression? Could cytokines be involved in telomere attrition and serve as a disease biomarker? Could telomere shortening be modified by modulating cytokine networks?
There is a need to expand research assessing integrative research in cytokine networks, telomere length, and the physiology of the aging lung concerning disease development and progression.
To achieve that aim, we would like to compile a diverse range of interdisciplinary studies that explore a comparative and multi-layered analysis of possible mechanisms responsible for inefficient immune responses impacting aging, including novel approaches, i.e., multi-omics or epigenetic signaling. We also seek to incorporate studies from different fields, including basic and clinical research and translational immunology.
We welcome the submission of Original Research, Reviews, Mini-Review, Methods, Case reports, and Perspective articles that cover, but are not limited to, the following topics:
• The role of inflammaging in interstitial lung diseases and its influence in telomere attrition.
• Cytokine networks modulating metalloproteinases related to fibrosis in lung diseases.
• Cytokine networks modulating aging-related mechanisms, such as telomere attrition, in infectious lung diseases.
• Genetic/genomic, epigenetic/epigenomic studies elucidating molecular mechanisms related to inflammaging and telomere length/attrition in lung diseases.
• Role of innate alterations in the development of interstitial lung diseases.
• Alterations in the activity of inflammasomes that favor the development of degenerative lung pathologies.
• Relationship between inflammasome activity and immunological senescence in infectious and non-infectious respiratory diseases.
Age is also a significant risk factor for certain infectious diseases such as severe coronavirus disease 2019 (COVID-19) and influenza A(H1N1) pdm09 H1N1, yet the mechanisms behind this relationship have remained poorly understood. Older adults, especially those who are frail, had notably worse outcomes in the COVID-19 and influenza A pandemic. This disparity continues today when COVID-19 vaccination has been applied globally, largely due to a waning vaccination response with age. A key contributor to this attenuated vaccination response is immunosenescence, the age-related physiological alterations of cellular and humoral immunity and inflammaging, a state of persistent elevation of circulating pro-inflammatory proteins secondary to continuous antigenic stimulation.
Although cytokine network participation in aging-related to respiratory diseases has been implicated in various lung diseases, many questions remain to be answered. What do we know about cytokine networks with alteration in the metalloproteinases system concerning respiratory disease development and progression? Could cytokines be involved in telomere attrition and serve as a disease biomarker? Could telomere shortening be modified by modulating cytokine networks?
There is a need to expand research assessing integrative research in cytokine networks, telomere length, and the physiology of the aging lung concerning disease development and progression.
To achieve that aim, we would like to compile a diverse range of interdisciplinary studies that explore a comparative and multi-layered analysis of possible mechanisms responsible for inefficient immune responses impacting aging, including novel approaches, i.e., multi-omics or epigenetic signaling. We also seek to incorporate studies from different fields, including basic and clinical research and translational immunology.
We welcome the submission of Original Research, Reviews, Mini-Review, Methods, Case reports, and Perspective articles that cover, but are not limited to, the following topics:
• The role of inflammaging in interstitial lung diseases and its influence in telomere attrition.
• Cytokine networks modulating metalloproteinases related to fibrosis in lung diseases.
• Cytokine networks modulating aging-related mechanisms, such as telomere attrition, in infectious lung diseases.
• Genetic/genomic, epigenetic/epigenomic studies elucidating molecular mechanisms related to inflammaging and telomere length/attrition in lung diseases.
• Role of innate alterations in the development of interstitial lung diseases.
• Alterations in the activity of inflammasomes that favor the development of degenerative lung pathologies.
• Relationship between inflammasome activity and immunological senescence in infectious and non-infectious respiratory diseases.
Keywords: Interstitial lung diseases, inflammaging, chronic respiratory diseases, infectious lung diseases, cytokine networks, metalloproteinases, inflammasome, inflammatory cytokines, telomere length
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