The cellular and humoral components of the immune system build a dynamically regulated entity, which beyond its function to discriminate between ‘self’ and ‘non-self’ and to fight against infections has been increasingly recognized as an important contributor to organ development, health, (patho-) physiological processes and tissue repair. The potential harms causing tissue stress or damage in cardiorespiratory disease induce along the physiological alterations humoral and cell bound danger signals that trigger inflammation and activate antigen-presenting cells followed by a plethora of innate and adaptive immune responses. Although these responses to sterile inflammatory processes and infection are first and foremost of protective nature, a fine balance between pro- and anti-inflammatory mediators adjusts between benefit and harm. Understanding the immunodynamics at the gas-blood interface and of inter-organ communication between heart and lung guides interdisciplinary science into new frontiers of pulmonary and cardiovascular diseases.
The capacity to self-renew and to undergo local proliferation allows tissue-resident immune cells to populate heart and lungs early in life and to get long-lived. They participate in essential housekeeping functions throughout life and can affect the pathophysiology. In addition, during sterile inflammation (e.g., myocardial infarction, heart failure, pulmonary hypertension) or in response to infection (e.g., pneumonia, myocarditis), many innate immune cells are recruited to the site of injury to remove dying tissue, scavenge pathogens or promote healing. However, under some circumstances, immune cells can also cause irreversible damage, contributing to organ dysfunction and accelerating disease progression. Notably, maladaptation of the adaptive immunity to heart or lung infections (e.g., bacterial/viral pneumonia and myocarditis) or inflammatory cardiopulmonary conditions (e.g., pulmonary hypertension) has been recognized as cause of chronic inflammation or autoimmunity.
This Research Topic will feature a collection of articles that highlight the role of resident and recruited immune cells in both homeostasis of heart and lung, and cardiopulmonary disease. We welcome submissions that focus on:
• signaling pathways identifying new targets to subdue inflammation
• contribution of pro-inflammatory cytokines in cardiorespiratory disease
• cardiopulmonary immune responses
• inflammatory aspects of inter-organ communication
• technical advances in analyses and modelling
• translational as well as bedside to bench approaches
The cellular and humoral components of the immune system build a dynamically regulated entity, which beyond its function to discriminate between ‘self’ and ‘non-self’ and to fight against infections has been increasingly recognized as an important contributor to organ development, health, (patho-) physiological processes and tissue repair. The potential harms causing tissue stress or damage in cardiorespiratory disease induce along the physiological alterations humoral and cell bound danger signals that trigger inflammation and activate antigen-presenting cells followed by a plethora of innate and adaptive immune responses. Although these responses to sterile inflammatory processes and infection are first and foremost of protective nature, a fine balance between pro- and anti-inflammatory mediators adjusts between benefit and harm. Understanding the immunodynamics at the gas-blood interface and of inter-organ communication between heart and lung guides interdisciplinary science into new frontiers of pulmonary and cardiovascular diseases.
The capacity to self-renew and to undergo local proliferation allows tissue-resident immune cells to populate heart and lungs early in life and to get long-lived. They participate in essential housekeeping functions throughout life and can affect the pathophysiology. In addition, during sterile inflammation (e.g., myocardial infarction, heart failure, pulmonary hypertension) or in response to infection (e.g., pneumonia, myocarditis), many innate immune cells are recruited to the site of injury to remove dying tissue, scavenge pathogens or promote healing. However, under some circumstances, immune cells can also cause irreversible damage, contributing to organ dysfunction and accelerating disease progression. Notably, maladaptation of the adaptive immunity to heart or lung infections (e.g., bacterial/viral pneumonia and myocarditis) or inflammatory cardiopulmonary conditions (e.g., pulmonary hypertension) has been recognized as cause of chronic inflammation or autoimmunity.
This Research Topic will feature a collection of articles that highlight the role of resident and recruited immune cells in both homeostasis of heart and lung, and cardiopulmonary disease. We welcome submissions that focus on:
• signaling pathways identifying new targets to subdue inflammation
• contribution of pro-inflammatory cytokines in cardiorespiratory disease
• cardiopulmonary immune responses
• inflammatory aspects of inter-organ communication
• technical advances in analyses and modelling
• translational as well as bedside to bench approaches
