Congenital diaphragmatic hernia is a deadly malformation of the lungs and diaphragm that causes underdeveloped lungs, leading to high mortality rates. Researchers discovered increased numbers of inflammatory cells in human lung tissue, both before and after birth, which may influence lung structure development.
A study found that exposure to β-glucan reprograms immune cells in the lungs, causing them to overreact and worsen lung damage. The research suggests that trained immunity in the lungs may have negative consequences in certain contexts.
Researchers Ana Ivonne Vazquez-Armendariz and Jan Hasenauer are using their prize money to study the functions of scavenger cells in the lungs, combining mathematics and medicine. Their new models aim to understand how these immune cells behave in the lung, potentially unlocking better defense mechanisms.
Researchers at Texas Biomedical Research Institute developed a human cell culture model of alveolar macrophages, which helped make a key finding about the role of tumor necrosis factor (TNF) in tuberculosis (TB). The study found that TNF is critical to protect against TB but not other infectious diseases.
Researchers found that interstitial macrophages in the lungs are most susceptible to infection by SARS-CoV-2, leading to pneumonia and organ damage. Blocking this step could prove a major therapeutic advance, but the virus's unusual entry mechanism presents a new challenge.
Researchers found that expression of CiDRE in alveolar macrophages makes patients more susceptible to SARS-CoV-2 invasion and promotes cytokine storm. The genetic quirk is associated with severe COVID-19 symptoms, suggesting potential treatments targeting IL-10R and CiDRE.
Researchers at Texas Biomedical Research Institute have developed a new cell culture model to generate human alveolar macrophages, the most critical immune cells in the lungs. This model allows for easier and inexpensive investigation of lung inflammatory diseases and testing of new therapies.
Researchers from Nara Institute of Science and Technology found that alveolar macrophages act as antigen-presenting cells to prime CD8+ T cell expansion in the lungs. This process involves the production of interleukin 18, leading to the development of resident memory-type cell populations.
Researchers discovered that a lipid called prostaglandin E2 weakens lung immune cells with age. This increased PGE2 production impairs alveolar macrophage health and leads to a suppressed immune response, making older people more vulnerable to flu infections.
A deficiency in gene regulation disrupts the clearance of surfactant lipids in alveolar macrophages, leading to their bloating and foaming. This defect is associated with conditions like pulmonary alveolar proteinosis, obesity, and atherosclerosis.
A study reveals that alveolar macrophages, responsible for filtering bacteria and viruses from the lungs, fail to function properly when lacking a crucial transcription factor called C/EBPb. This leads to an accumulation of surfactant in the lungs, causing pulmonary alveolar proteinosis (PAP), a hitherto incurable disease.
Researchers studied two strains of Mycobacterium tuberculosis with different lung attack mechanisms, finding that high-transmission strains trigger granulomas that may aid bacterial escape into the airways. In contrast, low-transmission strains cause inflammation that traps bacteria, reducing transmissibility.
After recovering from pneumonia, alveolar macrophages transform and retain a memory of their prior experience, influencing future responses to infections. This finding may lead to improved lung defenses against pneumonia in young adults.
A new study published in Science Translational Medicine reveals that monitoring Zinc finger and BTB domain-containing protein 7A (ZBTB7A) can be an early predictor of chronic lung allograft dysfunction (CLAD). This discovery fills the void for a reliable marker, opening new opportunities for diagnosis and prevention.
The immunoproteasome regulates alternative macrophage activation by inhibiting IL-4 signaling, reducing repair and clean-up functions. Targeted treatment with specific inhibitors may accelerate healing processes in the lung after acute pneumonia.
Researchers have identified alveolar macrophages as key contributors to cystic fibrosis airway inflammation, with the overabundance of XBP-1 protein mediating their inflammatory effect. This discovery bolsters the case for targeting this pathway in therapy.
The lung has a unique innate immune system, protected by alveolar macrophages that are repressed in steady state, activated when needed, and then re-repressed. This complex circuit allows for brief activation periods to fight invading microorganisms.