Macrophages are formed from peripheral blood precursors called monocytes. They are the first line of defense against invading disease-causing organisms. Macrophages attack invaders by a process of phagocytosis (engulfment and breakdown of particles). They can also help initiate immune responses by T lymphocytes.
A new study finds that chronic stress leads to recruitment of myeloid macrophages to the hippocampus, weakening the brain’s capacity for spatial memory. This finding may have broad implications for sufferers of stress-induced disorders.
Stress is part of our lives. Whether it occurs over finishing a term paper five milliseconds before the deadline, navigating the complicated social undercurrents in the office, juggling your teenaged offspring’s wishes against the budgetary restrictions of your existence, or getting delayed on the freeway on your way to an interview / concert / meeting / [insert absolutely crucial event here] – we all experience stress to varying degrees. Our bodies are equipped to handle stress, by pumping more oxygen to the brain, making us more alert and responsive.
Scientists discover and visualize the astonishing capability of microglia, macrophages circulating in the brain, to repair broken blood vessels. This finding may open up new avenues for treatment of hemorrhagic strokes and brain microbleeds associated with dementia and cognitive decline.
Every four minutes, a person dies from a stroke in the US. A staggering 15 million people worldwide suffer from an occurrence of this disease every year. Strokes are thus incredibly common and extremely serious. The majority of these strokes is caused by a disruption of the blood flow to the brain, and therapy approaches using pluripotent stem cells show much promise. However, about 13% of strokes are hemorrhagic in nature, where brain blood vessels rupture and blood flows freely into the brain tissue.
The 1976 convention of the American Legion in Philadelphia turned out to be an ill-fated event: Around 200 attendees contracted pneumonia, and about 30 eventually succumbed to the disease, which was caused by a hitherto unknown but quickly famed bacterium: Legionella pneumophila. This microbe evades the immune response by a particularly sneaky mechanism. It lets itself be eaten by the host’s macrophages, and instead of perishing, like regular pathogens, it makes itself a cozy home within those immune cells. It does this by preventing the fusion of the phagosome, where the bacteria reside, with the lysosome, which carries the killer enzymes that usually tackle the invading microbes, inside the macrophages. Instead, the bacteria continue to replicate happily inside the immune cells until these burst, releasing thousands of new bacteria that can hunt for new macrophages, thereby spreading all over the body. The disease is often deadly, especially when antibiotic treatment is delayed.