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Body reveals its inflammation 'off switch'
Researchers have shed light on how the body switches off its immune response, a key step towards understanding autoimmune diseases and controlling inflammation.
When immune cells die, they transform into “sponges†that soak up the molecules responsible for causing inflammation, researchers have discovered. The new information may lead to better drugs to treat inflammatory disorders, such as eczema.
Inflammation is characterised by a red, painful swelling around a wound caused by blood fluids, proteins and immune cells flooding into an area of the body in response to germs or damage. Its biological purpose is to allow immune cells to get from the blood to the trouble spot to fight infection.
But too much inflammation can be devastating. It is what causes death in diseases such as flu, while chronic, misdirected inflammation causes conditions from eczema to arthritis. As a result, researchers have been looking for ways to "turn-off" the inflammatory response.
Ultimate scavengers
Now, Charles Serhan and colleagues at Harvard University in Boston, US, have discovered an important natural braking mechanism. In a healthy inflammatory response, immune cells called leukocytes are attracted to the site of injury, where they are activated by molecules called chemokines. The leukocytes emit powerful germ-killing chemicals, and then commit suicide.
The researchers discovered that dying leukocytes act like sponges, soaking up chemokines, preventing them from attracting more leukocytes. It is the body’s way of controlling inflammation – a good thing, since too much of their germ-killing chemicals can damage healthy surrounding tissue.
These dying leukocytes are the “ultimate scavenging entityâ€, Serhan says. As they die, they even produce more of the molecules – called CCR5 – that help them soak up chemokines. Then the whole lot is gobbled by debris-removing cleaner cells called macrophages.
Complete turnaround
This system is just one part of a complicated web of inflammation controls. But understanding this natural chemokine-soaking mechanism is vital to learning more about how inflammation and autoimmune disorders progress, the team says. For example, mice bred to lack another molecule that soaks up chemokines develop a skin inflammation similar to psoriasis in humans.
Serhan told New Scientist that one day it may be possible to control chronic inflammatory disease by making drugs that promote the natural signals that turn inflammation off.
Such drugs could also be used to turn off the chronic inflammation underlying many auto-immune diseases. “This is a complete 180° turn from the drugs sought today and used in the last century,†he says, which have focused on drugs that block the signals that turn inflammation on in the first place
Researchers have shed light on how the body switches off its immune response, a key step towards understanding autoimmune diseases and controlling inflammation.
When immune cells die, they transform into “sponges†that soak up the molecules responsible for causing inflammation, researchers have discovered. The new information may lead to better drugs to treat inflammatory disorders, such as eczema.
Inflammation is characterised by a red, painful swelling around a wound caused by blood fluids, proteins and immune cells flooding into an area of the body in response to germs or damage. Its biological purpose is to allow immune cells to get from the blood to the trouble spot to fight infection.
But too much inflammation can be devastating. It is what causes death in diseases such as flu, while chronic, misdirected inflammation causes conditions from eczema to arthritis. As a result, researchers have been looking for ways to "turn-off" the inflammatory response.
Ultimate scavengers
Now, Charles Serhan and colleagues at Harvard University in Boston, US, have discovered an important natural braking mechanism. In a healthy inflammatory response, immune cells called leukocytes are attracted to the site of injury, where they are activated by molecules called chemokines. The leukocytes emit powerful germ-killing chemicals, and then commit suicide.
The researchers discovered that dying leukocytes act like sponges, soaking up chemokines, preventing them from attracting more leukocytes. It is the body’s way of controlling inflammation – a good thing, since too much of their germ-killing chemicals can damage healthy surrounding tissue.
These dying leukocytes are the “ultimate scavenging entityâ€, Serhan says. As they die, they even produce more of the molecules – called CCR5 – that help them soak up chemokines. Then the whole lot is gobbled by debris-removing cleaner cells called macrophages.
Complete turnaround
This system is just one part of a complicated web of inflammation controls. But understanding this natural chemokine-soaking mechanism is vital to learning more about how inflammation and autoimmune disorders progress, the team says. For example, mice bred to lack another molecule that soaks up chemokines develop a skin inflammation similar to psoriasis in humans.
Serhan told New Scientist that one day it may be possible to control chronic inflammatory disease by making drugs that promote the natural signals that turn inflammation off.
Such drugs could also be used to turn off the chronic inflammation underlying many auto-immune diseases. “This is a complete 180° turn from the drugs sought today and used in the last century,†he says, which have focused on drugs that block the signals that turn inflammation on in the first place