Post by steve201 on Sept 28, 2009 22:19:02 GMT -5
this is really hopeful if you can get thru all of this
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Healing Wounded Lungs
(Ivanhoe Newswire) -- Scientists at Johns Hopkins have mapped out the steps a set of white blood cells takes toward recovery after serious lung injury.
The white blood cells are called regulatory T cells -- “Tregs” for short -- and their best known function is to keep the body's immune system from attacking its own healthy tissues.
"When a patient develops acute lung injury, we want the critical care medicine team to be able to do more than just stabilize the patient on a ventilator," Landon King, M.D., study senior investigator and director of pulmonary and critical care medicine at the Johns Hopkins University School of Medicine, was quoted as saying.
King said the study opens the door to a new field in research and development of drugs that either speed up the post-injury activation of Tregs, or supplement levels of Tregs in people who may be relatively deficient from either lung disease or chemotherapy.
Some 200,000 Americans suffer some form of sudden, acute lung injury (ALI) each year, in which inflammation spreads across both lungs, making breathing difficult and starving the body of oxygen. Among them are people with severe acute respiratory distress syndrome caused by infection, the most severe form of ALI. Also included are burn victims, people with chest injuries from car accidents, and cancer patients who have had adverse reactions to donated platelets from blood transfusion. Almost all people with ALI require breathing assistance from mechanical ventilators, and nearly 75,000 die each year.
Spurred by the lack of treatment options, King and his team started to track and map out the biological steps involved in ALI recovery with an experiment in mice that were already serving as a lab model for lung injury. As part of the lab model, mice inhaled a bacterial substance well known to critically injure both lungs within 24 hours, with inflammation, on average, peaking after four days. In mice that survived, the average recovery time was 10 days.
Researchers had long assumed that an initial spike in blood lymphocyte levels deep inside lung tissue cavities was the immune system's first response to inflammation from injury. But the Hopkins scientists were surprised to find a higher death rate in mice that had been genetically modified to be lymphocyte deficient, at 40 percent, while the death rate in mice with lymphocytes was just 10 percent.
After determining that lymphocytes were key to mice recovering from lung injury, the team set out to determine the various roles, if any, played by specific lymphocytes.
Further experiments led by Johns Hopkins pulmonologist Franco D'Alessio, M.D., showed that blood levels of one subset of lymphocytes, the regulatory T cells, jumped proportionally in the lung spaces from the first day of injury, before peaking at day seven and remaining high throughout recovery at day 10. This demonstrated to D'Alessio and colleagues that the spike was not just a response to injury, but also part of the lung's immediate and natural process of wound repair. When researchers removed Tregs from the damaged lungs in mice, leaving all other lymphocytes behind, lung healing was slowed by half.
"T cells and the body's active immune system play a crucial role in recovery from acute lung injury," D'Alessio, an instructor based at Johns Hopkins Bayview Medical Center, is quoted as saying. "It is by no means a passive process as previously thought."
To test the prospects of Tregs as a potential therapy, the team doubled bacterial toxin exposures, increasing death rates to 50 percent in untreated mice. But mice injected with Tregs within an hour of exposure had just a 10 percent death rate, with many showing signs of accelerated recovery after just six days. Similar doses of Tregs provided days after exposure also showed lowered deaths rates in mice with ALI.
King concluded, "Our study should spark lung experts here and elsewhere to shift their research focus from nearly universal interest in the onset of acute lung injury to new mechanisms underlying resolution of lung injury."
Steve
-------------------------------------------------------------------------------
Healing Wounded Lungs
(Ivanhoe Newswire) -- Scientists at Johns Hopkins have mapped out the steps a set of white blood cells takes toward recovery after serious lung injury.
The white blood cells are called regulatory T cells -- “Tregs” for short -- and their best known function is to keep the body's immune system from attacking its own healthy tissues.
"When a patient develops acute lung injury, we want the critical care medicine team to be able to do more than just stabilize the patient on a ventilator," Landon King, M.D., study senior investigator and director of pulmonary and critical care medicine at the Johns Hopkins University School of Medicine, was quoted as saying.
King said the study opens the door to a new field in research and development of drugs that either speed up the post-injury activation of Tregs, or supplement levels of Tregs in people who may be relatively deficient from either lung disease or chemotherapy.
Some 200,000 Americans suffer some form of sudden, acute lung injury (ALI) each year, in which inflammation spreads across both lungs, making breathing difficult and starving the body of oxygen. Among them are people with severe acute respiratory distress syndrome caused by infection, the most severe form of ALI. Also included are burn victims, people with chest injuries from car accidents, and cancer patients who have had adverse reactions to donated platelets from blood transfusion. Almost all people with ALI require breathing assistance from mechanical ventilators, and nearly 75,000 die each year.
Spurred by the lack of treatment options, King and his team started to track and map out the biological steps involved in ALI recovery with an experiment in mice that were already serving as a lab model for lung injury. As part of the lab model, mice inhaled a bacterial substance well known to critically injure both lungs within 24 hours, with inflammation, on average, peaking after four days. In mice that survived, the average recovery time was 10 days.
Researchers had long assumed that an initial spike in blood lymphocyte levels deep inside lung tissue cavities was the immune system's first response to inflammation from injury. But the Hopkins scientists were surprised to find a higher death rate in mice that had been genetically modified to be lymphocyte deficient, at 40 percent, while the death rate in mice with lymphocytes was just 10 percent.
After determining that lymphocytes were key to mice recovering from lung injury, the team set out to determine the various roles, if any, played by specific lymphocytes.
Further experiments led by Johns Hopkins pulmonologist Franco D'Alessio, M.D., showed that blood levels of one subset of lymphocytes, the regulatory T cells, jumped proportionally in the lung spaces from the first day of injury, before peaking at day seven and remaining high throughout recovery at day 10. This demonstrated to D'Alessio and colleagues that the spike was not just a response to injury, but also part of the lung's immediate and natural process of wound repair. When researchers removed Tregs from the damaged lungs in mice, leaving all other lymphocytes behind, lung healing was slowed by half.
"T cells and the body's active immune system play a crucial role in recovery from acute lung injury," D'Alessio, an instructor based at Johns Hopkins Bayview Medical Center, is quoted as saying. "It is by no means a passive process as previously thought."
To test the prospects of Tregs as a potential therapy, the team doubled bacterial toxin exposures, increasing death rates to 50 percent in untreated mice. But mice injected with Tregs within an hour of exposure had just a 10 percent death rate, with many showing signs of accelerated recovery after just six days. Similar doses of Tregs provided days after exposure also showed lowered deaths rates in mice with ALI.
King concluded, "Our study should spark lung experts here and elsewhere to shift their research focus from nearly universal interest in the onset of acute lung injury to new mechanisms underlying resolution of lung injury."
Steve
