A study published in this month's Anesthesiology highlights the potential of cell-based therapies for the treatment of acute lung injury and acute respiratory distress syndrome (ARDS). This discovery may represent a milestone in acute lung injury therapy, which is based on removing and then reintroducing cells from the same individual.
In contrast to more controversial stem cell transplantation, the new technique employs a subject's own progenitor cells, which are present in adults and are more restricted than stem cells in the type of tissues they can subsequently form.
Chen-Fuh Lam, M.D., Ph.D., and colleagues from the National Cheng Kung University College of Medicine and Hospital in Taiwan, found convincing evidence that autologous (meaning transferred from the same individual) transplantation of cells that eventually form blood vessel linings ‚Äö?Ñ??‚àö?ë‚àö?ò so-called endothelial progenitor cells (EPCs) ‚Äö?Ñ??‚àö?ë‚àö?ò had markedly positive effects on animals being treated for acute lung injury.
'Acute lung injury and acute respiratory distress syndrome continue to be major causes of death in seriously ill patients,' said Dr Lam. 'Despite advances in current medical therapeutics, the overall mortality of acute lung injury remains as high as 40 percent, and even people who survive may suffer from certain respiratory complications.'
Dr Lam further explained that several pharmacologic agents have been examined in the management of acute lung injury over the past decades, but few of them have met with much success.
In Dr Lam's study, EPCs, which are derived from circulating bone marrow, were removed from a healthy animal and allowed to grow for one week in a laboratory culture. These cells were then reintroduced into the circulatory system of the same animal that had undergone induced acute lung injury.
'Our results obtained from a rabbit model of acute lung injury showed that transplantation of these premature EPCs significantly improved the function of lung blood vessels, reduced the amount of water that leaked into lungs, and decreased bleeding in the lungs.'
Dr Lam and colleagues also performed additional laboratory experiments on the antioxidant capacity of premature human EPCs compared to relatively more mature endothelial cells derived from human umbilical cords. They found that certain helpful antioxidant effects were greater in the premature EPCs than in the more mature endothelial cells.
In a companion editorial, Ellen L. Burnham, M.D., of the University of Colorado Health Sciences Centre, lauded Dr Lam's study and touted its potential influence in this field of research.
'These findings suggest a potential mechanism whereby infusion of premature EPCs acts to normalise the oxidative environment of the injured lung and potentially lay the groundwork for adequate lung repair and normalisation of cellular function.'
Both Dr Burnham and Dr Lam, however, emphasised that more animal studies need to be performed before EPC transplantation for acute lung injury can be considered safe for human subjects.
Again, Dr Burnham: 'Although cell-based therapies for lung injury are still a faraway goal, studies such as this by Dr Lam and his colleagues provide important information that will undoubtedly aid in the development of novel therapies for acute lung injury and ARDS,' she said.
While a number of animal studies have provided useful direction for further research, it is important to note that animal studies are considered basic science, and their findings do not always translate to the complex physiological system of human beings.
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