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Long before last spring’s H1N1 epidemic, Adrienne G. Randolph, MD, MSc, of Children’s Division of Critical Care Medicine, was concerned to see otherwise healthy school-aged children becoming critically ill from influenza. Why were children without any prior known risk factors developing deep pneumonias, sometimes requiring ventilation and heart-lung bypass, and succumbing to serious co-infections such as Staphylococcus aureus?
Dr. Randolph and her colleagues in the Pediatric Acute Lung Injury and Sepsis Investigators Network have launched an investigation that has so far enrolled 175 critically ill flu patients (50 percent with H1N1, the rest with seasonal flu) from more than 22 ICUs in the United States and Canada. Using blood and lung-fluid samples, they are exploring possible genetic and immunologic differences, co-infecting pathogens and potential susceptibility factors such as vitamin D levels.
Cellular immune responses and cytokines are being closely quantified in the blood and lungs. T-lymphocytes, for example, are sometimes virtually absent in the blood; aided by a team led by
Raif S. Geha, MD, of the Division of Immunology, Dr. Randolph’s group is investigating whether these cells have died or simply moved to the lungs. With the help of Louis Kunkel, PhD, director of the Program in Genomics, the researchers are investigating the genes that control the innate immune response, looking for individual differences.
Results from laboratory analyses of the first 126 critically ill children are being analyzed and Dr. Randolph hopes the data will help in targeting treatments. For example, some patients may have an extremely weak immune response, while others may need suppression of an over-active response. Meanwhile, a separate project with the Dana-Farber Cancer Institute is testing people’s ability to make antibodies to the stalk of the flu virus. Dr. Randolph hopes this will yield clues to better vaccines.
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