MinHo Kim and Jennifer Granick from the Simon Lab have published their latest work online in Blood, The official journal of the American Hematological Society. They studied skin wounding using real-time fluorescence imaging of the innate immune response in a mouse model. Remarkably, they found that Staphylococcus Aureus infection in wounds can cause the emigration of bone marrow hematopoietic progenitor cells that differentiate into neutrophils- the key innate immune cell that fights this infection. Blocking this migration and local proliferation results in marked infection and the demise of the host. The implication of this study is that one can actually engineer the innate immune response to improve wound healing during immunodeficiency as can occur in patients with diabetes or undergoing chemotherapy for cancer.
Neutrophil survival and c-kit+ progenitor proliferation in Staphylococcus aureus infected skin wounds promote resolution. Min-Ho Kim, Jennifer L. Granick, Cindy Kwok, Naomi J. Walker, Dori L. Borjesson, Fitz-Roy E. Curry, Lloyd S. Miller and Scott I. Simon,Prepublished online Jan 28, 2011; doi:10.1182/blood-2010-07-296970