Abstract
The high incidence of serious opportunistic infections that follow thermal injuries is well documented. Normal levels of functioning leukocytes are essential to the host's ability to resist infection. This study examined alterations in murine granulopoiesis after the inducement of a standardized, sublethal, third-degree burn covering 10%, 20%, or 30% of the dorsal body surface area. Significant alterations arose in peripheral leukocyte concentrations after inducement of uncomplicated thermal injury. In general, within the first day of injury, all three trauma levels produced a peripheral leukocytosis that lasted for 35 days or more. The leukocytoses that followed 20% and 30% injuries were similar and in numerous respects paralleled previously reported human peripheral responses after similar levels of thermal trauma. Differential examinations of peripheral blood demonstrated the peripheral leukocytosis to be due primarily to the influx of morphologically mature-appearing polymorphonuclear neutrophils. Premature bone marrow release did not appear to be a factor as immature polymorphonuclear neutrophils were seldom greater than 2% of polymorphonuclear neutrophil totals. Bone marrow granulopoietic activity was examined by in vitro clonal cell culture techniques and assessed over a period of 35 days after injury. Granulocyte-macrophage colony forming cells (GM-CFC), indicative of marrow progenitor cell concentrations, were significantly increased for 28 to 35 days after 10% injury and 11 to 14 days after 20% or 30% injury. Normal or increased progenitor cell concentrations and a lack of morphologically appearing premature forms suggest that the leukocytosis is the result of injury-induced alteration(s) in polymorphonuclear neutrophil margination or release mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
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