muramidase and Multiple-Organ-Failure

It has been recently suggested that multiple organ failure (MOF) is caused by activation of inflammatory cells and subsequent release soluble factors from these cells. However, morphologic data to support this hypothesis is lacking. Thus, the present study was conducted to evaluate the activation of Kupffer cells in multiple organ failure by applying immunohistochemical techniques to formalin-fixed, paraffin-embedded autopsy materials. Eleven liver samples of multiple organ failure were stained for lysozyme, alpha 1-antichymotrypsin, and by lectins, such as ConA, RCA-I, WGA and PNA. Normal livers and diseased livers of miscellaneous origins were also stained and compared. In normal livers, Kupffer cells were generally negative or weakly positive for lysozyme, alpha 1-antichymotrypsin, ConA, RCA-I, and PNA, while they were positive for WGA. In multiple organ failure, by contrast, Kupffer cells showed stronger staining for alpha 1-antichymotrypsin, lysozyme, ConA, RCA-I, WGA, and PNA, indicating activation of Kupffer cells. Increased reaction to WGA and RCA-I was also observed in diseased livers of miscellaneous origins. These results are in agreement with the current hypothesis that activation of Kupfer cells is involved in the pathogenesis of MOF. Our findings also indicate, however, that activation of Kupffer cells is not a phenomenon unique to MOF.

Topics: alpha 1-Antichymotrypsin; Carbohydrates; Humans; Immunohistochemistry; Kupffer Cells; Lectins; Macrophage Activation; Multiple Organ Failure; Muramidase; Retrospective Studies