Abstract
Endotoxin-treated mice exhibit a rapid rise in the level of the serum amyloid A (SAA) protein, but this effect is not observed in endotoxin-resistant C3H/HeJ mice. To evaluate the role of lymphoid cells in the production of SAA protein, C3H/HeJ mice were adoptively transfused with endotoxin-sensitive (C3H/HeN) bone marrow cells. After such adoptive transfer, endotoxin treatment of C3H/HeJ mice resulted in high serum levels of SAA protein. The ability of chimeric mice to make SAA protein correlated with the presence of endotoxin-sensitive B lymphocytes and macrophages. These findings suggest that lymphocytes and/or macrophages play an important role in initiating SAA protein synthesis after endotoxin treatment and suggest a possible mechanism by which chronic infection or inflammation leads to amyloidosis.
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