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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Influence of an established acute phase response on the severity of experimental nephritis.

Small doses of lipopolysaccharide (LPS) induced an acute phase response (APR), and a number of studies have also shown that this greatly enhances the severity of glomerular injury in the heterologous phase of nephrotoxic nephritis (hNTN), an experimental model of anti-glomerular basement membrane (GBM) disease. Here, we examined the influence of pre-existing subclinical infection and raised APR, assessed by plasma alpha 2-macroglobulin (alpha 2-M) concentration, on the degree of injury in this model of nephritis. Studies were initially performed to determine the normal range of alpha 2-M in rats and its modulation by IL-6 and different doses of LPS. Plasma concentration of alpha 2-M was found to be variable and dependent on the weight of the rats. Single injections of either LPS or IL-6 had a comparable effect, and continuous perfusions of LPS caused a progressive increase in alpha 2-M which peaked at 48 h and declined gradually over 1 week. Following induction of nephritis with 10 mg of anti-GBM antibody, rats with raised alpha 2-M had 14 +/- 3 mg/24 h albuminuria compared with 4 +/- 1 mg/24 h in rats with normal alpha 2-M (P < 0.001, Wilcoxon). Injection of 20 mg anti-GBM antibody caused 36 +/- 11 mg/24 h albuminuria compared with 16 +/- 4 mg/24 h (P < 0.001), respectively. However, all these rats remained active and none of them died. In contrast, injection of 0.25 microgram LPS before induction of nephritis with 10 mg anti-GBM antibody, in rats with raised alpha 2-M, caused severe albuminuria (115 +/- 23 mg/24 h) compared with rats having normal levels of alpha 2-M (72 +/- 15 mg/24 h, P < 0.05). Furthermore, rats with raised alpha 2-M also had severe systemic manifestations characterized by pulmonary haemorrhage and extensive glomerular thrombosis, and many of them died. These results demonstrate the potential effect of pre-existing subclinical infection and raised APR on severity of glomerular injury which may affect the outcome of experimental studies.[1]


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