The relationship between intensity of inflammatory stimulation and production of α2-macroglobulin (α2M) and α1-acid glycoprotein (AAG) in rats was investigated. Sprague-Dawley rats were injected with turpentine oil at doses of 0.05, 0.2 or 0.4 mL/rat. Serum levels of α2M, interleukin (IL)-6 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) were measured by enzyme-linked immunosorbent assay, and AAG was measured by single radial immunodiffusion. Peak serum levels of α2M and AAG in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. However, no significant differences were observed for peak serum levels of these acute-phase proteins between 0.2 and 0.4 mL/rat. Furthermore, peak serum levels of IL-6 and CINC-1 in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. Thus, the production of these acute-phase proteins has upper limits, even under increased strength of inflammatory stimulation in rats injected with turpentine oil.

Abstract:We investigated the effects of interleukin-6 (IL-6) and cytokine-induced neutrophil chemoattractant-1 (CINC-1) on α 2 -macroglobulin (α2M) production in rats. IL-6-rich and CINC-1-rich fractions were separated from serum obtained from rats 12 h after injection with turpentine oil using gel-chromatography. Sexual dimorphism was observed in the peak levels of α2M after injection of IL-6-, CINC-1-, or a mixture of IL-6-and-CINC-1-rich fractions. No significant differences in α2M levels were observed in males after injection with IL-6-or CINC-1-rich fractions and those injected with normal serum obtained from healthy rats (control). In contrast, serum levels of α2M, 6 to 120 h after injection of a mixture of IL-6-and CINC-1-rich fractions were significantly higher than in control rats. These results suggest that IL-6 and CINC-1 contribute to α2M production in rats only when IL-6 and CINC-1 act synergistically.

These results suggest that colostral antibodies against VT2, flagellum and somatic cells are effective against E. coli O157:H7 infection.

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These results suggest that absorption of VT2 from the intestine was inhibited by repeated administration of bovine immune colostral antibody against VT2 at early stages of Escherichia coli O157:H7 infection, whereas VT2 in the intestine remained at low levels.