It has been argued that stimulation of the immune system depresses performance. Accordingly, an experiment was conducted to determine the effect of dietary xylitol (150 g/kg diet) on growth and selected inflammatory responses in male broiler chickens. During the final 6 d of the experimental periods, chicks were injected with antigens: Escherichia coli lipopolysaccharide (LPS) on days 1, 3 and 5 and with Sephadex-G50 superfine on days 2 and 4 to stimulate macrophage functions. The immune stimulation reduced body weight gain and food intake, but enhanced alpha 1 acid glycoprotein (AGP) concentration and interleukin (IL-1) like activity in plasma. Feeding the xylitol diet partially, but significantly, prevented the reductions in body weight gain and food intake, without affecting the early stage of inflammatory responses triggered by LPS and Sephadex injections.

Tumor suppressor p53 plays an integral role in DNA-damage induced apoptosis, a biological process that protects against tumor progression. Cell shape dramatically changes when cells undergo apoptosis, which is associated with actomyosin contraction; however, it remains entirely elusive how p53 regulates actomyosin contraction in response to DNA-damaging agents. To identify a novel p53 regulating gene encoding the modulator of myosin, we conducted DNA microarray analysis. We found that, in response to DNA-damaging agent doxorubicin, expression of myotonic dystrophy protein kinase (DMPK), which is known to upregulate actomyosin contraction, was increased in a p53-dependent manner. The promoter region of DMPK gene contained potential p53-binding sequences and its promoter activity was increased by overexpression of the p53 family protein p73, but, unexpectedly, not of p53. Furthermore, we found that doxorubicin treatment induced p73 expression, which was significantly attenuated by downregulation of p53. These data suggest that p53 induces expression of DMPK through upregulating p73 expression. Overexpression of DMPK promotes contraction of the actomyosin cortex, which leads to formation of membrane blebs, loss of cell adhesion, and concomitant caspase activation. Taken together, our results suggest the existence of p53-p73-DMPK axis which mediates DNA-damage induced actomyosin contraction at the cortex and concomitant cell death.

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