Fock Ricardo Ambrósio, Vinolo Marco Aurélio Ramirez, Crisma Amanda Rabello, Nakajima Karina, Rogero Marcelo Macedo, Borelli Primavera
Experimental Hematology Laboratory, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, SP, Brazil.
J Nutr Sci Vitaminol (Tokyo). 2008 Oct;54(5):371-7. doi: 10.3177/jnsv.54.371.
Malnutrition modifies resistance to infection by impairing a number of physiological processes including hematopoesis and the immune response. In this study, we examined the production of Interleukin-4 (IL-4) and IL-10 in response to lipopolysaccharide (LPS) and also evaluated the cellularity of the blood, bone marrow, and spleen in a mouse model of protein-energy malnutrition. Two-month-old male Swiss mice were subjected to protein-energy malnutrition (PEM) with a low-protein diet (4%) as compared to the control diet (20%). When the experimental group lost approximately 20% of their original body weight, the animals from both groups received 1.25 microg of LPS intravenously. The cells in the blood, bone marrow, and spleen were counted, and circulating levels of IL-4 and IL-10 were evaluated in animals stimulated with LPS. Cells from the spleen, bone marrow, and peritoneal cavity of non-inoculated animals were collected for culture to evaluate the production of IL-4 and IL-10 after stimulating these cells with 1.25 microg of LPS in vitro. Malnourished animals presented leucopenia and a severe reduction in bone marrow, spleen, and peritoneal cavity cellularity before and after stimulus with LPS. The circulating levels of IL-10 were increased in malnourished animals inoculated with LPS when compared to control animals, although the levels of IL-4 did not differ. In cells cultured with LPS, we observed high levels of IL-10 in the bone marrow cells of malnourished animals. These findings suggest that malnourished mice present a deficient immune response to LPS. These alterations may be partly responsible for the immunodeficiency observed in these malnourished mice.
营养不良会损害包括造血和免疫反应在内的许多生理过程,从而改变对感染的抵抗力。在本研究中,我们检测了蛋白质 - 能量营养不良小鼠模型中,白细胞介素 - 4(IL - 4)和IL - 10对脂多糖(LPS)的反应,并评估了血液、骨髓和脾脏的细胞数量。将两个月大的雄性瑞士小鼠与对照饮食(20%)相比,用低蛋白饮食(4%)使其遭受蛋白质 - 能量营养不良(PEM)。当实验组体重减轻约20%时,两组动物均静脉注射1.25微克LPS。对血液、骨髓和脾脏中的细胞进行计数,并评估LPS刺激动物后IL - 4和IL - 10的循环水平。收集未接种动物的脾脏、骨髓和腹腔细胞进行培养,以评估在体外用1.25微克LPS刺激这些细胞后IL - 4和IL - 10的产生情况。营养不良的动物在LPS刺激前后均出现白细胞减少,骨髓、脾脏和腹腔细胞数量严重减少。与对照动物相比,接种LPS的营养不良动物中IL - 10的循环水平升高,尽管IL - 4水平没有差异。在用LPS培养的细胞中,我们观察到营养不良动物的骨髓细胞中IL - 10水平较高。这些发现表明,营养不良的小鼠对LPS的免疫反应不足。这些改变可能部分导致了这些营养不良小鼠中观察到的免疫缺陷。