Li J, Kudsk K A, Hamidian M, Gocinski B L
Department of Surgery, University of Tennessee, Memphis, USA.
Arch Surg. 1995 Nov;130(11):1164-9; discussion 1169-70. doi: 10.1001/archsurg.1995.01430110022005.
Our prior studies show that intravenous (IV) total parenteral nutrition (TPN) produces atrophy of the small intestine-related gut-associated lymphoid tissue and significant decreases in intestinal IgA levels, the major system of mucosal immunity. Others have noted increased small intestinal permeability, bacterial adherence and translocation, and decreased IgA levels in TPN-fed animals. Bombesin, a neuropeptide, may play a regulatory role in mucosal immunity. It is not clear whether bombesin attenuates the TPN-associated gut-associated lymphoid tissue atrophy.
To examine the effect of bombesin on gut-associated lymphoid tissue integrity and function during IV TPN feeding.
Randomized animal study.
A university laboratory.
Male ICR mice weighing 25 to 30 g were randomized to chow plus IV saline solution (n = 12), IV TPN (n = 12), or IV TPN plus bombesin (15 micrograms/kg, administered intramuscularly three times a day) (n = 12). Animals were killed after 5 days of receiving the experimental diet. Total small intestinal IgA level was quantified by enzyme-linked immunosorbent assay. Lymphocytes were isolated from Peyer's patches, intraepithelial spaces, and lamina propria and were stained with specific antibodies for B and T cells and for T-cell expression of CD4 and CD8 by flow cytometric analysis. Data were analyzed by analysis of variance.
Bombesin prevented the IV TPN decreases in (1) total cell yield and B-cell yield from the Peyer's patches, intraepithelial spaces, and lamina propria; (2) T-cell yield in the intraepithelial spaces and lamina propria; and (3) small intestinal IgA levels. Bombesin also reversed IV TPN decreases in CD4+ and CD8+ T cells in the intraepithelial spaces and Peyer's patches and prevented the decrease in the CD4/CD8 ratio in the lamina propria.
Bombesin prevents the TPN-associated atrophy and dysfunction of gut-associated lymphoid tissue, supporting the concept of close neuroimmunologic interaction.
我们之前的研究表明，静脉内（IV）全胃肠外营养（TPN）会导致小肠相关的肠道相关淋巴组织萎缩，并使肠道IgA水平显著降低，而IgA是粘膜免疫的主要系统。其他人已经注意到，接受TPN喂养的动物小肠通透性增加、细菌粘附和移位，以及IgA水平降低。蛙皮素是一种神经肽，可能在粘膜免疫中起调节作用。目前尚不清楚蛙皮素是否能减轻TPN相关的肠道相关淋巴组织萎缩。
研究蛙皮素在静脉内TPN喂养期间对肠道相关淋巴组织完整性和功能的影响。
随机动物研究。
大学实验室。
将体重25至30 g的雄性ICR小鼠随机分为普通饲料加静脉内生理盐水组（n = 12）、静脉内TPN组（n = 12）或静脉内TPN加蛙皮素组（15微克/千克，每天肌肉注射3次）（n = 12）。接受实验饮食5天后处死动物。通过酶联免疫吸附测定法定量小肠总IgA水平。从派尔集合淋巴结、上皮内间隙和固有层分离淋巴细胞，并用针对B细胞和T细胞以及T细胞CD4和CD8表达的特异性抗体进行染色，通过流式细胞术分析。数据采用方差分析进行分析。
蛙皮素可防止静脉内TPN导致的以下情况降低：（1）派尔集合淋巴结、上皮内间隙和固有层的总细胞产量和B细胞产量；（2）上皮内间隙和固有层的T细胞产量；（3）小肠IgA水平。蛙皮素还可逆转静脉内TPN导致的上皮内间隙和派尔集合淋巴结中CD4 +和CD8 + T细胞的减少，并防止固有层中CD4/CD8比值的降低。
蛙皮素可防止TPN相关的肠道相关淋巴组织萎缩和功能障碍，支持神经免疫密切相互作用的概念。
