Westermann J, Michel S, Lopez-Kostka S, Bode U, Rothkötter H J, Bette M, Weihe E, Straub R H, Pabst R
Center of Anatomy, Medical School of Hannover, Germany.
J Neuroimmunol. 1998 Aug 1;88(1-2):67-76. doi: 10.1016/s0165-5728(98)00081-2.
The loss of spleen may lead to fatal bacterial infections. To prevent this, splenic autotransplantation has been performed in humans and experimental animals. However, there is still controversy about the protective function of this procedure. Since innervation plays an important role in splenic function, we investigated whether splenic regenerates are re-innervated, and whether this depends on the donor and host age. Splenic tissue (30 mg) was implanted into the greater omentum of either young (2 days) or old (12 months) rats, from either young or old syngeneic animals. After 3 months of regeneration, the weight of the regenerates was determined, PGP+ nerve fibers were revealed by immunohistology, and subdivided into nerve fibers of sympathetic (TH+, NPY+) or sensory (SP+, CGRP+) origin. In addition, proliferating (Ki-67 proliferation antigen+) and apoptotic cells (TUNEL technique+) were likewise investigated. No innervation of splenic regenerates was observed after implantation into old hosts, correlating with poorly developed splenic compartments. In contrast, almost normal re-innervation occurred in young hosts after implantation of both young and old splenic tissue. These regenerates showed well-developed splenic compartments and a normal number and tissue distribution of proliferating and apoptotic cells. However, after the implantation of young tissue, the final size of splenic regenerates was three times larger (140 +/- 30 vs. 40 +/- 10 mg). Thus, re-innervation of splenic implants is necessary for their subsequent development. It is determined by host age, whereas the final size of the splenic regenerates is regulated by donor age-dependent factors. This model is useful for studying both the process leading to initial innervation and the consequences of this innervation.
脾脏缺失可能导致致命的细菌感染。为预防此情况，已在人类和实验动物中进行了脾自体移植。然而，关于该手术的保护功能仍存在争议。由于神经支配在脾脏功能中起重要作用，我们研究了脾脏再生组织是否会重新获得神经支配，以及这是否取决于供体和宿主的年龄。将脾脏组织（30毫克）植入年轻（2天）或年老（12个月）大鼠的大网膜中，供体动物也分为年轻和年老的同基因动物。再生3个月后，测定再生组织的重量，通过免疫组织学显示PGP +神经纤维，并将其细分为交感神经（TH +，NPY +）或感觉神经（SP +，CGRP +）起源的神经纤维。此外，同样研究了增殖细胞（Ki-67增殖抗原+）和凋亡细胞（TUNEL技术+）。将脾脏组织植入年老宿主后，未观察到脾脏再生组织的神经支配，这与发育不良的脾脏隔室相关。相反，在植入年轻和年老的脾脏组织后，年轻宿主中几乎出现了正常的重新神经支配。这些再生组织显示出发育良好的脾脏隔室以及增殖和凋亡细胞的正常数量和组织分布。然而，植入年轻组织后，脾脏再生组织的最终大小是其3倍（140±30对40±10毫克）。因此，脾脏植入物的重新神经支配对其后续发育是必要的。它由宿主年龄决定，而脾脏再生组织的最终大小由依赖供体年龄的因素调节。该模型对于研究导致初始神经支配的过程及其神经支配的后果均有用。
