Gustafsson Björn I, Bakke Ingunn, Hauso Øyvind, Kidd Mark, Modlin Irvin M, Fossmark Reidar, Brenna Eiliv, Waldum Helge L
Department of Gastroenterology, St Olavs Hospital HF, Trondheim University Hospital, Trondheim, Norway.
Scand J Gastroenterol. 2011 May;46(5):531-7. doi: 10.3109/00365521.2011.558113. Epub 2011 Feb 23.
Enterochromaffin-like (ECL) cells are central in the regulation of acid secretion. G cells release gastrin and activate ECL cell histamine secretion which stimulates parietal cell H(2) receptors initiating acid secretion. It is unclear whether histamine-mediated parietal cell activation is via a vascular or paracrine pathway. To assess this, we utilized immunohistochemistry (IHC) and electron microscopy to examine gastric tissue and used visualization of formalin fixed dispersed gastric cells and glands to investigate and define the anatomical relationship between ECL and parietal cells.
Sprague-Dawley rat stomachs were instilled with formalin. Thereafter fixed mucosal cells and whole gastric glands were dispersed by mechanical and chemical dissolution and enzymatic digestion. Smears with fixed isolated cells and whole glands were stained by IHC with histidine decarboxylase (HDC) and H+/K+-ATPase antibodies. Whole tissue samples of Sprague-Dawley and cotton rat oxyntic mucosa were investigated with IHC using HDC, VMAT2 and H+/K+-ATPase antibodies, and electron microscopy was performed to further delineate the precise anatomic relationship between ECL cells and parietal cells.
Each ECL cell generated a network of HDC- and VMAT2-positive dendritic-like elongations that were in direct contact with several parietal cells. Thus, ECL cells at the base of the gland were in communication with parietal cells in the middle of the gland. Electron microscopy confirmed that the cytoplasmic ECL cell elongations containing secretory vesicles were in direct juxtaposition to parietal cells.
These findings indicate that ECL cells directly regulate parietal cell function in a neurocrine manner via slender neuron-like elongations.
肠嗜铬样（ECL）细胞在胃酸分泌调节中起核心作用。G细胞释放胃泌素并激活ECL细胞组胺分泌，后者刺激壁细胞H₂受体引发胃酸分泌。目前尚不清楚组胺介导的壁细胞激活是通过血管途径还是旁分泌途径。为评估这一点，我们利用免疫组织化学（IHC）和电子显微镜检查胃组织，并通过可视化福尔马林固定的分散胃细胞和腺体来研究和确定ECL细胞与壁细胞之间的解剖关系。
向Sprague-Dawley大鼠胃内灌注福尔马林。此后，通过机械和化学溶解及酶消化使固定的黏膜细胞和整个胃腺体分散。用组氨酸脱羧酶（HDC）和H⁺/K⁺-ATP酶抗体对固定的分离细胞和整个腺体涂片进行IHC染色。使用HDC、囊泡单胺转运体2（VMAT2）和H⁺/K⁺-ATP酶抗体，通过IHC对Sprague-Dawley大鼠和棉鼠胃底黏膜的全组织样本进行研究，并进行电子显微镜检查以进一步描绘ECL细胞与壁细胞之间的确切解剖关系。
每个ECL细胞产生一个由HDC和VMAT2阳性的树突状样伸长结构组成的网络，这些结构与多个壁细胞直接接触。因此，腺体底部的ECL细胞与腺体中部的壁细胞相互连通。电子显微镜证实，含有分泌囊泡的ECL细胞胞质伸长结构与壁细胞直接并列。
这些发现表明，ECL细胞通过细长的神经元样伸长结构以神经分泌方式直接调节壁细胞功能。
