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Τρίτη 27 Ιουλίου 2021

Immunohistochemical study of inflammatory responses in septa arising from type I intestinal atresia

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Histol Histopathol. 2021 Jul 27:18364. doi: 10.14670/HH-18-364. Online ahead of print.

ABSTRACT

The purpose of this study was to evaluate defensive functional cells in intestinal septa during recanalization in the embryonic period, and to access immune responses in septa arising from type I intestinal atresia and normal intestinal walls. Tissue samples were of septa located in the intestinal wall at a distance <15cm from the ligament of Treitz, and normal intestine walls obtained from seven neonates who underwent surgery. Following serial tissue sectioning, the samples were subjected to hematoxylin and eosin (HE), periodic acid-Schiff (PAS) and immunohistochemical staining to determine the morphological features and markers of functional cells and immune responses in the septa and normal intestinal walls. Quantitative analysis was conducted to compare differences between them. Compared with normal intestinal wall, the mucosal layer of septa arising from type I intestinal atresia had fewer misaligned villi and no classic epithelial crypts. Immunohistochemical staining showed that the mucosal layer of septa arising from type I intestinal atresia had fewer Paneth cells and goblet cells and lower amounts of lysozyme and MUC2, than normal intestinal walls. The concentration of pro-inflammatory cytokines, including interlukin (IL)-6 and tumor necrosis factor (TNF) -α, as well as macrophage inflammatory protein 3α (MIP-3α) and its receptor, CCR6, were higher in the mucosal layer of septa arising from type I intestinal atresia than in normal intestinal walls. Moreover, the numbers of mature dendritic cells and CD4+ T lymphocytes were higher in the mucosal layer of septa than in normal intestinal walls. The defensive activity of septa arising from type I intestinal atresia is weaker than that of normal intestinal walls. This weaker activity may correlate with increases in mature dendritic cells and CD4+ T lymphocyte s, as well overexpression of proinflammatory cytokines.

PMID:34312829 | DOI:10.14670/HH-18-364

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