Pediatric surgery international · 2026
Macrophage subtypes distinguish the hepatic lobule from portal area as sites of inflammation and fibrosis in liver of patients with biliary atresia.
СтатьяНазвание и аннотация: Перевод в очереди
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Tsuruno Yudai, Muraji Toshihiro, Ohtani Haruo, Masuya Ryuta, Sugita Koshiro, Tohma Miki, Yanai Toshihiro, Tabata Yumiko, Nishida Nanako, Kedoin Chihiro, Nagano Ayaka, Murakami Masakazu, Yano Keisuke, Onishi Shun, Harumatsu Toshio, Kawano Takafumi, Bitoh Yuko, Ieiri Satoshi
Аннотация
PURPOSE: Biliary atresia (BA) has potential immune-mediated pathogenesis involving CD4 + Th1 and Th17 cells. We therefore examined antigen-presenting cells to elucidate their etiopathogenetic mechanisms.
METHODS: This study cohort included 17 patients with BA and 15 controls (8 normal controls [NCs] and 7 clinical inflammation controls [CICs]). We focused on CD86+ macrophages, which are antigen-presenting cells. We performed double immunohistochemistry for CD86/CD68, with double-positive and CD68-single-positive cells representing M1 and non-M1 macrophages, respectively. Macrophage subsets were morphometrically analyzed in the hepatic lobule (HL), portal area (PA), and interface (IF) and investigated in relation to clinical data.
RESULTS: In the BA group, M1 macrophages in all regions and non-M1 macrophages in the IF and PA were significantly increased compared to those in the NC group. Notably, M1 macrophages often clustered in the IF, and non-M1 macrophages in the PA showed a small spindle-shaped morphology. Non-M1 macrophages in the IF showed a significant positive correlation with alanine aminotransferase, direct bilirubin, and fibrotic area.
CONCLUSIONS: M1 macrophages were detected as the major population in the HL and IF in BA, whereas non-M1 macrophages in the PA were correlated with hepatic fibrosis. CD86+ and CD86- macrophages immunologically distinguish HL with IF from PA in BA.
METHODS: This study cohort included 17 patients with BA and 15 controls (8 normal controls [NCs] and 7 clinical inflammation controls [CICs]). We focused on CD86+ macrophages, which are antigen-presenting cells. We performed double immunohistochemistry for CD86/CD68, with double-positive and CD68-single-positive cells representing M1 and non-M1 macrophages, respectively. Macrophage subsets were morphometrically analyzed in the hepatic lobule (HL), portal area (PA), and interface (IF) and investigated in relation to clinical data.
RESULTS: In the BA group, M1 macrophages in all regions and non-M1 macrophages in the IF and PA were significantly increased compared to those in the NC group. Notably, M1 macrophages often clustered in the IF, and non-M1 macrophages in the PA showed a small spindle-shaped morphology. Non-M1 macrophages in the IF showed a significant positive correlation with alanine aminotransferase, direct bilirubin, and fibrotic area.
CONCLUSIONS: M1 macrophages were detected as the major population in the HL and IF in BA, whereas non-M1 macrophages in the PA were correlated with hepatic fibrosis. CD86+ and CD86- macrophages immunologically distinguish HL with IF from PA in BA.