低聚果糖通过调整肠道菌群改善川崎病小鼠冠状动脉损伤的机制

doi:10.3969/j.issn.2095-9400.2021.06.001

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Abstract Objective: To investigate the underlying mechanism for fructo-oligosaccharide to attenuate coronary artery injury in mice with Kawasaki disease (KD) by regulating intestinal flora. Methods: Mice were given water-soluble components of Candida albicans cell wall (CAWS) to establish KD model and randomly assigned as normal control group (PBS), KD model group (CAWS), and FOS+KD group (FOS). After 28 days of modeling, feces and hearts were collected. The structural changes of coronary arteries and the infiltration degree of monocyte-macrophages were detected by HE and immunofluorescence with CD68 antibody, respectively. The differences in intestinal flora and metabolites of short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and gas chromatography/mass spectrometry (GS-MS). Results: HE results showed that after KD modeling, many normal structures of coronary arteries disappeared. Wall edema and a large number of inflammatory
cells were infiltrated. Immunofluorescence showed significant enhancement of CD68, the monocyte-macrophage markers, around coronary arteries. After FOS treatment, the above coronary artery injury and inflammation decreased significantly. 16S rRNA sequencing showed that intestinal flora in CAWS group was obviously
disturbed, SCFAs producing flora and fecal SCFAs content decreased. However, intestinal flora composition and SCFAs recovered after FOS treatment. Conclusion: FOS alleviated coronary artery injury of KD mice through regulating intestinal flora disturbance to increase SCFAs production

Key words： Kawasaki disease gut microbiota short-chain fatty acids inflammation -oligosaccharide

Received: 14 February 2021

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	QIAN Fanyu
	ZHANG Qihao
	CEN Jianke
	ZHOU Jinhui
	LI Ruixin
	YE Zi
	WU Menghan
	WANG Fangyan
	CHU Maoping
	ZHANG Chunxiang

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2021.06.001 OR https://xb.wmu.edu.cn/EN/Y2021/V51/I6/431

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