Abstract：
In infants with suspected food protein induced proctocolitis (sFPIP) only a minority of patients are finally diagnosed with the disease following diagnostic dietary intervention (DDI). There is a need for a pathophysiological explanation for the cause of hematochezia in the majority of sFPIP infants.
We prospectively recruited infants with sFPIP and healthy controls. Fecal samples were collected at inclusion, week 4 (end of DDI in sFPIP), and week 8. For 16S rRNA sequencing (515F/806R) we used Illumina MiSeq sequencing system. Amplicon sequence variants were generated using Qiime2 and DADA2. Qiime diversity alpha and beta group comparisons and linear discriminant analysis effect size analysis was performed. For shotgun metagenomic analysis on species level we used KneadData and MetaPhlAn2.
Fourteen sFPIP infants were compared to 55 healthy infants. At inclusion overall microbial composition of sFPIP infants differed significantly from controls (weighted UniFrac; Pairwise PERMANOVA, P = 0.002, pseudo- F = 5.008). On genus level healthy infant microbiota was significantly enriched with Bifidobacterium ( B ) compared to sFPIP patients (linear discriminant analysis [LDA] = 5.5, P < 0.001, 31.3% vs 12.1%). sFPIP stool was significantly enriched by Clostridium sensu stricto 1 over controls (LDA = 5.3, P = 0.003, 3.5% vs 18.3%). DDI caused a significant and sustained increase of Bifidobacterium (LDA = 5.4, P = 0.048, 27.9%) in sFPIP infants. Species level analysis revealed significant reduction of abundance of B longum in sFPIP patients, which after DDI was reversed by B. species other than B longum .
We revealed a gut microbiota dysbiosis phenomenon in sFPIP infants. DDI induces a microbiota composition comparable to that of healthy infants. In most sFPIP infants hematochezia might be triggered by a gut microbiota dysbiosis phenomenon.
We prospectively recruited infants with sFPIP and healthy controls. Fecal samples were collected at inclusion, week 4 (end of DDI in sFPIP), and week 8. For 16S rRNA sequencing (515F/806R) we used Illumina MiSeq sequencing system. Amplicon sequence variants were generated using Qiime2 and DADA2. Qiime diversity alpha and beta group comparisons and linear discriminant analysis effect size analysis was performed. For shotgun metagenomic analysis on species level we used KneadData and MetaPhlAn2.
Fourteen sFPIP infants were compared to 55 healthy infants. At inclusion overall microbial composition of sFPIP infants differed significantly from controls (weighted UniFrac; Pairwise PERMANOVA, P = 0.002, pseudo- F = 5.008). On genus level healthy infant microbiota was significantly enriched with Bifidobacterium ( B ) compared to sFPIP patients (linear discriminant analysis [LDA] = 5.5, P < 0.001, 31.3% vs 12.1%). sFPIP stool was significantly enriched by Clostridium sensu stricto 1 over controls (LDA = 5.3, P = 0.003, 3.5% vs 18.3%). DDI caused a significant and sustained increase of Bifidobacterium (LDA = 5.4, P = 0.048, 27.9%) in sFPIP infants. Species level analysis revealed significant reduction of abundance of B longum in sFPIP patients, which after DDI was reversed by B. species other than B longum .
We revealed a gut microbiota dysbiosis phenomenon in sFPIP infants. DDI induces a microbiota composition comparable to that of healthy infants. In most sFPIP infants hematochezia might be triggered by a gut microbiota dysbiosis phenomenon.
摘要：
目的：在疑似食物蛋白诱导的直肠结肠炎（sFPIP）的婴儿中，只有少数患者在诊断性饮食干预（DDI）后最终被诊断为该病。需要对大多数sFPIP婴儿中便血的原因进行病理生理学解释。
方法：我们前瞻性招募sFPIP患儿和健康对照者。在包含时收集粪便样本，第4周（sFPIP中的DDI结束），第8周对于16SrRNA测序(515F/806R),我们使用IlluminaMiSeq测序系统。使用Qime2和DADA2产生扩增子序列变体。进行了Qime多样性α和β组比较和线性判别分析效应大小分析。对于物种水平的shot弹枪宏基因组分析，我们使用了KneadData和MetaPhlAn2。
结果：将14名sFPIP婴儿与55名健康婴儿进行了比较。在包含sFPIP婴儿的总体微生物组成与对照组显着不同（加权UniFrac；成对PERMANOVA，P=0.002,伪F=5.008)。在属水平上，与sFPIP患者相比，健康婴儿微生物群明显富含双歧杆菌（B）（线性判别分析[LDA]=5.5，P<0.001，31.3％vs12.1％）。与对照组相比，严格梭状芽孢杆菌1显着富集了sFPIP粪便（LDA=5.3，P=0.003，3.5％vs18.3％）。DDI引起sFPIP婴儿双歧杆菌的显着和持续增加（LDA=5.4，P=0.048，27.9％）。物种水平分析显示sFPIP患者中长B丰度显著降低，DDI后被B长株以外的B.物种逆转。
结论：我们揭示了sFPIP婴儿的肠道菌群失调现象。DDI诱导与健康婴儿相当的微生物群组成。在大多数sFPIP中，婴儿便血可能是由肠道微生物群菌群失调现象引发的。
方法：我们前瞻性招募sFPIP患儿和健康对照者。在包含时收集粪便样本，第4周（sFPIP中的DDI结束），第8周对于16SrRNA测序(515F/806R),我们使用IlluminaMiSeq测序系统。使用Qime2和DADA2产生扩增子序列变体。进行了Qime多样性α和β组比较和线性判别分析效应大小分析。对于物种水平的shot弹枪宏基因组分析，我们使用了KneadData和MetaPhlAn2。
结果：将14名sFPIP婴儿与55名健康婴儿进行了比较。在包含sFPIP婴儿的总体微生物组成与对照组显着不同（加权UniFrac；成对PERMANOVA，P=0.002,伪F=5.008)。在属水平上，与sFPIP患者相比，健康婴儿微生物群明显富含双歧杆菌（B）（线性判别分析[LDA]=5.5，P<0.001，31.3％vs12.1％）。与对照组相比，严格梭状芽孢杆菌1显着富集了sFPIP粪便（LDA=5.3，P=0.003，3.5％vs18.3％）。DDI引起sFPIP婴儿双歧杆菌的显着和持续增加（LDA=5.4，P=0.048，27.9％）。物种水平分析显示sFPIP患者中长B丰度显著降低，DDI后被B长株以外的B.物种逆转。
结论：我们揭示了sFPIP婴儿的肠道菌群失调现象。DDI诱导与健康婴儿相当的微生物群组成。在大多数sFPIP中，婴儿便血可能是由肠道微生物群菌群失调现象引发的。
