Abstract
BackgroundMesenteric adipose tissue (mAT) hyperplasia, known as creeping fat is a pathologic characteristic of Crohn’s disease (CD). The reserve of creeping fat in surgery is associated with poor prognosis of CD patients, but the mechanism remains unknown.MethodsMesenteric microbiome, metabolome, and host transcriptome were characterized using a cohort of 48 patients with CD and 16 non-CD controls. Multidimensional data including 16S ribosomal RNA gene sequencing (16S rRNA), host RNA sequencing, and metabolome were integrated to reveal network interaction. Mesenteric resident bacteria were isolated from mAT and functionally investigated both in the dextran sulfate sodium (DSS) model and in the Il10 gene-deficient (Il10−/−) mouse colitis model to validate their pro-inflammatory roles.ResultsMesenteric microbiota contributed to aberrant metabolites production and transcripts in mATs from patients with CD. The presence of mAT resident microbiota was associated with the development of CD. Achromobacter pulmonis (A. pulmonis) isolated from CD mAT could translocate to mAT and exacerbate both DSS-induced and Il10 gene-deficient (Il10−/−) spontaneous colitis in mice. The levels of A. pulmonis in both mAT and mucous layer from CD patients were higher compared to those from the non-CD group.ConclusionsThis study suggests that the mesenteric microbiota from patients with CD sculpt a detrimental microenvironment and promote intestinal inflammation.5k89f_PEiAcxa3djQxTmu9Video abstract
Highlights
Mesenteric adipose tissue hyperplasia, known as creeping fat is a pathologic characteristic of Crohn’s disease (CD)
Flow chart of sample collection and analysis In order to elucidate a potential interaction between mesenteric adipose tissue microbiome and host responses in CD patients, a prospective cohort of 48 patients was recruited consisting of individuals with diagnosed CD
Taxonomic analysis of mesenteric adipose tissue (mAT) microbiome using principal component analysis (PCA) and principal coordinates analysis (PCoA) of 16S rRNA gene sequencing data showed that the mesenteric microbiome from CD and non-CD controls exhibited slight but significant separation (Fig. 1a and Fig. S2b)
Summary
Mesenteric adipose tissue (mAT) hyperplasia, known as creeping fat is a pathologic characteristic of Crohn’s disease (CD). Hyperplasia of mesenteric adipose tissue (mAT), known as “creeping fat,” is a pathologic characteristic of CD and is associated with postoperative recurrence [4]. Previous studies have provided evidences for the presence of bacteria in adipose tissue from chronic inflammation, such as obesity, insulin resistance, and type 2 diabetes in animal models and humans [7,8,9]. Human studies have demonstrated that intestinal permeability is associated with visceral adiposity [12] and metabolic syndrome in obese individuals [13]. A recent study has provided evidence for the presence of bacteria and bacterial DNA in several mAT in metabolic sequelae of obesity [9]. It is still a noteworthy question to clarify the role of mAT-associated microbiota in CD development
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