The gut microbiota of siblings offers insights into microbial pathogenesis of inflammatory bowel disease

Abstract

Siblings of patients with Crohn's disease (CD) have elevated risk of developing CD and display aspects of disease phenotype, including faecal dysbiosis. In our recent article we have used 16S rRNA gene targeted high-throughput sequencing to comprehensively characterize the mucosal microbiota in healthy siblings of CD patients, and determine the influence of genotypic and phenotypic factors on the gut microbiota (dysbiosis). We have demonstrated that the core microbiota of both patients with CD and healthy siblings is significantly less diverse than controls. Faecalibacterium prausnitzii contributed most to core metacommunity dissimilarity between both patients and controls and between siblings and controls. Phenotype/genotype markers of CD risk significantly influenced microbiota variation between and within groups, of which genotype had the largest effect. Individuals with elevated CD-risk display mucosal dysbiosis characterized by reduced diversity of core microbiota and lower abundance of F. prausnitzii. The presence of this dysbiosis in healthy people at-risk of CD implicates microbiological processes in CD pathogenesis.

Relatively rare root endophytic bacteria drive plant resource allocation patterns and tissue nutrient concentration in unpredictable ways

“…However, methodological limitations (Konopka, ), the assumption of high functional redundancy (Nannipieri et al., ; Rousk et al., ), and the legacy of the mass–ratio hypothesis (Mariotte, ) have hindered investigations on subordinate, rare, transient, or low abundance taxa until recently (Shade et al., ; Lynch and Neufeld, ; Jousset et al., ). Our results suggest that low‐abundance taxa within the plant microbiome may drive host plant function, which is in agreement with recent investigations of the human microbiome (Gerritsen et al., ; Gilbert et al., ; Hedin et al., ), marine systems (Sogin et al., ; Ziegler et al., ), and plant–soil microbial interactions (De Boer et al., ; Hol et al., , , b; Marra et al., ). Although investigations of the effects of low‐abundance taxa within the plant microbiome are rare, in one prominent study, Hol et al.…”

“…Surprisingly, there have been relatively few empirical tests of the mass–ratio hypothesis in species‐rich microbial communities, likely because functional redundancy is assumed to be high (Nannipieri et al., ). Nevertheless, recent studies question the applicability of the mass–ratio hypothesis in microbial communities (Hol et al., , , ; Jousset et al., ; Ziegler et al., ) and find that low‐abundant microbes can: mediate plant–herbivore interactions via changes in plant nutritional resources (Hol et al., ; Marra et al., ), drive ecosystem function (Jousset et al., ), contribute to the resilience and stability of the systems in which they reside (van Elsas et al., ; Vivant et al., ; Ziegler et al., ), and elicit disease symptoms within the human microbiome (Gerritsen et al., ; Gilbert et al., ; Hedin et al., ).…”

Recent Development of Prebiotic Research—Statement from an Expert Workshop

“…It is also one of the main butyrate producers in the gut with proven anti-inflammatory properties [ 42 , 43 , 58 ]. The number of F. prausnitzii is reduced in patients with inflammatory bowel disease, especially with Crohn’s disease [ 42 , 59 , 60 , 61 ] probably due to the increased oxidative stress created by the inflamed gut.…”

LogMPIE, pan-India profiling of the human gut microbiome using 16S rRNA sequencing

“…An increasing body of evidence now substantiates that the gut microbiome plays a critical role in digestion, nutrition, and immune system maturation 2–7 . A non-exhaustive list of physiological disorders associated with gut microbiome dysbiosis includes Crohn’s disease 8 , 9 , type II diabetes 10 , 11 , colorectal cancer 12 , 13 and metabolic disorders 14 , 15 . With advancements in the gut microbiome field, modulation of host physiology and biochemistry by the microbiome is being investigated in greater detail 16 .…”