Decreased enteric bacterial composition and diversity in South American Crohn’s disease vary with the choice of treatment strategy and time since diagnosis.
J Crohns Colitis. 2019 Nov 23;:
Authors: Cruz-Lebrón A, D’argenio Garcia L, Talla A, Joussef-Piña S, Quiñones-Mateu ME, Pierre Sekaly R, Carvalho KIL, Levine AD
BACKGROUND AND AIMS: The symptomology of Crohn’s disease (CD), a chronic inflammatory disease of the digestive tract, correlates poorly with clinical, endoscopic, or immunological assessments of disease severity. Prevalence of CD in South America is rising, reflecting changes in socio-economic stability. Many treatment options are available to CD patients, including biological agents and corticosteroids, each of which offers variable efficacy attributed to host genetics and environmental factors associated with alterations in the gut microbiota.
METHODS: The fecal microbial population was determined by 16S rRNA sequencing and taxonomic differences compared between Brazilian patients with CD treated with corticosteroid or anti-TNF immunotherapy. Fecal calprotectin and plasma sCD14 levels were quantified as markers for local and systemic inflammation, respectively.
RESULTS: Anti-TNF treatment led to an increased relative abundance of Proteobacteria and a decreased level of Bacteroidetes. In contrast, corticoid treatment was associated with an increase in the relative abundance of Actinobacteria, which has been linked with inflammation in CD. Disruption of the fecal microbiota was related to decreased bacterial diversity and composition. Moreover, the choice of clinical regimen and time since diagnosis modulate the character of the resulting dysbiosis.
CONCLUSIONS: Enteric microbial populations in treated CD patients are modulated by disease pathogenesis, local inflammatory microenvironment, and treatment strategy. The dysbiosis that remains after anti-TNF treatment due to decreased bacterial diversity and composition abates restoration of the microbiota to a healthy state, suggesting that the identification and development of new clinical treatments for CD must include their capacity to normalize the gut microbiota.
PMID: 31758685 [PubMed – as supplied by publisher]