Patients with ankylosing spondylitis demonstrate a distinct fecal microbiota signature that is linked to levels of fecal calprotectin, but not other clinical parameters, according to data published in Arthritis Research & Therapy.
“The gastrointestinal tract is the home of more than 1,000 species of bacteria, but also fungi and viruses, which coexist with the host in a reciprocal relationship,” Eva Klingberg, MD, PhD, of the Sahlgrenska Academy at the University of Gothenburg, in Sweden, and colleagues wrote. “The gut microbiota is necessary for the development and shaping of the immune system, and the host genetics play a role in the establishing and shaping of the gut microbiota.”
“Intestinal microbiota most likely play a role in initiating and triggering the immune system in individuals who are genetically susceptible for [inflammatory bowel disease], leading to the typical gut inflammation of [Crohn’s disease] and [ulcerative colitis],” they added. “Aberrations in the gut microbiome, dysbiosis with decreased bacterial diversity, expansion of potentially pro-inflammatory bacteria, and reduction of potentially anti-inflammatory, protective bacteria have repeatedly been shown in IBD. However, it is still unclear whether the dysbiosis in IBD is a cause or a consequence of the gut inflammation.”
To evaluate differences in fecal microbiota among patients with AS, ulcerative colitis and healthy individuals, as well as analyze the relationship between fecal microbiota, fecal calprotectin and disease-related variables in AS, Klingberg and colleagues studied a cohort from Western Sweden across the 5-year period. Participants included 204 patients recruited in 2009, with the same patients invited back for a follow-up in 2014. For this analysis, the researchers focused on 150 participants with AS, 18 with ulcerative colitis and 17 healthy controls with no history of gastrointestinal or other chronic disorders.
Patients with AS demonstrate a distinct fecal microbiota signature that is linked to levels of fecal calprotectin, but not other clinical parameters, according to data.
Klingberg and colleagues examined fecal microbiota in participants using GA-map Dysbiosis Test, developed by Genetic Analysis in Oslo, Norway. The test also reports the degree of deviation of the microbiota composition compared with a healthy control population. Patients with AS were assessed using questionnaires, back mobility tests, fecal calprotectin, erythrocyte sedimentation rate and C-reactive protein.
According to the researchers, a principal component analysis demonstrated highly separate clustering of fecal microbiota from the patients with AS, ulcerative colitis and healthy individuals. For example, fecal microbiota in AS was characterized by a higher abundance of Proteobacteria, Enterobacteriaceae, Bacilli and Streptococcus species, as well as Actinobacteria, but lower abundance of Bacteroides and Lachnospiraceae.
In addition, fecal microbiota composition varied between patients with normal and increased fecal calprotectin. Patients with increased fecal calprotectin demonstrated lower abundance of bacteria with anti-inflammatory properties, such as Faecalibacterium prausnitzii and Clostridium, as well as a higher amount of the genus Streptococcus. Meanwhile, 87% of patients with AS demonstrated dysbiosis.
“We have demonstrated a distinct fecal microbiota signature in the patients with AS, which differed from the patients with UC and healthy controls,” Klingberg and colleagues wrote. “In the AS patients, fecal microbiota signature was linked to fecal calprotectin levels, a marker of intestinal inflammation, but not to other clinical parameters. This suggests that the intestinal microbiota may be involved in an interplay with subclinical gut inflammation in AS.” – by Jason Laday
Disclosure: The researchers report no relevant financial disclosures.