Alterations of the Gut Microbiota in Hashimoto’s Thyroiditis Patients Original paper
Researched by:
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Karen Pendergrass
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Karen Pendergrass
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
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Autoimmune Diseases
Autoimmune Diseases
Autoimmune disease is when the immune system mistakenly attacks the body's tissues, often linked to imbalances in the microbiome, which can disrupt immune regulation and contribute to disease development.
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Hashimoto’s Thyroiditis
Hashimoto’s Thyroiditis
OverviewHashimoto’s Thyroiditis (HT) is an autoimmune disorder characterized by the progressive destruction of thyroid follicles due to chronic inflammation, often leading to hypothyroidism. It affects 10-12% of the global population, with a significantly higher prevalence among women. While its etiology involves genetic, environmental, and epigenetic factors, increasing evidence highlights the role of gut microbiota in […]
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Karen Pendergrass
Researched by:
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Karen Pendergrass
ID
Karen Pendergrass
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass
What Was Studied?
This study systematically investigated alterations in the gut microbiota composition in patients with Hashimoto’s thyroiditis (HT), an organ-specific autoimmune disease, compared to healthy controls. The researchers used 16S rRNA sequencing to profile and compare the gut microbiota of 50 HT patients and 27 matched healthy controls. The study aimed to identify microbial biomarkers associated with HT and their correlations with clinical parameters, such as thyroid peroxidase antibody (TPO-Ab) and thyroglobulin antibody (TG-Ab) levels.
Who Was Studied?
The study involved two cohorts: an exploration cohort of 28 HT patients and 16 healthy controls, and a validation cohort of 22 HT patients and 11 healthy controls. All participants were of Han Chinese ethnicity, aged between 18 and 65 years, and matched for age, sex, and BMI. Patients included were euthyroid and free from confounding conditions or recent medications that could affect the gut microbiota.
Key Findings
The study revealed significant differences in the gut microbiota composition between HT patients and healthy controls, though overall bacterial diversity and richness were similar. HT patients exhibited a marked increase in Firmicutes and a reduction in Bacteroidetes, with a significantly higher Firmicutes-to-Bacteroidetes (F/B) ratio. At the genus level, the abundances of Blautia, Roseburia, Ruminococcus_torques_group, and Eubacterium_hallii_group were significantly increased in HT patients. In contrast, beneficial genera like Bacteroides, Fecalibacterium, and Prevotella_9 were significantly decreased.
The researchers identified 27 genera with significant differences between HT patients and controls using linear discriminant analysis effect size (LEfSe). Ten genera, including Bacteroides and Fecalibacterium, were highlighted as potential biomarkers, achieving high diagnostic accuracy with AUC values of 0.91 and 0.88 in the exploration and validation cohorts, respectively.
Microbiota changes were correlated with clinical parameters. For instance, increased levels of Blautia and Dorea were positively associated with TPO-Ab and TG-Ab, while reduced levels of Fecalibacterium and Bacteroides correlated inversely with these antibodies.
Greatest Implications
The findings highlight the potential role of gut dysbiosis in the pathogenesis of HT. The observed microbial shifts suggest a loss of anti-inflammatory and barrier-supporting taxa, such as Fecalibacterium, and an increase in pro-inflammatory or mucin-degrading taxa, such as Ruminococcus_torques_group. This dysbiosis may contribute to immune activation and thyroid autoimmunity through mechanisms like increased intestinal permeability and molecular mimicry. Additionally, the identified microbial biomarkers could serve as non-invasive tools for HT diagnosis and disease monitoring. However, longitudinal studies and experimental validation are needed to confirm causality and explore therapeutic interventions targeting the gut microbiota.