Published: 7.5.2026
Text: Sonia Sarfraz
Editing: Viestintätoimisto Jokiranta Oy
Image: Created using Bing Image Creator

Juvenile idiopathic arthritis (JIA) is defined as arthritis that has persisted for at least six weeks in a child under the age of 16 without a known cause. JIA is the most common paediatric rheumatic disease with a multifactorial pathogenesis – including microbial influences. If inadequately treated, the disease causes significant damage to the musculoskeletal system and can result in early disability. Antirheumatic drugs have greatly improved the prognosis, but joint changes and functional limitations still occur in many cases.

Association between gut microbiome and JIA

We have previously published a study demonstrating that the gut microbiome of a JIA patient differs from the microbiome of a healthy child. Intestinal mucosa is the largest, constantly active organ of the immunological system, and it is subjected regularly to food and microbes. It can be reasonably suspected of being an important factor in the development of autoimmune diseases. It has been suggested that bacterial particles from the intestine could be transported to the synovial membrane, where they would cause an immune reaction. In children, associations have been identified between inflammatory bowel disease (IBD) and the enthesitis-related subtype of JIA, which resembles spondyloarthritis in adults. 

Novel biomarkers and diagnostic approaches

Traditional biomarkers in JIA include rheumatoid factor, antinuclear antibodies, C-reactive protein and blood counts, which mainly reflect systemic rather than local inflammation. More recently studied biomarkers include S100 proteins (e.g., calprotectin, S100A8), matrix metalloproteinases and interleukin-18. Faecal calprotectin reflects intestinal inflammation in paediatric IBD, while blood calprotectin in JIA at diagnosis correlates with disease activity and future course. Additionally, microvesicles have emerged as novel biomarkers, acting as intercellular messengers within the immune system.

The influence of extracellular vesicles on immune responses

Extracellular vesicles (EVs) are lipid bilayer-covered nanosized particles secreted by all cell types, including bacteria. Bacteria can pack various biomolecules, such as proteins, nucleic acids and metabolites, into EVs to communicate with other bacterial cells and their environment. EVs secreted by human gut microbiota have been identified as one mechanism of communication between the gut microbiota and the body. Gut microbiota-derived EVs have been found to be able to cross the intestinal epithelial barrier, allowing them to enter the bloodstream and interact with target cells throughout the body. Gut microbiota-derived vesicles have been studied in many diseases, such as various cancers as well as metabolic and inflammatory diseases. Bacterial extracellular vesicles (bEVs) can enter systemic circulation and modulate host immune responses.

Looking for answers by means of multiomics

Our research hypothesis is that bacterial vesicles in synovial fluid are one possible mechanism in the development of JIA. Using medical data from newly diagnosed JIA patients, collected through careful clinical monitoring and a range of laboratory methods, we are examining how bacterial particles in synovial fluid influence immune activation in the synovial membrane and their role in disease pathogenesis. In addition, an ongoing follow-up will allow us to assess these effects over the long term, including their relationship to disease progression and treatment response. 

We will use a multiomics approach, which is an advanced biological approach that integrates data from multiple ‘omics’ layers – such as genomics (DNA), transcriptomics (RNA), proteomics (proteins) and metabolomics (small molecules) – to comprehensively characterise the biomolecules composition of bacterial EVs in synovial fluid and the gut.

Assistance from machine learning

We use machine learning, a method where computers learn patterns from large volumes of data, to combine different types of omics data. This helps us identify bacterial EV biomarkers in JIA and explore how patient clinical characteristics relate to our research findings. By combining multiomics and machine learning, we aim to identify key molecules and molecular signatures that direct EV targeting to specific tissues and cells, such as epithelial cells and macrophages. These processes may play a critical role in the onset and persistence of JIA. 

Overall, this research will enhance our understanding of how bacterial EVs interact with the epithelial barrier, immune cells and the broader disease environment, providing new insights into the development of JIA.

 

 

 

Dr. Sonia Sarfraz earned her Ph.D. in Medical Microbiology by studying bacterial adhesion on patient-specific implant materials. In her current position as a post-doctoral researcher in the Research Unit of Clinical Medicine, University of Oulu, she is exploring the role of EVs in the pathogenesis of juvenile idiopathic arthritis (JIA) and gut-derived bacterial EVs in colorectal cancer.