Our bodies are a lot like well-constructed houses built on solid foundations. It seems like they should last forever, but the fact is that even the best houses require constant maintenance and repairs, especially as they age. And, just like houses, vigilant maintenance and earlier repairs of our bodies can often stave off bigger problems.
But what happens when the maintenance and repairs fail? This can and does happen unfortunately. During an injury, our immune system engages to facilitate repairs, e.g., of a torn anterior cruciate ligament (ACL) in a weekend warrior. However, this repair process can also lay the foundations for osteoarthritis to set in for many of the afflicted (King et al., 2018).
Using the SOMAscan® Assay to study proteomics, King et al. set out to look at the joint fluid surrounding the area of the injury to better understand what is occurring at the repair site that leads to the unwanted effects of inflammation (King et al., 2018). In their findings, the team found the anticipated protein biomarkers, but also many markers typically associated with a different form of arthritis, i.e., rheumatoid arthritis. The researchers surmise that these findings could provide insights into the underlying mechanism of the immune “cannibalization” of joints and offer possibilities for new drug targets to help patients return to a state of normalcy.
While similar to osteoarthritis in terms of symptoms and suffering, rheumatoid arthritis differs in several ways, such patients also show an increase in immune cell production (B and T cells) in the synovium (membrane lining the joints). Medications are available to treat rheumatoid arthritis, but they may not always return the patient back to a pre-arthritis state. Tasaki et al. decided to use multiple approaches, including proteomics via SomaLogic® technology, to understand patients’ response to medication and determine if patients can return to a pre-arthritic state at the molecular level (Tasaki et al., 2018). For the different medications tested, a wide variety of responses were observed. One drug – tocilizumab – was found to fix the molecular imbalance more effectively and to restore the affected systems that remained untouched by other drugs tested. From their work, the researchers also identified the molecular signs that suggest a patient may be resistant to the treatment tested in the study.
Though osteoarthritis and rheumatoid arthritis are different conditions, they both are remarkable examples of what can go wrong when repairs have untoward effects. With a proteomic way of monitoring the body’s repair job, intervention can happen before a problem arises. Through proper intervention, joint cannibalization accompanied by detrimental pain can perhaps be avoided entirely.
King, J. D., Rowland, G., Villasante Tezanos, A. G., Warwick, J., Kraus, V. B., Lattermann, C., & Jacobs, C. A. (2018). Joint Fluid Proteome after Anterior Cruciate Ligament Rupture Reflects an Acute Posttraumatic Inflammatory and Chondrodegenerative State. Cartilage, 1947603518790009.doi:10.1177/1947603518790009
Tasaki, S., Suzuki, K., Kassai, Y., Takeshita, M., Murota, A., Kondo, Y., . . . Takeuchi, T. (2018). Multi-omics monitoring of drug response in rheumatoid arthritis in pursuit of molecular remission. Nat Commun, 9(1), 2755. doi:10.1038/s41467-018-05044-4