Hematopoietic prostaglandin D synthase–derived prostaglandin D2ameliorates adjuvant‐induced joint inflammation in mice

What is it about?

Rheumatoid arthritis (RA) is chronic inflammatory disease, which develops mainly in the joints of the feet and hands. RA occurs in approximately 1% of the world population. The major symptoms of RA are swelling, stiffness, and pain in the joints. The pathological features of RA include synovial hyperplasia, infiltration of inflammatory leukocytes, vascular hyper-permeability, neo-angiogenesis, and bone destruction in the joints. RA is assumed to be a consequence of an inappropriate and continuous inflammatory response to self-antigens. Certain pro-inflammatory cytokines, e.g., tumor necrosis factor (TNF)-α, interleukin (IL)-6 are well-known to promote RA and antibodies against these are now commonly used to treat. However, the etiology of RA remains virtually unknown. Prostaglandins (PGs) as well as cytokines and chemokines are produced in response to inflammation. There are several experimental studies showed that major PGs such as PGE2 and PGI2 exacerbate RA progression. However, the role of another type of PG, PGD2 in RA progression remained unknown. In the present study, we identified macrophage-derived PGD2 as an anti-inflammatory mediator in joint inflammation. We also demonstrated the therapeutic potential of pharmacological stimulation of PGD2 receptor against RA. PGD2 is a very rare negative regulator to inhibit excessive inflammatory responses in joint. Future medical application of this signaling is expected.

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