Role of Hyaluronan in Inflammatory Effects on Human Articular Chondrocytes
Mary K Cowman, Claire Shortt, Shivani Arora, Yuhong Fu, Jemma Villavieja, Jai Rathore, Xiayun Huang, Tatini Rakshit, Gyu Ik Jung, Thorsten Kirsch
Key takeaways
In this lab study, hyaluronan fragments did not cause or worsen inflammation in human cartilage cells already exposed to an inflammatory substance.
Hyaluronan (HA) fragments have been proposed to elicit defensive or proinflammatory responses in many cell types. For articular chondrocytes in an inflammatory environment, studies have failed to reach consensus on the endogenous production or effects of added HA fragments. The present study was undertaken to resolve this discrepancy. Cultured primary human articular chondrocytes were exposed to the inflammatory cytokine IL-1beta, and then tested for changes in HA content/size in conditioned medium, and for the expression of genes important in HA binding/signaling or metabolism, and in other catabolic/ anabolic responses. Changes in gene expression caused by enzymatic degradation of endogenous HA, or addition of exogenous HA fragments, were examined. IL-1beta increased the mRNA levels for HA synthases HAS2/HAS3 and for the HA-binding proteins CD44 and TSG-6. mRNA levels for TLR4 and RHAMM were very low and were little affected by IL- 1beta. mRNA levels for catabolic markers were increased, while type II collagen (alfa1(II)) and aggrecan were decreased. HA concentration in the conditioned medium was increased, but the HA was not degraded. Treatment with recombinant hyaluronidase or addition of low endotoxin HA fragments did not elicit pro-inflammatory responses. Our findings showed that HA fragments were not produced by IL-1beta-stimulated human articular chondrocytes in the absence of other sources of reactive oxygen or nitrogen species, and that exogenous HA
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