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by claude@2026-07, 2026-07-04
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The study developed a microfluidic co-culture system that supports human osteoblasts, chondrocytes, fibroblasts, and macrophages, including quiescent (M0) and pro-inflammatory (M1) macrophage phenotypes, to model joint inflammation. Using IFN-γ and LPS supplementation, the researchers induced an M1 phenotype and compared a healthy (M0-based) versus diseased (M1-based) joint model, assessing cell viability (fluorescent live/dead staining), cytotoxicity (LDH release), and metabolic activity (PrestoBlue). Co-culture maintained similar viability in healthy and diseased models (~83% mean) with no measurable LDH increase, while metabolic activity was elevated 5.3–5.9× over standard monolayer conditions. A key caveat noted implicitly by the design is that characterization is reported at 24 hours of co-culture, not longer-term behavior. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
Here we present a microfluidic model that allows for co-culture of human osteoblasts, chondrocytes, fibroblasts, and macrophages of both quiescent (M0) and pro-inflammatory (M1) phenotypes, maintaining initial viability of each cell type at 24 h of co-culture. We established healthy (M0-based) and diseased (M1-based) joint models within this system. An established disease model based on supplementation of IFN-γ and LPS in cell culture media was used to induce an M1 phenotype in macrophages to recapitulate inflammatory conditions found in OA. Cell viability was assessed using NucBlue™ Live and NucGreen™ Dead fluorescent stains, with mean viability of 83.9% ± 14% and 83.3% ± 12% for healthy and diseased models, respectively, compared with 93.3% ± 4% for cell in standard monoculture conditions. Cytotoxicity was assessed via a lactate dehydrogenase (LDH) assay and showed no measurable increase in LDH release into the culture medium under co-culture conditions, indicating that neither model promotes a loss of cell membrane integrity due to cytotoxic effects. Cellular metabolic activity was assessed using a PrestoBlue™ assay and indicated increased cellular metabolic activity in co-culture, with levels 5.9 ± 3.2 times mean monolayer cell metabolic activity levels in the healthy joint model and 5.3 ± 3.4 times mean monolayer levels in the diseased model. Overall, these findings indicate that the multi-tissue nature of in vivo human joint conditions can be recapitulated by our microfluidic co-culture system at 24 h and thus this model serves as a promising tool for studying the pathophysiology of rheumatic diseases and testing potential therapeutics.
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Abstract
Here we present a microfluidic model that allows for co-culture of human osteoblasts, chondrocytes, fibroblasts, and macrophages of both quiescent (M0) and pro-inflammatory (M1) phenotypes, maintaining initial viability of each cell type at 24 h of co-culture. We established healthy (M0-based) and diseased (M1-based) joint models within this system. An established disease model based on supplementation of IFN-γ and LPS in cell culture media was used to induce an M1 phenotype in macrophages to recapitulate inflammatory conditions found in OA. Cell viability was assessed using NucBlue™ Live and NucGreen™ Dead fluorescent stains, with mean viability of 83.9% ± 14% and 83.3% ± 12% for healthy and diseased models, respectively, compared with 93.3% ± 4% for cell in standard monoculture conditions. Cytotoxicity was assessed via a lactate dehydrogenase (LDH) assay and showed no measurable increase in LDH release into the culture medium under co-culture conditions, indicating that neither model promotes a loss of cell membrane integrity due to cytotoxic effects. Cellular metabolic activity was assessed using a PrestoBlue™ assay and indicated increased cellular metabolic activity in co-culture, with levels 5.9 ± 3.2 times mean monolayer cell metabolic activity levels in the healthy joint model and 5.3 ± 3.4 times mean monolayer levels in the diseased model. Overall, these findings indicate that the multi-tissue nature of in vivo human joint conditions can be recapitulated by our microfluidic co-culture system at 24 h and thus this model serves as a promising tool for studying the pathophysiology of rheumatic diseases and testing potential therapeutics.
Competing Interest Statement
SW is an inventor on a patent that pertains to the methods described in this publication for which he is entitled to receive royalties and/or equity. US Patent No. 12098354B2 was issued to the South Dakota Board of Regents. In addition, SW is a partner in a company, CellField Technologies, Inc., that has licensed related technology from the South Dakota Board of Regents.
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