TrackMate is an automated tracking software used to analyze bioimages and is distributed as a Fiji plugin. Here we introduce a new version of TrackMate. TrackMate 7 is built to address the broad spectrum of modern challenges researchers face by integrating state-of-the-art segmentation algorithms into tracking pipelines. We illustrate qualitatively and quantitatively that these new capabilities function effectively across a wide range of bio-imaging experiments. Main textIn biosciences, object tracking is an essential image analysis technique used to quantify dynamic processes. In Life Sciences, tracking is used, for instance, to follow single particles, subcellular organelles, bacteria, cells, and whole animals. While tech developments have drastically improved image acquisition capabilities and allowed increasingly sophisticated experimental setups, they have also led to bottlenecks in downstream image analyses. Due to the sheer diversity of images, no single software can address every Life Science research tracking challenge. This has prompted the development of flexible and extensible software tracking platforms 1-5 , including TrackMate, that enable biologists to build automated tracking pipelines tailored to a specific problem.

Chronic inflammation is a hallmark of obesity and is linked to the development of numerous diseases. The activation of toll-like receptor 4 (TLR4) by long-chain saturated fatty acids (lcSFAs) is an important process in understanding how obesity initiates inflammation. While experimental evidence supports an important role for TLR4 in obesity-induced inflammation in vivo, via a mechanism thought to involve direct binding to and activation of TLR4 by lcSFAs, several lines of evidence argue against lcSFAs being direct TLR4 agonists. Using multiple orthogonal approaches, we herein provide evidence that while loss-of-function models confirm that TLR4 does, indeed, regulate lcSFA-induced inflammation, TLR4 is not a receptor for lcSFAs. Rather, we show that TLR4-dependent priming alters cellular metabolism, gene expression, lipid metabolic pathways, and membrane lipid composition, changes that are necessary for lcSFA-induced inflammation. These results reconcile previous discordant observations and challenge the prevailing view of TLR4's role in initiating obesity-induced inflammation.