Artificial urine has many advantages over human urine for research and educational purposes. By closely mimicking healthy individuals’ urine, it may also be important in discovering novel biomarkers. However, up until now, there has not been any specific protocol to prove the similarity in terms of the chemical composition at the molecular level. In this study, a new artificial urine protocol is established to mimics the urine of healthy individuals. The multi-purpose artificial urine (MP-AU) presented here is compared with two other protocols most cited in literature. Furthermore, these three protocols are also compared with samples from 28 healthy young individuals. To do so, attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR) is used, according to which MP-AU shows a significantly close similarity with human urine. In formulating MP-AU, the infrared spectra of nine compounds is provided, making possible the band assignment of some absorption bands to certain compounds. Given its properties, the MP-AU protocol introduced here is both economical and practical, making it useful when designing comparative-controlled experiments.
Barrier tissues are populated by functionally plastic CD4+ resident memory T (TRM) cells. Whether the barrier epithelium regulates CD4+ TRM cell locations, plasticity and activities remains unclear. Here we report that lung epithelial cells, including distinct surfactant protein C (SPC)lowMHChigh epithelial cells, function as anatomically-segregated and temporally-dynamic antigen presenting cells. In vivo ablation of lung epithelial MHC-II results in altered localization of CD4+ TRM cells. Recurrent encounters with cognate antigen in the absence of epithelial MHC-II leads CD4+ TRM cells to co-express several classically antagonistic lineage-defining transcription factors, changes their cytokine profiles, and results in dysregulated barrier immunity. In addition, lung epithelial MHC-II is needed for surface expression of PD-L1, which engages its ligand PD-1 to constrain lung CD4+ TRM cell phenotypes. Thus, we establish epithelial antigen presentation as a critical regulator of CD4+ TRM cell function and identify epithelial-CD4+ TRM cell immune interactions as core elements of barrier immunity.
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