TR-AMs were incubated overnight (16 hr) under 21 or 1.5% O2, then stimulated with 20 ng/ml LPS for 6 hr while maintaining pretreatment conditions. For IL-1β measurements, 5 mM ATP was added to TR-AMs for 30 min following 6 hr LPS treatment to activate caspase 1, ensuring IL-1β release. (A) We measured cytokine (TNFα, IL-6, KC, CCL2, and IL-1β) levels in media using ELISA. Data represent at least three independent experiments; n = 3 per group. Significance was determined by unpaired, two-tailed t-test. (B) qPCR was used to measure mRNA expression (Tnfa, Il6, Kc, Ccl2, and Il1b). Gene expression was normalized to corresponding gene ct values in 21% group and represented as fold change using the ∆∆ct method. Data represent at least three independent experiments; n = 3 per group. Significance was determined by unpaired, two-tailed t-test. (C) Western blot analysis of whole-cell extracts at 6 and 24 hr post LPS treatment. (D) Extracellular acidification rate (ECAR) was measured in following acute LPS injection (final concentration: 20 ng/ml) in TR-AMs conditioned in 1.5% O2. (E) Capillary electrophoresis-mass spectrometry (CE-MS) metabolite heatmap for glycolytic intermediates. All error bars denote mean ± SD. *p<0.05.
Figure 3—source data 1. Changes in lipopolysaccharide (LPS)-induced expression of proIL-1β protein in tissue-resident alveolar macrophages (TR-AMs) under normoxia and hypoxia.Uncropped Western blot images of proIL-1β protein in TR-AMs treated with LPS for 6 or 24 hr under normoxia or hypoxia.