ALVEOLAR EPITHELIUM DOWN-MODULATES ENDOTOXIN—BUT NOT TUMOR NECROSIS FACTOR ALPHA—INDUCED ACTIVATION OF ENDOTHELIUM AND SELECTIVELY INHIBITS NEUTROPHIL TRANSENDOTHELIAL MIGRATION
Why this work is in the frame
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Bibliographic record
Abstract
In a previous study, the authors reported the development of an optimized model bilayer of endothelium with alveolar epithelium using A549 cells, and that neutrophil transendothelial migration across endotoxin (lipopolysaccharide [LPS])-activated endothelial cells was attenuated by the apposition of the epithelium. Here the authors investigated whether this modulation by the epithelium extended to other stimuli such as tumor necrosis factor (TNF)-alpha, which, like LPS, activates proinflammatory gene transcription via nuclear factor (NF)-kappa B-dependent mechanisms to induce neutrophil transendothelial migration. Unlike the response to LPS, neutrophil migration in response to TNF-alpha was not altered by the presence of lung epithelial cells, except at a low concentration of TNF-alpha upon alveolar directional exposure of the endothelium, i.e., from the epithelial side of the bilayer. Epithelial cells in the bilayer reduced expression of E-selectin on the endothelium in response to LPS, but not with TNF-alpha stimulation. The production of the chemokine CXCL8 was also differentially modulated by epithelium in response to these 2 mediators. The expression of Toll-like receptor 4 (TLR4), which is involved in LPS recognition by endothelium, was not altered by epithelial cells, suggesting that the anti-inflammatory effect on endothelium may be via downstream LPS-induced signaling events. Inhibition of some candidate anti-inflammatory mediators produced by epithelium, such as nitric oxide, or the activity of interleukin (IL)-10 or transforming growth factor (TGF)-beta had no effect on the inhibitory influence of the epithelium in the bilayers. The authors' findings demonstrate a selective role for alveolar epithelial cells, via either direct cell-cell contact or yet-to-be-identified but short-range or short-lived product(s) in attenuating endothelial responses to endotoxin.
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Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.001 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it