CellModelDB

Public Schema V2 · Lung Census V1

A549

A04 · stable entity ID: LUNG-ENT-002

Provenance and Evidence

Species
Homo sapiens
Tissue origin
Lung
Provenance summary
Lung V1 frozen scientific record
Evidence summary
Lung V1 frozen scientific record
Identity caveat
NOT_ASSESSED
Public omics readiness
NOT ASSESSED

Relationships

No parent relationship recorded.

Disease Applications

Disease context

Acute lung injury

Inflammatory lung injury

LITERATURE SUPPORTED
Stimulus
Lipopolysaccharide
Experimental context
A549 + LPS
Stimulus parameters
dose: NOT_REPORTED; exposure duration: NOT_REPORTED

Application purpose

  • Inflammatory epithelial injury response
  • ALI-like model context

Evidence summary: Directly supports LPS-stimulated A549 alveolar epithelial inflammatory/injury-response applications. A549 cells were exposed to LPS; SP-A expression, c-Jun/AP-1 signaling and TLR2-related effects were assessed over concentration/time conditions. Provides independent LPS-response support in the A549 lung epithelial context and distinguishes alveolar/bronchial response pathways. LPS, soluble CD14 and LPS-binding protein were evaluated in A-549 type-II-like pneumocytes with IL-6/IL-8 release and signaling readouts.

Interpretation: Used to study LPS-associated alveolar epithelial signaling and injury-response readouts in A549.

Limitation: A549 is lung adenocarcinoma-derived and remains a tumour-control; the study does not make it a normal alveolar model or establish clinical disease fidelity. A549 is tumour-derived; response depends on accessory factors such as soluble CD14 and is not a complete acute-lung-injury model.

Supporting references

  • PMID 19712733 — Molecular mechanisms of lipopolysaccharide-caused induction of surfactant protein-A gene expression in human alveolar epithelial A549 cells
  • PMID 12193231 — Differences in LPS-induced activation of bronchial epithelial cells (BEAS-2B) and type II-like pneumocytes (A-549)

Disease application evidence describes documented experimental use. It does not change model identity, database role, physiological relevance, Disease Fidelity, or overall model ranking.

Physiological Relevance

PR evaluates baseline similarity between a cell model and its intended normal human target-cell reference. It is not overall model quality, a universal ranking, or Disease Fidelity; PR and DF are independent.

Status
FORMAL
PR version
V2
Target reference
alveolar cells type 2
Spearman rho
0.728273
Reference rank
11/154
Percentile
93.464%
Delta rho
-0.0331284011
NES
NOT_DEFINED
Gene-set size
295
Method route
DIRECT_TPM_V1_COMPATIBLE

Caveat: Tumour-control role retained; PR does not change database role.

The displayed row is read from the approved PUBLIC_RC1 SQLite release and is not recalculated by the website.

Uncertainty and Limitations

No structured uncertainty flag is recorded.

Analysis layers

Physiological Relevance and Disease Fidelity are separate analysis layers. No overall score or ranking is generated by this page.

Physiological Relevance
NOT_ASSESSED
Disease Fidelity
NOT_ASSESSED
Availability
REPOSITORY OR VENDOR SIGNAL

Lung V1 scientific context

Coverage
2 adequate · 4 partial · 2 under-covered
Saturation
SATURATION LIMITED BY MODEL ECOSYSTEM
Module state
FROZEN
Freeze ID
LUNG-CENSUS-V1-FROZEN

These module-level statements preserve the frozen scientific limitation context; they do not rank or reclassify this entity.