Mouse lung macrophage

Where it participates (unsigned role)

1. GABA-A receptor subunits were expressed by primary lung macrophages of mice and the mouse macrophage cell line RAW264.7, the expression levels of these subunits decreased or increased concurrently with classical M1 or alternative M2 activation respectively, moreover activation or blockade of the receptors distinctively influenced the phenotypic characteristics of the macrophages, and these results suggested that microenvironments leading to macrophage phenotypic polarization concurrently modulate autocrine GABA signaling and its role in macrophage activation.

   Classical M1-like and alternative M2-like macrophage activation → GABA-A receptor anion channels source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/gaba-research/30017085.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8c2d49008808726bf766218eb51ab5ec08e9790897619e750b8caacc1afad63b", "start_char": 0, "end_char": 1120, "text_sha256": "8c2d49008808726bf766218eb51ab5ec08e9790897619e750b8caacc1afad63b"}

   experimental_model

   Subunit expression and phenotype in primary lung macrophages and a macrophage cell line under polarising conditions

   exposure

   Classical and alternative activating conditions, with GABA-A receptor activation or blockade

   limitations

   Expression changes and phenotype rather than disease outcome. It shows the receptor tracks polarisation rather than that it drives it.

   nutrient_topic

   GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid

   organism

   Mouse

   plain_language

   The receptor goes up as the cell takes the repair-type phenotype and down as it takes the inflammatory one.

   primary_references

   [gb-p30017085] Autocrine GABA signaling distinctively regulates phenotypic activation of mouse pulmonary macrophages. (2018). https://pubmed.ncbi.nlm.nih.gov/30017085/ DOI: 10.1016/j.cellimm.2018.07.001

   tissue_or_cell_type

   Lung macrophage

   GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 573–584

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Subunit expression and phenotype in primary lung macrophages and a macrophage cell line under polarising conditions · source_derived_draft · unverified_draft

   ### gb-the-receptor-tracks-polarisation GABA-A receptor subunits were expressed by primary lung macrophages of mice and the mouse macrophage cell line RAW264.7, the expression levels of these subunits decreased or increased concurrently with classical M1 or alternative M2 activation respectively, moreover activation or blockade of the receptors distinctively influenced the phenotypic characteristics of the macrophages, and these results suggested that microenvironments leading to macrophage phenotypic polarization concurrently modulate autocrine GABA signaling and its role in macrophage activation. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The receptor goes up as the cell takes the repair-type phenotype and down as it takes the inflammatory one. organism: Mouse tissue_or_cell_type: Lung macrophage experimental_model: Subunit expression and phenotype in primary lung macrophages and a macrophage cell line under polarising conditions limitations: Expression changes and phenotype rather than disease outcome. It shows the receptor tracks polarisation rather than that it drives it. exposure: Classical and alternative activating conditions, with GABA-A receptor activation or blockade evidence_span: {"source_cache": "artifacts/gaba-research/30017085.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8c2d49008808726bf766218eb51ab5ec08e9790897619e750b8caacc1afad63b", "start_char": 0, "end_char": 1120, "text_sha256": "8c2d49008808726bf766218eb51ab5ec08e9790897619e750b8caacc1afad63b"} [gb-p30017085] Autocrine GABA signaling distinctively regulates phenotypic activation of mouse pulmonary macrophages. (2018). https://pubmed.ncbi.nlm.nih.gov/30017085/ DOI: 10.1016/j.cellimm.2018.07.001

   Complete structured claim and evidence