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SCGB1A1 encodes a small secreted homodimeric secretoglobin
(uteroglobin/CC10/CC16/CCSP) whose function is best supported as an
extracellular immunomodulator at the airway barrier rather than as a
metabolic enzyme.
"SCGB1A1 encodes a highly abundant, secreted airway protein (often referred to as CCSP/CC16/CC10) produced constitutively primarily by airway club cells (non-ciliated secretory epithelial cells), with protein readily detectable in airway lining fluid and also measurable in blood and urine
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The protein is a secretoglobin homodimer with an antiparallel
dimerization architecture and a central hydrophobic cavity that binds
phospholipids, steroids and inflammatory mediators.
"structure is described as antiparallel dimerization with a central hydrophobic cavity that can bind hydrophobic ligands (e.g., phospholipids, steroids, inflammatory mediators)
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SCGB1A1/CC10 antagonizes phospholipase A2 activity, with increased
PLA2 activity observed in CCSP-deficient contexts.
"Multiple sources describe SCGB1A1/CC10 as a phospholipase A2-inhibitory protein and note increased PLA2 activity in CCSP-deficient contexts
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Recombinant CCSP/SCGB1A1 binds CXCL8/IL-8 and inhibits neutrophil
chemotaxis; CCSP deficiency increases airway neutrophilia after injury.
"Recombinant human CCSP/SCGB1A1 can bind CXCL8/IL-8 and inhibit neutrophil chemotaxis, and CCSP deficiency in animal models is associated with greater airway neutrophilia after injurious stimuli
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CCSP is described as antagonizing neutrophil adhesion through
interaction with VLA-4 (alpha4beta1 integrin).
"CCSP is described as potentially antagonizing neutrophil adhesion through interaction with VLA-4 (α4β1 integrin)
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A 2024 mechanistic study reports CC10/SCGB1A1 suppresses Th2-type
allergic airway inflammation by modulating lung dendritic cell subsets
and activation through an NF-kappaB-linked pathway, rather than acting
directly on T helper cells.
"CC10/SCGB1A1 suppresses Th2-type inflammation largely by modulating lung DC subsets and activation through an NF-κB–linked pathway
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SCGB1A1 expression is cytokine-regulated; Th2 cytokines can
downregulate SCGB1A1 while Th1-related pathways regulate expression via
JAK-STAT/FOXA factors.
"Th2 cytokines can downregulate SCGB1A1 and Th1-related pathways can regulate expression via JAK–STAT/FOXA factors
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The protein is secreted into airway lumen/lining fluid with measurable
spillover into blood and urine, and is detectable across serum/plasma,
sputum, BALF, nasal secretions and urine.
"detectable in serum/plasma, sputum, bronchoalveolar lavage fluid (BALF), nasal secretions, and urine, consistent with secretion into airway lumen and translocation into the circulation
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