Table 1.
Summary table of the evidence for NF-κB involvement in response to CO2
| Experimental model | Cellular Effect | Evidence of NF-κB involvement | Reference |
|---|---|---|---|
| Rat hepatic IRI | ↓ TNFα | ↓ NF-κB staining by IHC | Li et al. |
| ↑ IL-10 | |||
| ↓ Apoptosis | |||
| ↓ Liver injury | |||
| In vitro buffered hypercapnia (MEF, A549 lung epithelial cells and others) | ↓ TNFα, ICAM-1 and CCL2 | ↓ NF-κB luciferase promoter reporter | Cummins et al. |
| ↑ IL-10 | ↓ Nuclear p65 accumulation | ||
| ↓ IκBα degradation | |||
| ↑ Nuclear lKKα | |||
| In vitro hypercapnic acidosis (pulmonary endothelial cells) | ↓ ICAM-1, IL-8 | ↓ Nuclear p65 binding (EMSA) | Takeshita et al. |
| ↓ Neutrophil adherence | ↓ IκBα degradation | ||
| In vitro hypercapnia (macrophages) | ↓ IL-6, TNFα | No change in p65 or IκBα | Wang et al. |
| IL-10 unaffected | ↓ IL-6 promoter activity | ||
| ↓ Phagocytosis | |||
| In vitro hypercapnia acidosis (wound healing model in A549 lung epithelial cells) | ↓ Wound healing | ↓ IκBα degradation | O’Toole et al. |
| ↓ Cell migration | ↓ NF-κB luciferase promoter reporter | ||
| Effect of HCA lost when NF-κB inhibited | |||
| Drosophila (flies +/− pathogen at a range of CO2 concentrations) | ↑ Mortality | Proteolytic cleavage of Relish unchanged | Helenius et al. |
| ↓ Antimicrobial peptide genes | Hypercapnia inhibits Rel targets in parallel or downstream of proteolytic activation of Rel |