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