Viktig studie som nevner at økt CO2 kan dempe betennelser.

http://www.jimmunol.org/content/185/7/4439.long

In this study, we demonstrate that mammalian cells (mouse embryonic fibroblasts and others) also sense changes in local CO2 levels, leading to altered gene expression via the NF-κB pathway. IKKα, a central regulatory component of NF-κB, rapidly and reversibly translocates to the nucleus in response to elevated CO2. This response is independent of hypoxia-inducible factor hydroxylases, extracellular and intracellular pH, and pathways that mediate acute CO2-sensing in nematodes and flies and leads to attenuation of bacterial LPS-induced gene expression. These results suggest the existence of a molecular CO2 sensor in mammalian cells that is linked to the regulation of genes involved in innate immunity and inflammation.

FIGURE 7.Hypercapnia promotes an anti-inflammatory profile of gene expression. A PCR array of genes known to be involved in the NF-κB signaling cascade was performed on A549 cells exposed to ambient or 10% CO2 ± LT (100 ng/ml) for 4 h. A selection of differentially expressed genes from the array were chosen for validation. CCL2 (A), ICAM1 (B), TNF-α (C), and IL-10 (D) message levels were determined by quantitative real-time PCR and expressed as a percentage of LT-induced gene expression at 0.03% CO2 (n = 3 ± SEM, one-way ANOVA, Tukey post-test).

Traditionally, CO2 has been considered a waste product of respiration, and its biologic activity is poorly understood in terms of gene expression. However, a recent study reported differential gene expression in elevated CO2 (9).

This study suggests the existence of an intracellular CO2 sensor that is associated with anti-inflammatory and immunosuppressive signaling, is independent of intracellular and extracellular pH, and could account for the above clinical observations. CO2 can profoundly influence the transcriptional activation of the NF-κB pathway but its transcriptional effects may extend to other as yet uncharacterized pathways. Understanding the molecular mechanisms of CO2-dependent intracellular signaling could lead to new therapies in which the suppression of immunity or inflammation is clinically desirable.