Infectious disease: CO₂ levels contribute to infection

In some diseases that affect pulmonary function, such as cystic fibrosis and chronic obstructive pulmonary disease (COPD), carbon dioxide levels in the blood accumulate owing to the inability of the body to properly regulate ventilation. The resulting condition is called hypercapnia acidosis, which can disrupt cardiac and neurological function, and impair the immune response. Helenius et al. found that when Drosophila were exposed to high levels of carbon dioxide, they changed their gene profiles and suppressed their production of antimicrobial peptides. Hypercapnia in flies impaired their ability to survive infection with a variety of bacterial strains by inhibiting their resistance to infection. In mammals, hypercapnia can suppress immune function through its inhibition of the NFκB pathway. In hypercapnic flies, the downregulated immune peptides are regulated by Relish, which is a conserved member of this pathway. Flies exposed to high carbon dioxide levels also exhibit developmental and reproductive changes. The genetic tractability of Drosophila, and the molecular conservation of its innate immune response with mammals, make this a useful model to understand some of the ways that hypercapnia acidosis impairs immunity and possibly contributes to the poor outcomes of patients with obstructive lung disease.