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Differential Expression of Inflammatory Response Genes During Acute High‐Altitude Exposure

Inflammatory signaling and hypoxia responses are linked via HIF and NF‐kB crosstalk. Upon high‐altitude exposure, the inflammatory profile adapts to the hypoxic environment. However, these evolutionarily conserved inflammatory responses to oxygen limitation likely contribute to pathologies such as Acute and Chronic Mountain Sickness, a progressive fatal disease characterized by excessive erythrocytosis. We hypothesize that pro‐inflammatory gene expression will increase upon acute high‐altitude exposure. We compared the inflammatory profiles in whole blood samples collected in the morning during fasting at sea level and after one night at high altitude (3800 m elevation) in 14 healthy sojourners (4 women, 10 men). Expression of 255 inflammation‐related genes was determined via the NanoString Inflammation panel. 15 genes showed significant differential expression at altitude. These include upregulation of LY96, TGFBR1, HSPB2, IL13, IL9, as well as multiple chemokines (p < 0.0003 for all). Additionally, HIF1A expression was significantly correlated with the expression of multiple genes including TLR4 (R = 0.66, p=0.0003), IL6R (R = 0.68, p=0.001), and IFNG (R = −0.71, p = 0.001). The upregulation of chemotactic proteins provides evidence that acute high‐altitude exposure induces pro‐inflammatory signaling. Furthermore, LY96 encodes MD2, a coreceptor with toll‐like receptor 4, which is upregulated in macrophages via HIF and involved in modulating the inflammatory response to lipopolysaccharide. Therefore, this data suggests that at high‐altitude, hypoxic stress may increase susceptibility to subsequent infection.