Immunomodulation is integral to the body's adaptation to varying altitudes. Nevertheless, the effects of immune regulation on the onset of high-altitude pulmonary edema (HAPE) are not well understood. This research aimed to explore the influence of immune regulation on HAPE pathogenesis through the assessment of cytokine levels.

We analyzed the cytokine profiles of 28 HAPE patients at high altitudes and compared them to 25 healthy individuals who had successfully acclimatized. The levels of seven cytokines released by T helper cells (Th)1/2/17, alongside monocyte chemoattractant protein-1 (MCP-1), interleukin (IL)-8, and IL-1β in serum, were quantified using cytometric bead array (CBA) technology.

Our findings revealed significantly higher concentrations of IL-2, IL-10, and tumor necrosis factor (TNF) in the peripheral blood of HAPE patients when contrasted with those of healthy individuals (P < 0.001). A comprehensive analysis of these cytokines indicated a robust diagnostic capability for predicting HAPE, achieving an area under the curve (AUC) of 0.98. Conversely, no significant differences were observed in the levels of IL-6, IL-8, interferon-γ (IFN-γ), IL-4, IL-17 A, MCP-1, and IL-1β between the two cohorts.

Elevated IL-2, IL-10, and TNF in HAPE patients underscore immune dysregulation as a disease driver. Clinically, these cytokines may guide risk prediction (IL-2-hypoxemia link) and targeted therapies (anti-TNF for vascular leakage). Future work should define hypoxia-specific cytokine networks, validate interventions in altitude cohorts, and integrate multi-omics to map immune-vascular crosstalk.