Objective:

To identify specific immune cell drivers and potential therapeutic targets for precision intervention in traumatic lung injury (TLI).

Approach:

Key Findings:

• Classical monocytes showed the greatest disturbance post-trauma, with the ISG15+STAT1+ subpopulation expanding and driving an inflammatory response.
• PIM1 was identified as a core pathogenic gene co-upregulated in peripheral blood and lung tissue.
• Elevated PIM1 expression was confirmed as a causal risk factor for ARDS.
• The JAK2/STAT3/PIM1 pathway is activated during the acute trauma phase.
• Fedratinib effectively inhibits M1 polarization and inflammatory gene expression by interfering with the JAK2/STAT3/PIM1 signaling axis.

Interpretation:

The JAK2/STAT3/PIM1 signaling axis within the ISG15+STAT1+ monocyte subpopulation is a key driver of TLI.

Conclusion:

Fedratinib is a candidate for targeted treatment of TLI.

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