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Inhaling hydrogen sulfide continuously induces lung injury via IL-6/IL-10 and occludin
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DOI：10.1080/15569543.2026.2612777.png)
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Abstract
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Background and aimHydrogen sulfide (H2S) is a common gas with an unpleasant odor similar to rotten eggs. The extent of injury from inhaled H2S depends on the gas concentration. Chronic exposure to H2S has been reported to cause immunotoxicity and inflammatory effects in the lung. However, the molecular mechanisms underlying lung injury induced by continuous, low-concentration H2S exposure remain unclear.Experimental approachTwenty male ICR mice, 6-7 weeks old, were randomly assigned to two groups. The control group was exposed to clean air (21.9% O2, 0 ppm H2S), while the H2S group was exposed to air containing H2S (21.9% O2, 5 +/- 1 ppm H2S) for 21 days.Key findings and conclusionsInhaled H2S induced pulmonary injury and fibrosis, promoted the release of pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1 beta), and inhibited the anti-inflammatory cytokine IL-10. Additionally, H2S inhalation altered the expression of occludin, a tight junction-related protein. These findings enhance understanding of H2S-associated occupational health risks.
Keywords:
Hydrogen sulfide
lung injury
lung fibrosis
IL-6/IL-10
occludin
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