In vitro exposure to dust storm PM modulates IL-6, IL-8, IL-32, and TNF-α secretion from PBMCs: evidence for biphasic pro-inflammatory activity and potential immune suppression at high concentrations in STEMI patients
Exposure to dust storm particulate matter (PM) is recognized as a risk factor for cardiovascular diseases; however, the inflammatory immune responses of peripheral blood mononuclear cells (PBMCs) from patients with acute ST-segment elevation myocardial infarction (STEMI) compared to healthy individuals following acute exposure to such particles remain poorly understood. This study investigated the effects of PMs on the secretion of inflammatory cytokines from PBMCs of STEMI patients compared to healthy individuals. Dust samples were collected using a quartz filter sampler, and PBMCs from five patients and five healthy controls were exposed to 0 (control), 10, and 100 µg/mL of the dust particles for 24/48 hours. The levels of IL-6, IL-8, IL-32, and TNF-α in the supernatant were measured by ELISA. The results showed that at 10 µg/mL, the PMs significantly increased secretion of all measured the measured cytokines in patients compared to healthy individuals, but at 100 µg/mL, the levels decreased relative to 10 µg/mL. The most significant differences between two groups were observed in IL-32 secretion at all three concentrations (0,10, and 100 µg/mL) and in IL-8 secretion at 10 µg/mL after 24 h. Although IL-6 and TNF-α were also higher in patients than healthy individuals, these differences weren’t statistically significant, likely due to the small sample size. These findings suggest that PMs may act as a risk factor for the development of cardiovascular diseases and potentially pose an additional hazard to individuals already affected by conditions such as STEMI. Furthermore, the decrease in pro-inflammatory cytokines at the high concentration (100 µg/mL) of PMs may indicate immune system suppression due to high-dose exposure, which, given the ability of PMs to carry microbial components into the body, could increase susceptibility to infections in both patients and healthy individuals.
Authors
- Heidar Maleki (ORCID: https://orcid.org/0000-0002-9820-2908)
- Mehdi Sheikhi
- Gholamreza Goudarzi (ORCID: https://orcid.org/0000-0001-5387-0761)
- Narges Baharifar
- Abdolkarim Sheikhi (ORCID: https://orcid.org/0000-0002-3559-5548)
- Hakimeh Saadatifar (ORCID: https://orcid.org/0000-0002-0966-1150)
- Aziz Kassani (ORCID: https://orcid.org/0000-0001-5188-5249)
- Myron R. Szewczuk (ORCID: https://orcid.org/0000-0001-8471-5481)
- Ali Sadeghi Moghaddam (ORCID: https://orcid.org/0000-0003-2660-3064)
- FOROUGH CHAMAEINEJAD
- Mehdi Baghersheidaee
- Negar Soleimani
Institutions
- Ahvaz Jundishapur University of Medical Sciences (IR)
- Queen's University (CA)
- Dezful University of Medical Sciences (IR)
Publication Details
- Journal
- Scientific Reports
- Published
- 2026-09-09
- DOI
- https://doi.org/10.1038/s41598-026-70941-4
- Primary Topic
- Air Quality and Health Impacts
- Type
- article
- Field-Weighted Citation Impact
- 0.00