Analysis of Inflammatory Cytokine Levels in Sinonasal Secretions of Gulf War Veterans with and without Gulf War Illness

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Background: Gulf war illness (GWI) is a chronic, multisystemic disease that has been reported to impact one third of Veterans from the Persian Gulf War (1990–1991). Symptoms of chronic rhinosinusitis (CRS), including nasal congestion and fatigue, have been identified as the 1st (47%) and 3rd (41%) most common complaints associated with GWI. Although the precise etiology is unknown, chronic inflammation has been postulated to contribute to its pathogenesis. Objective: The purpose of this study was to compare inflammatory cytokine levels of sinonasal secretions from Gulf War Veterans with and without GWI associated CRS. Methods: Sinonasal secretions were collected from 13 GWV with associated GWI CRS, 11 GWV without GWI, 4 patients without GW exposures but with CRS, and 4 patients without GW exposures or CRS. The Luminex 38-plex assay was performed for chemokine/cytokine analysis and levels compared among the various groups. Results: Significantly higher levels of the proinflammatory cytokines gamma-IFN, IL-4, IL-5, IL-7, IL-10, IL-12, IL-13, IL-15, IL-17F, IL-22, TNFb, MIG/CXCL9, and IP-10 in GWV with GWI versus GWV without GWI ( p ≤ 0.05). In addition, when comparing GWV with GWI associated CRS to non-GWV with CRS, there were significantly higher levels of MCP1, IL-4, IL-10, IL-17F, IL-22, TNFb, M-CSF, and IP-10 in GWI patients. These findings indicate that GWI associated CRS is characterized by a more severe inflammatory response than what could be attributed to CRS alone. Furthermore, when comparing non-GWV without CRS to GWV without GWI/CRS, GWV had significantly higher IL-10 but lower M-CSF levels ( p < 0.05). These findings suggest that GW exposures alone may alter the sinonasal milieu even without manifestation of GWI . Conclusion: To the best of our knowledge, this pilot study is the first to demonstrate differences in inflammatory signatures of the sinonasal milieu in GWV with and without GWI, and is consistent with the hypothesis that chronic inflammation contributes to the underlying pathophysiology of GWI. Publication History Article published online: 07 February 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

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