Staphylococcus aureus Biofilm-Secreted Factors Cause Mucosal Damage, Mast Cell Infiltration, and Goblet Cell Hyperplasia in a Rat Rhinosinusitis Model

• Published in: International journal of molecular sciences 2024-03, Vol.25 (6), p.3402
• Main Authors: Houtak, Ghais, Nepal, Roshan, Bouras, George, Shaghayegh, Gohar, Bennett, Catherine, Finnie, John, Fenix, Kevin, Psaltis, Alkis James, Wormald, Peter-John, Vreugde, Sarah
• Format: Article
• Language: English
• Subjects: Animals; biofilm; Biofilms; Chronic Disease; Chronic rhinosinusitis; Cytokines; eosinophilic; Goblet Cells - pathology; Histopathology; Humans; Hyperplasia; Hyperplasia - pathology; IgE; Inflammation; Mast Cells - pathology; Neutrophils; Pathophysiology; Patients; Rats; Rhinitis - pathology; Rhinosinusitis; Sinusitis - pathology; Staphylococcus aureus
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms25063402

Chronic rhinosinusitis (CRS) is an inflammatory condition of the sinonasal mucosa. Despite being a common health issue, the exact cause of CRS is yet to be understood. However, research suggests that , particularly in its biofilm form, is associated with the disease. This study aimed to investigate the impact of long-term exposure to secreted factors of biofilm (SABSFs), harvested from clinical isolates of non-CRS carrier and CRS patients, on the nasal mucosa in a rat model. Animals were randomised (n = 5/group) to receive daily intranasal instillations of 40 μL (200 μg/μL) SABSFs for 28 days or vehicle control. The sinonasal samples were analysed through histopathology and transcriptome profiling. The results showed that all three intervention groups displayed significant lymphocytic infiltration ( ≤ 0.05). However, only the SABSFs collected from the CRSwNP patient caused significant mucosal damage, mast cell infiltration, and goblet cell hyperplasia compared to the control. The transcriptomics results indicated that SABSFs significantly enriched multiple inflammatory pathways and showed distinct transcriptional expression differences between the control group and the SABSFs collected from CRS patients ( ≤ 0.05). Additionally, the SABSF challenges induced the expression of IgA and IgG but not IgE. This in vivo study indicates that long-term exposure to SABSFs leads to an inflammatory response in the nasal mucosa with increased severity for isolated from a CRSwNP patient. Moreover, exposure to SABSFs does not induce local production of IgE.