Staphylococcus aureus controls interleukin-5 release in upper airway inflammation.

Area of Science:

• Immunology
• Microbiology
• Otolaryngology

Background:

• Staphylococcus aureus frequently colonizes airways in chronic rhinosinusitis with nasal polyps.
• Secreted staphylococcal proteins, like enterotoxins and serine proteases, are known to induce cytokine release, including Interleukin-5 (IL-5).

Purpose of the Study:

• To investigate the spontaneous IL-5 production in nasal polyp tissue.
• To determine the role of Staphylococcus aureus and its secreted proteins in IL-5 release within nasal polyps.
• To evaluate the efficacy of antibiotics and bacteriophages in reducing IL-5 production.

Main Methods:

• Analysis of freshly obtained nasal polyp tissue with and without cultivatable S. aureus.
• Incubation of tissue cultures for 24 and 72 hours to monitor IL-5 production.
• Intervention using antibiotics or specific intravenous staphylococcal phages (ISP) to eliminate S. aureus.
• Identification of S. aureus proteins using high-resolution mass spectrometry.
• Assessment of phage specificity using heat inactivation and anti-phage antibodies.

Main Results:

• Cultivatable S. aureus was identified in type-2 inflamed nasal polyps, replicating within 24 hours and secreting proteins.
• The presence of S. aureus was significantly associated with increased IL-5 release.
• Elimination of S. aureus by antibiotics or active ISP significantly reduced IL-5 release.
• Heat-inactivated ISP and ISP neutralized by antibodies did not suppress IL-5 release, confirming phage specificity.

Conclusions:

• Staphylococcus aureus plays a direct role in regulating IL-5 production in nasal polyps.
• Bacterial proteins, including enterotoxins and serine proteases, likely contribute to the observed IL-5 release.
• Targeting S. aureus with bacteriophages presents a potential therapeutic strategy for managing type-2 inflammation in chronic rhinosinusitis with nasal polyps.