Association between H1N1 infection and pro-inflammatory Th-1 and Th-17 cytokines production

Objectives The pandemic H1N1 influenza A virus is considered one of the main causes of outbreaks of respiratory infection among humankind. Resident immune cells in the mucosal sites of the respiratory tract maintain an appropriate balance between protection and disease. Our research aims in the current study to investigate a profile of cytokines production, including TNF-α, IL-4, IFN-γ, IL-17A, IL-10, and IL-2, following stimulation of tonsillar MNCs using pH1N1 (A/California/04/2009 strain). Methods Patients who underwent tonsillectomy because of snoring and obstructive sleep apnoea (n = 31) were recruited in the current pilot study. Tonsillar monocular cells (MNCs) were isolated and then stimulated using the H1N1 viral antigen of the A/California/04/2009 strain. A BD™ Cytometric Bead Array Experiment (CBA) method was utilized to analyze different target pro-inflammatory cytokine markers in the cell-culture supernatants of H1N1-stimulated MNCs. The cytokine profiles comprise TNF-α, IL-4, IFN-γ, IL-17A, IL-10, and IL-2. Results A noticeable pro-inflammatory Th-1 and Th-17 response was seen in H1N1-stimulated MNCs, with significantly increased concentrations of IFN-γ, IL-10, and IL-17A compared to un-stimulated controls (p-value less than 0.001, and 0.01, respectively). TNF-α, IL-4, and IL-2 levels presented no significant differences between H1N1-stimulated MNCs compared to un-stimulated controls (P > 0.05). The results demonstrate a marked Th-1 and Th-17 cytokine response following stimulation of MNCs with the H1N1 viral antigen. Conclusions Stimulation of MNCs using pH1N1 viral antigen presented the vital role of T-cells in mucosal immunity against pH1N1 and its importance when considering designing and developing intranasal vaccine candidates that can trigger cellular in addition to humoral immune responses.