Influenza infection directly alters innate IL-23 and IL-12p70 and subsequent IL-17A and IFN-[gamma] responses to pneumococcus in vitro in human monocytes

• Published in: PloS one Vol. 13; no. 9; p. e0203521
• Main Authors: Loughran, Sinead T, Power, Patrick A, Maguire, Paula T, McQuaid, Samantha L, Buchanan, Paul J, Jonsdottir, Ingileif, Newman, Robert W, Harvey, Ruth, Johnson, Patricia A
• Format: Journal Article
• Language: English
• Published: Public Library of Science 07-09-2018
• Subjects: Genetic aspects; Health aspects; Influenza viruses; Interleukins; Monocytes; Physiological aspects; Ireland
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0203521

It is well accepted that influenza A virus predisposes individuals to often more severe superinfections with Streptococcus pneumonia. However, the mechanisms that lead to this synergy are not clearly understood. Recent data suggests that competent Th17 immunity is crucial to clearance and protection from invasive pneumococcal disease of the lung. We demonstrate that early influenza infection significantly reduced levels of pneumococcus driven IL-12p70, IL-23 and IL-27 in human monocytes with significant impairment of IL-17A and IFN-[gamma] in HKSP-treated allogeneic mixed lymphocyte cultures. We also provide evidence to suggest that the hemagglutinin component of the virus is at least partially responsible for this downward pressure on IL-17 responses but surprisingly this suppression occurs despite robust IL-23 levels in hemagglutinin-treated monocyte cultures. This study demonstrates that influenza can directly affect the immunological pathways that promote appropriate responses to Streptococcus pneumonia in human immune cells.