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Mitchell R White, I-Ni Hsieh, Xavier De Luna, Kevan L Hartshorn, Effects of serum amyloid protein A on influenza A virus replication and viral interactions with neutrophils, The Journal of Immunology, Volume 200, Issue Supplement_1, May 2018, Page 168.11, https://doi.org/10.4049/jimmunol.200.Supp.168.11
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Abstract
Innate immunity is vital for the early control of influenza A virus (IAV) infection. Serum amyloid A (SAA1) is an acute phase reactant produced in the liver and lung that rises dramatically during IAV infection. SAA has been reported to directly activate neutrophils and to recruit them to the lung during infectious and inflammatory processes. In this study we characterized the interactions of several forms of SAA with IAV and with neutrophils. The complex of SAA with HDL had some neutralizing activity against IAV. Similarly purified SAA containing amino acids 19–94 prepared from human serum had some viral neutralizing activity. In contrast recombinant SAA containing amino acids 19–123 (rSAA) did not. SAA preparations, including rSAA, increased various responses of neutrophils to the virus. Neither serum nor rSAA directly stimulated neutrophil respiratory burst responses on their own; however, both preparations increased these responses to IAV. rSAA also increased neutrophil uptake of IAV. rSAA alone did trigger neutrophil IL-8 production but modestly increased the strong neutrophil IL-8 response triggered by IAV. rSAA alone did trigger a neutrophil intracellular calcium response and also increased the peak calcium response to IAV. Combining rSAA with surfactant protein D (a known lung inhibitor of IAV) resulted in potentiation of viral neutralizing and aggregating activity of IAV. We provide evidence that the effects of SAA on neutrophil responses to IAV were not mediated by formyl peptide receptor 2 but were in part mediated by TLR2. These results suggest that SAA produced in the lung may significantly modulate the early neutrophilic host response to IAV.
