Low-level AFB1 promotes H1N1 swine influenza virus infection via macrophage polarization to M1/ M2

11^th International Veterinary Congress

July 02-03, 2018 Berlin, Germany

Yuhang Sun

Nanjing Agricultural University, China

Posters & Accepted Abstracts: J Vet Sci Technol

Abstract :

Swine Influenza Virus (SIV) is a major pathogen of both animals and humans. Aflatoxin B1 (AFB1) is one of the most common mycotoxins in feeds and food. However, the central contribution of AFB1 in SIV infection remains unclear. Here we investigated the involvement of AFB1 in SIV infection in vivo and in vitro, as well as its underlying mechanism using mouse and Porcine Alveolar Macrophage (PAM) models. The results of the study in vivo showed that low doses of AFB1 increased SIV infection and its severity as assessed by the increased expression levels of viral Matrix protein (M) mRNA, Nucleo-Protein (NP), matrix protein 1 and ion-channel protein, as well as weight loss, lung index and the lung histologic damage. In addition, increased SIV infection coupled with increases in TNF-�± in serum and spleen index but decreases in IL-10 in serum and thymus index were observed after low doses of AFB1 exposure in SIVinfected mice. The study in vitro also demonstrated that low concentrations of AFB1 promoted SIV replication as demonstrated by the increased viral titers, viral M mRNAand NP expression levels in SIV-infected PAMs, as well as the numbers of positive cells for the NP protein. Furthermore, AFB1 promoted PAM polarization to M1/M2 in SIV-infected PAMs, as measured by the increased M2 macrophage markers such as IL- 10 and morphological changes under scanning electron microscope. Administration of an immune-stimulant, LipoPoly-Saccharide (LPS), reversed PAM polarization to M1/M2, and thereby counteracted the promotion of influenza virus replication induced by AFB1. Take together, our results first time to confirm that low-level AFB1 promotes SIV infection via PAM polarization to M1/M2. This work reported here provides important data that point to a role for AFB1 in SIV infection and opens a new field of study.