Autophagy is a lysosomal degradative pathway responsible for recycling cytosolic proteins and organelles and also functions as an innate defense mechanism that host cells use against viral infection. While many viruses have evolved mechanisms to antagonize the antiviral effects of the autophagy pathway, others subvert autophagy to facilitate replication. For flaviviruses, both the positive and negative role of autophagy in virus replication has been reported. The interplay between autophagy and tick-borne encephalitis virus (TBEV) in innate immune cells is largely unknown. Here we report the relationship between an autophagy and TBEV replication in mouse macrophage cell line PMJ2-R using Hypr strain of TBEV. First, we examined the effect of Hypr infection on the autophagy pathway. We detected a mild and a temporary increase of autophagy marker LC3-II in Hypr-infected cells. The role of autophagy in TBEV replication was evaluated in autophagy related gene 5 (Atg5) knockdown cells (shAtg5). Our results showed that during an early stage of Hypr infection the viral titers were increased, while later on, at 72 hpi, the titers have declined in shAtg5 cells compared to control. Moreover, the higher number of virus-positive cells was observed in shAtg5 cells in early stage of infection and correlated with enhanced virus entry. Finally, we found an increased production of IFN-β in Hypr-infected shAtg5 cells in comparison to control at 48 and 72 hpi implicating that autophagy restricts the amount of IFN produced by TBEV-infected macrophages. To conclude, in mouse macrophages TBEV replication is controlled by autophagy in time dependent manner, having temporally an antiviral and then a pro-viral role during infection. Our study points out to a delicate and complex involvement of autophagy machinery at level of virus entry and IFN-β production when controlling TBEV infection.

• MeSH
• Antiviral Agents metabolism   MeSH
• Autophagy MeSH
• Interferon-beta genetics   metabolism   MeSH
• Encephalitis, Tick-Borne * genetics   MeSH
• Macrophages metabolism   MeSH
• Mice MeSH
• Virus Replication MeSH
• Encephalitis Viruses, Tick-Borne * genetics   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

The protective effect of Enterococcus faecium EFAL41 on chicken's caecum in relation to the TLR (TLR4 and TLR21) activation and production of luminal IgA challenged with Campylobacter jejuni CCM6191 was assessed. The activation of MIF, IFN-β, MD-2 and CD14 was followed-up after bacterial infection. Day-old chicks (40) were divided into four groups (n = 10): control (C), E. faecium AL41 (EFAL41), C. jejuni (CJ) and combined E. faecium AL41+C. jejuni (EFAL41+CJ). Relative mRNA expression of TLR4, TLR21 and CD14 was upregulated in the probiotic strain and infected (combined) group on day 4 and 7 post infection (p.i.). The caecal relative MD-2 mRNA expression was upregulated on day 4 p.i. in the EFAL41+CJ and CJ groups. MIF and IFN-β reached the highest levels in the combined groups on day 7 p.i. The concentration of the sIgA in intestinal flush was upregulated in EFAL41+CJ group on day 4 p.i. The results demonstrated that E. faecium EFAL41 probiotic strain can modulate the TLRs expression and modify the activation of MIF, IFN-β, MD-2 and CD14 molecules in the chickens caecum challenged with C. jejuni CCM 6191. The counts of EFAL41 were sufficient and high, similarly the counts of enterococci in both, caecum and faeces but without reduction of Campylobacter counts.

• MeSH
• Campylobacter jejuni growth & development   MeSH
• Cecum immunology   microbiology   MeSH
• Enterococcus faecium growth & development   immunology   MeSH
• Feces microbiology   MeSH
• Immunoglobulin A, Secretory genetics   MeSH
• Host-Pathogen Interactions MeSH
• Interferon-beta genetics   immunology   MeSH
• Campylobacter Infections diet therapy   immunology   microbiology   veterinary   MeSH
• Chickens MeSH
• Lipopolysaccharide Receptors genetics   immunology   MeSH
• Lymphocyte Antigen 96 genetics   immunology   MeSH
• Poultry Diseases diet therapy   genetics   immunology   microbiology   MeSH
• Animals, Newborn MeSH
• Probiotics pharmacology   MeSH
• Protein Isoforms genetics   immunology   MeSH
• Receptors, Immunologic genetics   immunology   MeSH
• Gene Expression Regulation MeSH
• Signal Transduction MeSH
• Toll-Like Receptor 4 genetics   immunology   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH