Gram's staining and molecular identification of Staphylococcus isolate.

<p>A. Gram's staining of the clinical Staphylococcus isolate. B. Identification of Staphylococcus subspecies by ITS-PCR analysis of ribosomal DNA in the isolates from natural EE (Lane 1) and experimental EE (Lane 2). C. Examination of exfoliative toxin gene of the Staphylococcus isolate by PCR. Lanes 1 through 5 represent the PCR products of Exh-A, Exh-B, Exh-C, Exh-D and 23s ribosomal DNA, respectively.</p

Reproduction of EE in newborn piglets inoculated with <i>S. sciuri</i> HBXX06 via <i>i.m.</i> injection or oral feeding.

<p>A. Four out of six newborn piglets treated with <i>S. sciuri</i> HBXX06 via <i>i.m.</i> injection or oral feeding at the dose of 1×10¹⁰ CFU per pig succumbed to death within 24 hours post infection. B–D. The skin lesions (indicated by arrows) of the survivals of the piglets on days 2, 3 and 4 respectively following oral feeding with 1×10¹⁰ CFU per piglet.</p

Clinical case of Exudative Epidermitis (EE) in piglets.

<p>A–B. Skin lesions (indicated by arrows) of five-day-old piglets with EE. C. Morbidity and mortality of suckling piglets from September of 2005 (n = 23), December of 2005 (n = 33) through March of 2006 (n = 95).</p

Image1.TIF

<p>Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). MicroRNAs (miRNAs) are involved in host-pathogen interactions and innate immune response to viral infection. However, the role of miRNAs in host response to IBDV infection is not clear. We report here that gga-miR-155 acts as an anti-virus host factor inhibiting IBDV replication. We found that transfection of DF-1 cells with gga-miR-155 suppressed IBDV replication, while blockage of the endogenous gga-miR-155 by inhibitors enhanced IBDV replication. Furthermore, our data showed that gga-miR-155 enhanced the expression of type I interferon in DF-1 cells post IBDV infection. Importantly, we found that gga-miR-155 enhanced type I interferon expression via targeting SOCS1 and TANK, two negative regulators of type I IFN signaling. These results indicate that gga-miR-155 plays a critical role in cell response to IBDV infection.</p

DataSheet1.XLS

<p>Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). MicroRNAs (miRNAs) are involved in host-pathogen interactions and innate immune response to viral infection. However, the role of miRNAs in host response to IBDV infection is not clear. We report here that gga-miR-155 acts as an anti-virus host factor inhibiting IBDV replication. We found that transfection of DF-1 cells with gga-miR-155 suppressed IBDV replication, while blockage of the endogenous gga-miR-155 by inhibitors enhanced IBDV replication. Furthermore, our data showed that gga-miR-155 enhanced the expression of type I interferon in DF-1 cells post IBDV infection. Importantly, we found that gga-miR-155 enhanced type I interferon expression via targeting SOCS1 and TANK, two negative regulators of type I IFN signaling. These results indicate that gga-miR-155 plays a critical role in cell response to IBDV infection.</p