Molecular mechanisms of primary and secondary mucosal immunity using avian infectious bronchitis virus as a model system.
ABSTRACT Although mucosal immune responses are critical for protection of hosts from clinical illness and even mortality caused by mucosal pathogens, the molecular mechanism of mucosal immunity, which is independent of systemic immunity, remains elusive. To explore the mechanistic basis of mucosal protective immunity, gene transcriptional profiling in mucosal tissues was evaluated after the primary and secondary immunization of animals with an attenuated avian infectious bronchitis virus (IBV), a prototype of Coronavirus and a well-characterized mucosal pathogen. Results showed that a number of innate immune factors including toll-like receptors (TLRs), retinoic-acid-inducible gene-1 (RIG-1), type I interferons (IFNs), complements, and interleukin-1 beta (IL-1beta) were activated locally after the primary immunization. This was accompanied or immediately followed by a potent Th1 adaptive immunity as evidenced by the activation of T-cell signaling molecules, surface markers, and effector molecules. A strong humoral immune response as supported by the significantly up-regulated immunoglobulin (Ig) gamma chain was observed in the absence of innate, Th1 adaptive immunity, or IgA up-regulation after the secondary immunization, indicating that the local memory response is dominated by IgG. Overall, the results provided the first detailed kinetics on the molecular basis underlying the development of primary and secondary mucosal immunity. The key molecular signatures identified may provide new opportunities for improved prophylactic and therapeutic strategies to combat mucosal infections.
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ABSTRACT: Infectious Bronchitis (IB) of chicken is a viral disease caused by a Coronavirus (IBV). It is worldwide distributed and characterized by its heavy economic impact on the poultry industry. The objective of this study is to elucidate the molecular aspect of the IBV, to describe the humoral and cellular immune responses, especially those played by cytotoxic T lymphocytes in the control of this infection in addition to the role played by each of the viral proteins S and N in the induction of those immune reactions. Biotechnological advances (especially gene therapy) in the IB control have been assessed by several researchers; however they are still facing some constraints. Development of new vaccines against IBV involves detailed knowledge of its antigenic structure and of the specific Cytotoxic T Lymphocytes (CTL) epitopes.Asian Journal of Poultry Science 03/2015; 9(2). DOI:10.3923/ajpsaj.2015.57.69
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ABSTRACT: The natural route of entry of Marek's disease virus (MDV) is via the respiratory system. However, little is known about host–virus interactions in the lungs. The objective of the present study was to examine MDV replication and induction of innate host responses in the lungs of chickens infected through inhalation. Replication of MDV in lungs was detectable as early as 12 hours post-infection (hpi). The expression of Toll-like receptor (TLR)3 and TLR7 genes was enhanced in response to MDV infection in the lungs. This was associated with the up-regulation of interleukin (IL)-1β and IL-8 genes. In response to MDV infection, the number of macrophages in lungs of infected chickens was significantly higher compared to uninfected control chickens. The expression of inducible nitric oxide synthase (iNOS) gene was also significantly higher in the lungs at 72 hpi following MDV infection. In conclusion, the present study demonstrates induction of innate host responses to MDV infection in the respiratory system. Further studies are needed to characterize other host responses generated in the lungs following MDV infection.Virology 10/2009; 393(2-393):250-257. DOI:10.1016/j.virol.2009.08.001 · 3.28 Impact Factor