Molecular mechanisms of primary and secondary mucosal immunity using avian infectious bronchitis virus as a model system

Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA.
Veterinary Immunology and Immunopathology (Impact Factor: 1.54). 03/2008; 121(3-4):332-43. DOI: 10.1016/j.vetimm.2007.09.016
Source: PubMed


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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    • "According to Juul-Madsen et al. (2007) a good complement activation and inhibition of the multiplication of IBV in the trachea are recorded in chickens with the highest serum rate of MBL. IBV stimulates the production of different chemokines (CXCR4, CCR6, factors derived from stromal cell), interferon type 1 and interleukin 1 beta (IL-1$) (Guo et al., 2008) which act in synergy to activate the migration of specific immune cells to sites of viruses entering (Caron, 2010). Cytotoxic T Lymphocytes (CTLs) play an important role in the anti-infectious poultry protection. "
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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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    • "However, our study indicated that this initial down-regulation of innate immune genes is associated with the increase in IBV replication and the virus induced histological changes in trachea and lung. Neither Guo et al. nor Wang et al. observed a down-regulation in expression of the these genes (Guo et al., 2008; Wang et al., 2006), which could be due to the use of the less virulent vaccine strains in their studies. Also, since production of IFN-γ is controlled by cytokines secreted by both antigen-presenting cells and from the adaptive arm of immune system, a slight delay in expression is expected in response to IBV infection (Frucht et al., 2001; Gessani and Belardelli, 1998; Golab et al., 2000). "
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    ABSTRACT: Infectious bronchitis virus (IBV) replicates in the epithelial cells of trachea and lungs of chicken, however the mechanism of generation of innate immune response against IBV infection in these tissues has not been fully characterized. Our objective was to study innate responses induced early following IBV infection in chickens. Initiation of the transcription of selected innate immune genes such as TLR3, TLR7, MyD88, IL-1β and IFN-β, as well as recruitment of macrophages, were evident following an initial down regulation of some of the observed genes (TLR3, IL-1β, and IFN-γ) in trachea and lung. This initial down-regulation followed by the induction of innate immune response to IBV infection appears to be inadequate for the control of IBV genome accumulation and consequent histopathological changes in these tissues. Potential induction of innate immunity before infection occurs may be necessary to reduce the consequences since vaccine induced immunity is slow to develop.
    Virology 02/2014; s 450–451:114–121. DOI:10.1016/j.virol.2013.12.001 · 3.32 Impact Factor
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    • "A case study of avian infectious bronchitis revealed potent TH1 adaptive immunity accompanied by IL-β activation after primary immunization, with strong activation of T cells and IgA upregulation, and a local memory response governed by IgG at the bronchial mucosal surface after second immunization.117 TGF-β in the gut is known to suppress mucosal inflammation and to heal damaged mucosa by upregulating the deposition of extracellular matrix in the mucosal mesenchymal cells. "
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    ABSTRACT: The body defense mechanism has evolved to protect animals from invading pathogenic microorganisms and cancer. It is able to generate a diverse variety of cells and molecules capable of specifically recognizing and eliminating a limitless variety of foreign invaders. These cells and molecules act together in a dynamic network and are known as the immune system. Innate mucosal immunity consists of various recognition receptor molecules, including toll-like receptors, NOD-like receptors, and RIG-I-like receptors. These recognition receptor molecules recognize various invading pathogens effectively, and generate an immune response to stop their entry and neutralize their adverse consequences, such as tissue damage. Furthermore, they regulate the adaptive response in cases of severe infection and also help generate a memory response. Most infections occur through the mucosa. It is important to understand the initial host defense response or innate immunity at the mucosal surface to control these infections and protect the system. The aim of this review is to discuss the effects and functions of various innate mucosal agents and their importance in understanding the physiological immune response, as well as their roles in developing new interventions.
    International Journal of General Medicine 04/2011; 4:299-311. DOI:10.2147/IJGM.S17525
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