Atlantic salmon bath challenged with Moritella viscosa – Pathogen invasion and host response

2009 ◽  
Vol 26 (6) ◽  
pp. 877-884 ◽  
Author(s):  
M. Løvoll ◽  
C.R. Wiik-Nielsen ◽  
H.S. Tunsjø ◽  
D. Colquhoun ◽  
T. Lunder ◽  
...  
1996 ◽  
Vol 157 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Min B. Rayachhetry ◽  
George M. Blakeslee ◽  
Thomas Miller

2012 ◽  
Vol 32 (5) ◽  
pp. 796-807 ◽  
Author(s):  
Tharangani K. Herath ◽  
James E. Bron ◽  
Kim D. Thompson ◽  
John B. Taggart ◽  
Alexandra Adams ◽  
...  

Author(s):  
W. Joost Wiersinga ◽  
Tom van der Poll

Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.


2007 ◽  
Vol 32 (1) ◽  
pp. 33-44 ◽  
Author(s):  
S. A. M. Martin ◽  
J. B. Taggart ◽  
P. Seear ◽  
J. E. Bron ◽  
R. Talbot ◽  
...  

Interferons (IFNs) are cytokines that have proinflammatory, antiviral, and immunomodulatory effects and play a central role during a host response to pathogens. The IFN family contains both type I and type II molecules. While there are a number of type I IFNs, there is only one type II IFN. Recently both type I and type II IFN genes have been cloned in salmonid fish and recombinant proteins produced showing IFN activity. We have stimulated an Atlantic salmon cell line (SHK-1) with both type I and type II recombinant salmonid IFNs and analyzed the transcriptional response by microarray analysis. Cells were exposed to recombinant IFNs for 6 or 24 h or left unexposed as controls. RNA was hybridized to an Atlantic salmon cDNA microarray (salmon 17K feature TRAITS/SGP array) in order to assess differential gene expression in response to IFN exposure. For IFN I and II, 47 and 72 genes were stimulated, respectively; most genes were stimulated by a single IFN type, but some were affected by both IFNs, indicating coregulation of the IFN response in fish. Real-time PCR analysis was employed to confirm the microarray results for selected differentially expressed genes in both a cell line and primary leukocyte cultures.


2012 ◽  
Vol 43 (1) ◽  
pp. 78 ◽  
Author(s):  
Cheng Xu ◽  
Tz-Chun Guo ◽  
Stephen Mutoloki ◽  
Øyvind Haugland ◽  
Øystein Evensen

2021 ◽  
Author(s):  
Enguo Wu ◽  
Long Liu ◽  
Mingqi Zhu ◽  
Huiqin Wu ◽  
Qinghua Yang ◽  
...  

Broomcorn millet smut caused by the fungus Anthracocystis destruens is one of the most destructive diseases in broomcorn millet production. The life cycle of A. destruens and host defense responses against A. destruens remain elusive. Here we investigated the disease symptom development and the parasitic process of A. destruens as well as the ultrastructure of the host-pathogen interface. The results showed that there are four typical symptoms of broomcorn millet smut, which are blackfly, cluster leaves, hedgehog head and incomplete fruiting. A. destruens colonizes all tissues of broomcorn millet but only produces teliospores in the inflorescence. After infection, A. destruens proliferates in the host likely in a systemic manner. Ultrastructural study of the infected inflorescence showed that the pathogen grows intercellularly and intracellular within the host. The host active defense response against pathogen invasion, includes host secrets callose analogs and highly electron-dense deposits to prevent pathogen infection.


2021 ◽  
Vol 9 (4) ◽  
pp. 746
Author(s):  
Michelle McCormack ◽  
Eugene Dillon ◽  
Ian O’Connor ◽  
Eugene MacCarthy

Amoebic Gill Disease (AGD), caused by the ectoparasite Paramoeba perurans is characterised by hyperplasia of the gill epithelium and lamellar fusion. In this study, the initial host response of naïve Atlantic salmon (Salmo salar) inoculated with P. perurans was investigated. Using gel-free proteomic techniques and mass spectrometry gill and serum samples were analysed at 7 timepoints (2, 3, 4, 7, 9, 11 and 14 days) post-inoculation with P. perurans. Differential expression of immune related proteins was assessed by comparison of protein expression from each time point against naïve controls. Few host immune molecules associated with innate immunity showed increased expression in response to gill colonisation by amoebae. Furthermore, many proteins with roles in immune signalling, phagocytosis and T-cell proliferation were found to be inhibited upon disease progression. Initially, various immune factors demonstrated the anticipated increase in expression in response to infection in the serum while some immune inhibition became apparent at the later stages of disease progression. Taken together, the pro-immune trend observed in serum, the lack of a robust early immune response in the gill and the diversity of those proteins in the gill whose altered expression negatively impact the immune response, support the concept of a pathogen-derived suppression of the host response.


Aquaculture ◽  
2017 ◽  
Vol 470 ◽  
pp. 1-10 ◽  
Author(s):  
Mar Marcos-López ◽  
Hamish D. Rodger ◽  
Ian O'Connor ◽  
Mark Braceland ◽  
Richard J.S. Burchmore ◽  
...  

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