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ARS Home » Southeast Area » Stoneville, Mississippi » Warmwater Aquaculture Research Unit » Research » Publications at this Location » Publication #261497

Title: Exploring the biology of disease resistance and susceptibility in catfish through proteomics and primary cell culture

item Booth, Natha
item Peterson, Brian

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/28/2010
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Each year more than 200 families of channel catfish are screened through experimental challenge with Edwardsiella ictaluri, the causative agent of Enteric Septicemia of Catfish, a disease that annually causes widespread economic losses in the catfish industry. These experiential challenges are designed and carried out in order to identify families that are extremely susceptible (> 70% mortality) to ESC and those that are extremely resistant (< 20% mortality). Once families displaying the desired high and low survival phenotype are identified, they are then used in proteomic and primary cell culture studies to discern the biological basis for these phenotypes. Head kidney tissue from high and low survivors was subjected to analysis by 2-D gel electrophoresis, followed by MALDI-TOF-MSMS analysis of uniquely expressed proteins in each of these. Three unique proteins were identified from each of these groups. All but one of these proteins were related to macrophage function or stress response. Proteomic studies of brain tissue and mucous from these two families are in process. Primary macrophages were prepared from both of these families and, in 2 replicate studies, each performed in triplicate, macrophages from the high survivors demonstrated significantly reduced ability to control intracellular replication of E. ictaluri over 8 and 10 hours post-infection. There was no significant difference in initial uptake of bacteria by the two cell types. TNF, which plays an important role in innate immunity, macrophage function, and the onset of the inflammatory response, was shown to be significantly higher in the spleen and liver of the high survivors at 48 and 72 hours, respectively. TNF expression was negligible in the low survivors at all time-point in the liver, but in the spleen increased between 48 and 72 hours to levels significantly higher than the high survivors by 72 hours.