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ARS Home » Southeast Area » Auburn, Alabama » Aquatic Animal Health Research » Research » Publications at this Location » Publication #357438

Research Project: Pathogen Characterization, Host Immune Response and Development of Strategies to Reduce Losses to Disease in Aquaculture

Location: Aquatic Animal Health Research

Title: Stress hormone cortisol helps to drive biofilm formation in Flavobacterium columnare

Author
item Declercq, Annelies - Ghent University
item Cai, Wenlong - Auburn University
item Naranjo, Eber - Auburn University
item Thongda, Wilawan - Auburn University
item Eckhaut, Venessa - Ghent University
item Bauwens, Eva - Ghent University
item Arias, Cova - Auburn University
item De La Fuente, Leonardo - Auburn University
item Beck, Benjamin
item Lange, Miles
item Peatman, Eric - Auburn University
item Haesebrougk, Freddy - Ghent University
item Aerts, Johan - Ghent University
item Decostere, Annemie - Ghent University

Submitted to: International Aquaculture Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 9/28/2018
Publication Date: 11/25/2018
Citation: Declercq, A., Cai, W., Naranjo, E., Thongda, W., Eckhaut, V., Bauwens, E., Arias, C., De La Fuente, L., Beck, B.H., Lange, M.D., Peatman, E., Haesebrougk, F., Aerts, J., Decostere, A. 2018. Stress hormone cortisol helps to drive biofilm formation in Flavobacterium columnare [abstract]. 5th International Conference of Members of the Genus Flavobacterium 2018. p. 42.

Interpretive Summary:

Technical Abstract: The impact of cortisol on biofilm formation by Flavobacterium columnare, the causative agent of columnaris disease, was evaluated. Firstly, the dynamics of biofilm formation by one high (HV) and another low virulent (LV) F. columnare isolate supplemented either or not with the stress hormone cortisol under microfluidic flow conditions was characterized. In both isolates, cell aggregates resembling biofilms occurred within 7-h post-inoculation. Consequently, cell clusters were sloughed away, immediately followed by a rebuilding of bacterial cell aggregates, occurring four times and once in the 24-h observation period for the HV and LV isolate, respectively, suggestive for a higher spreading capacity of the former. The LV isolate only revealed upstream cell aggregates upon cortisol supplementation. Secondly, the expression of genes belonging to the Type IX secretion system (gldK, gldL, gldM, gldN, sprA, sprE, and sprT, and porV) was investigated in planktonic and biofilm cells of a HV and LV isolate to which no, a low or high dose of cortisol was added. Significantly lower expression of gliding genes gldK, gldL, gldM and gldN, and of protein secretion regulator porV was seen in the planktonic cells of the LV isolate supplemented with a high cortisol dose. The LV isolate biofilm cells treated with the high cortisol dose showed a significant upregulation of sprT, encoding mobile surface adhesion which is important in bacterial colonization. This is the first evidence for the co-regulatory effect of cortisol on biofilm formation and on F. columnare gliding gene expression, thereby launching new research perspectives for microbial endocrinology.