Molecular interactions in an holobiont-pathogen model: Integromics in gilthead seabream infected with Sparicotyle chrysophrii

Mucosal affairs: glycosylation and expression changes of gill goblet cells and mucins in a fish–polyopisthocotylidan interaction

“…A total of 273 sequences annotated as silialidases, mannosidases, fucosyltransferases, acetylglucosaminyltransferases, sialyltransferases, mannosyltransferases glucosyltransferases, and phosphomannomutases were found in the gilthead seabream genome ( Supplementary Table S2A ). Examination of the differential expression results from the RNA sequencing experiments by Piazzon et al ( 31 ) and Toxqui-Rodríguez et al ( 43 ) revealed that 29 of these sequences were differentially expressed in at least one of the experiments when comparing control and S. chrysophrii -infected fish ( Supplementary Table S2B ). Marked downregulation was found in fish with low infection intensity ( 31 ), whereas fish with high infection intensities ( 43 ) presented both significant upregulation and downregulation ( Figure 5 ).…”

“…Examination of the differential expression results from the RNA sequencing experiments by Piazzon et al ( 31 ) and Toxqui-Rodríguez et al ( 43 ) revealed that 29 of these sequences were differentially expressed in at least one of the experiments when comparing control and S. chrysophrii -infected fish ( Supplementary Table S2B ). Marked downregulation was found in fish with low infection intensity ( 31 ), whereas fish with high infection intensities ( 43 ) presented both significant upregulation and downregulation ( Figure 5 ). Half of these modulated genes responded with opposite trends depending on the infection intensity of the fish, except for the five sialyltransferase genes, which had the same regulation patterns regardless of the parasite load.…”

“…In fact, the current S. chrysophii -infected fish had developed epitheliocystis at the later sampling point. Sparicotyle chrysophrii and epitheliocystis co-infection in gilthead seabream are common under farm and experimental conditions ( 39 , 50 , 54 ), and its specific bacterial etiology was a matter of discussion until recently ( 43 , 55 , 56 ).…”

“…We are still far from understanding the entire interplay occurring between host mediators and effectors, microbiota and microbiota-derived factors, and parasites and their excretory–secretory products. However, this study helps to understand how the gill mucosal microhabitat responds to the S. chrysophrii offender and consequent microbiota shift ( 43 ) by increased goblet cell differentiation leading to neutral goblet cell hyperplasia on gill lamellae, acutely increased mucin expression, and a probable increase in more complex glycoconjugates with sialylated, fucosylated, and branched structures.…”

“…The gilthead seabream genome ( 40 ) was mined for sequences annotated as sialilidases, mannosidases, fucosyltransferases, acetylglucosaminyltransferases, sialyltransferases, mannosyltransferases glucosyltransferases, and phosphomannomutases. Identified sequences were used to mine RNA sequencing results from two previous studies of gilthead seabream infected with S. chrysophrii : a study on fish with a mild natural infection [( 31 ); SRA accession PRJNA507368; n = 4 control and n = 4 infected fish, mean intensity of infection 2.73 parasites/fish] and other on fish with high intensity of infection during an experimental challenge [( 43 ); SRA accession PRJNA992062; n = 5 control and n = 5 infected fish, mean intensity of infection 121.2 parasites/fish]. Gill-normalized expression values (FPKM) for each identified enzyme were retrieved from the count tables, and differential expression was checked for the DESeq results obtained from each of the studies.…”