The Interaction between Phagocytes and Streptococcus agalactiae (GBS) Mediated by the Activated Complement System is the Key to GBS Inducing Acute Bacterial Meningitis of Tilapia

Abstract

Simple SummaryStreptococcus agalactiae (GBS) is a serious threat to farmed tilapia, which results in high mortality and seriously hinders tilapia farming development. The pathogenic mechanism of tilapia infected with GBS which die rapidly in production remains unknown. We provided a comprehensive comparative analysis of the tilapias infected with fish-derived GBS attenuated strain YM001 and its parental virulent strain HN016. The present study indicates that the interaction between phagocytes and GBS mediated by the activated complement system is key to GBS inducing tilapia acute bacterial meningitis. The low survival ability caused by reduced β-lactam antibiotics resistance is one of the important reasons YM001 lost its pathogenicity to tilapia. Our study provided a comprehensive cognition of the mechanism of acute bacterial meningitis caused by GBS.AbstractStreptococcus agalactiae is an important pathogen for tilapia meningitis. Most of the infected tilapia die rapidly in production, when the way to study the pathogenic mechanism of bacteria on host through chronic infection in laboratory is not comprehensive and accurate enough to elucidate the real pathogenic mechanism. The objective of this study was to investigate the mechanism of acute bacterial meningitis of tilapia caused by Streptococcus agalactiae (GBS), and provide a theoretical basis for its prevention and treatment. Duel RNA-seq, proteome analysis, histopathological analysis, plasma biochemical indexes, and blood routine examination were performed on tilapias infected with fish-derived GBS attenuated strain YM001 and its parental virulent strain HN016. The results showed that the contents of white blood cell (WBC), monocytes (MON), and neutrophil (NEU) were significantly lower in the HN016 group compared to that in the YM001 group (p < 0.05). Histopathological examination showed that there were partially lesions in the examined tissues of tilapia infected by HN016, while no obvious histopathological changes occurred in the YM001 group. The differential expressed genes (DEGs) and differential expressed proteins (DEPs) between YM001 and HN016 were mainly enriched in the beta-lactam resistance pathway (oppA1, oppA2, oppB, oppC, oppD, oppF, and mrcA). The DEGs DEPs between YM001-brain and HN016-brain were mainly enriched in the complement and coagulation cascades signaling pathway (C2a, c4b, c3b, c7, CD59, ITGB2, and ITGAX). The present study indicates that the interaction between phagocytes and GBS mediated by the activated complement system is the key to GBS inducing tilapia acute bacterial meningitis. The low survival ability caused by reduced β-lactam antibiotics resistance is one of the important reasons for why YM001 lost its pathogenicity to tilapia.

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“…Differentially expressed proteins (DEPs) were identified and assigned to Gene Ontology (GO) categories . The GO enrichment analysis was performed when the p value < 0.05 . A protein–protein interaction network analysis was performed as described in our previous study .…”

“…Total proteins were extracted, and their concentrations were evaluated . One hundred micrograms of protein from each sample was reduced, alkylated, digested, and labeled with a tandem mass tag (TMT). , Then, the labeled samples were analyzed as described in previous studies. , …”

Acetylome and Succinylome Profiling of Edwardsiella tarda Reveals Key Roles of Both Lysine Acylations in Bacterial Antibiotic Resistance

“…Additionally, some MDR-related proteins were also found to be Kac- or Ksu-modified in this study. Among these, OppD is a major component of the β-lactam antibiotic resistance of S. agalactiae [ 57 ]; ArnA is a bifunctional polymyxin resistance protein targeted to peptide antibiotics by altering the antibiotic target of the host [ 58 ]. Moreover, the protein EmrA is involved in the regulation of multidrug resistance in various bacterial species [ 59 , 60 ].…”

Research Advances on Tilapia Streptococcosis

“…Besides the aforementioned virulence factors, there are also other virulence factors, which have not been experimentally confirmed in tilapia GBS infections, but, which have been widely studied in mammalian GBS infections, including, for example, fibrinogen receptor ( FbsA, FbsB and FbsC) [ 62 ] , superoxide dismutase (SOD), serine-threonine protein kinase (STPK), C5a peptidase (scp) [ 14 ] , serine-rich repeat glycoproteins (srr1 and srr2) [ 63 ] , β-hemolysin/cytolysin (cylE) [ 64 ], pili [ 65 ] , proteins Cα (bca) [ 66 ], neul [ 67 ], and α-like protein ( Alp ) [ 68 ], among others.…”