Comparative multi-omics systems analysis reveal the glycolysis / gluconeogenesis signal pathway play an important role in virulence attenuation in fish-derived GBS YM001

Liu, Yu; Li, Liping; Huang, Ting; Wang, Rui; Liang, Weizheng; Yang, Qiong; Lei, Aiying; Chen, Ming

doi:10.1371/journal.pone.0221634

Cited by 3 publications

(2 citation statements)

References 50 publications

(45 reference statements)

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“…RNA-seq provides a sensitive method for global gene expression analysis in infection biology [21]. Previous combined transcriptomic and proteomic studies on HN016 and its attenuated strain YM001 cultured in vitro have shown that the pentose phosphate pathway and pyruvate metabolism pathway that affecting the growth of the strain may be one of the important reasons for the virulence attenuation in HN016 [28]. However, as bacterial infections of eucaryon involve two interacting organisms, there are interactions between the bacteria and the host.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Huang

et al. 2019

Animals

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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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Section: Discussionmentioning

confidence: 99%

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

Liu

Huang

et al. 2019

Animals

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“…Refer to our previous study [29], the cultured strains were stored in TRizol and transported with liquid nitrogen. RNA sequencing was performed by Novogene Co, LTD (Beijing, China).…”

Section: Rna-sequencingmentioning

confidence: 99%

Arginine Deiminase and Biotin Metabolism Signaling Pathways Play an Important Role in Human-Derived Serotype V, ST1 Streptococcus agalactiae Virulent Strain upon Infected Tilapia

Liu

Luo³

et al. 2020

Animals

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Our previous study showed that human-derived Streptococcus agalactiae (serotype V) could infect tilapia, but the mechanism underlying the cross-species infection remains unrecognized. In this study, a multi-omics analysis was performed on human-derived S.agalactiae strain NNA048 (virulent to tilapia, serotype V, ST1) and human-derived S.agalactiae strain NNA038 (non-virulent to tilapia, serotype V, ST1). The results showed that 907 genes (504 up/403 down) and 89 proteins (51 up/38 down) were differentially expressed (p < 0.05) between NNA038 and NNA048. Among them, 56 genes (proteins) were altered with similar trends at both mRNA and protein levels. Functional annotation of them showed that the main differences were enriched in the arginine deiminase system signaling pathway and biotin metabolism signaling pathway: gdhA, glnA, ASL, ADI, OTC, arcC, FabF, FabG, FabZ, BioB and BirA genes may have been important factors leading to the pathogenicity differences between NNA038 and NNA048. We aimed to provide a comprehensive analysis of the human-derived serotype V ST1 S.agalactiae strains, which were virulent and non-virulent to tilapia, and provide a more comprehensive understanding of the virulence mechanism.

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Re-framing the importance of Group B Streptococcus as a gut-resident pathobiont

Ling,

Hryckowian

2024

Infect Immun

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Streptococcus agalactiae (Group B Streptococcus , GBS) is a Gram-positive bacterial species that causes disease in humans across the lifespan. While antibiotics are used to mitigate GBS infections, it is evident that antibiotics disrupt human microbiomes (which can predispose people to other diseases later in life), and antibiotic resistance in GBS is on the rise. Taken together, these unintended negative impacts of antibiotics highlight the need for precision approaches for minimizing GBS disease. One possible approach involves selectively depleting GBS in its commensal niches before it can cause disease at other body sites or be transmitted to at-risk individuals. One understudied commensal niche of GBS is the adult gastrointestinal (GI) tract, which may predispose colonization at other body sites in individuals at risk for GBS disease. However, a better understanding of the host-, microbiome-, and GBS-determined variables that dictate GBS GI carriage is needed before precise GI decolonization approaches can be developed. In this review, we synthesize current knowledge of the diverse body sites occupied by GBS as a pathogen and as a commensal. We summarize key molecular factors GBS utilizes to colonize different host-associated niches to inform future efforts to study GBS in the GI tract. We also discuss other GI commensals that are pathogenic in other body sites to emphasize the broader utility of precise de-colonization approaches for mitigating infections by GBS and other bacterial pathogens. Finally, we highlight how GBS treatments could be improved with a more holistic understanding of GBS enabled by continued GI-focused study.

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Comparative multi-omics systems analysis reveal the glycolysis / gluconeogenesis signal pathway play an important role in virulence attenuation in fish-derived GBS YM001

Cited by 3 publications

References 50 publications

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

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

Arginine Deiminase and Biotin Metabolism Signaling Pathways Play an Important Role in Human-Derived Serotype V, ST1 Streptococcus agalactiae Virulent Strain upon Infected Tilapia

Re-framing the importance of Group B Streptococcus as a gut-resident pathobiont

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