Lonicerae flos polysaccharides improve nonalcoholic fatty liver disease by activating the adenosine 5'-monophosphate-activated protein kinase pathway and reshaping gut microbiota.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver cirrhosis and cancer. Lonicerae flos polysaccharides (LPs) have been shown to be effective in treating metabolic diseases; however, the therapeutic effects and underlying molecular mechanisms of LPs in NAFLD remain unclear. PURPOSE: The objective of this study was to investigate the morphological characterization of Lonicerae flos polysaccharides (LPs) and the mechanism of LPs in relieving NAFLD. METHODS: The morphology of LPs was observed using atomic force microscopy (AFM), X-ray diffraction (XRD), thermal weight (TG), and thermal weight derivative (DTG); NAFLD mice were treated with LPs at the same time as they were induced with a Western diet, and then the indexes related to glycolipid metabolism, fibrosis, inflammation, and autophagy in the serum and liver of the mice were detected. RESULTS: The atomic force microscope analysis results indicated that the LPs displayed sugar-chain aggregates, exhibited an amorphous structure, and were relatively stable in thermal cracking at 150 °C. It was also found that LPs exerted therapeutic effects in NAFLD. The LPs prevented high-fat and -cholesterol diet-induced NAFLD progression by regulating glucose metabolism dysregulation, insulin resistance, lipid accumulation, inflammation, fibrosis, and autophagy. Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) inhibitor compound C abrogated LP-induced hepatoprotection in mice with NAFLD. The LPs further treated NAFLD by reshaping the structure of the gut microbiota, in which Desulfovibrio bacteria plays a key roles. CONCLUSION: Lonicerae flos polysaccharides exert protective effects against NAFLD in mice by improving the structure of the intestinal flora and activating the AMPK signaling pathway. © 2023 Society of Chemical Industry.

Maternal colonization with group B Streptococcus and antibiotic resistance in China: systematic review and meta-analyses.

BACKGROUND: Maternal rectovaginal colonization with group B Streptococcus (GBS) or Streptococcus agalactiae is the most common pathway for this disease during the perinatal period. This meta-analysis aimed to summarize existing data regarding maternal colonization, serotype profiles, and antibiotic resistance in China. METHODS: Systematic literature reviews were conducted after searching 6 databases. Meta-analysis was applied to analyze colonization rate, serotype, and antimicrobial susceptibility of GBS clinical isolates in different regions of China. Summary estimates are presented using tables, funnel plots, forest plots, histograms, violin plots, and line plots. RESULTS: The dataset regarding colonization included 52 articles and 195 303 pregnant women. Our estimate for maternal GBS colonization in China was 8.1% (95% confidence interval [CI] 7.2%-8.9%). Serotypes Ia, Ib, III, and V account for 95.9% of identified isolates. Serotype III, which is frequently associated with the hypervirulent clonal complex, accounts for 46.4%. Among the maternal GBS isolates using multilocus sequence typing (MLST), ST19 (25.7%, 289/1126) and ST10 (25.1%, 283/1126) were most common, followed by ST12 (12.4%, 140/1126), ST17 (4.8%, 54/1126), and ST651 (3.7%, 42/1126). GBS was highly resistant to tetracycline (75.1% [95% CI 74.0-76.3%]) and erythromycin (65.4% [95% CI 64.5-66.3%]) and generally susceptible to penicillin, ampicillin, vancomycin, ceftriaxone, and linezolid. Resistance rates of GBS to clindamycin and levofloxacin varied greatly (1.0-99.2% and 10.3-72.9%, respectively). A summary analysis of the bacterial drug resistance reports released by the China Antimicrobial Resistance Surveillance System (CARSS) in the past 5 years showed that the drug resistance rate of GBS to erythromycin, clindamycin, and levofloxacin decreased slowly from 2018 to 2020. However, the resistance rates of GBS to all 3 antibiotics increased slightly in 2021. CONCLUSIONS: The overall colonization rate in China was much lower than the global colonization rate (17.4%). Consistent with many original and review reports in other parts of the world, GBS was highly resistant to tetracycline. However, the resistance of GBS isolates in China to erythromycin and clindamycin was greater than in other countries. This paper provides important epidemiological information, to assist with prevention and treatment of GBS colonization in these women.

Identification of a Novel Linear B Cell Epitope on the Sao Protein of Streptococcus suis Serotype 2.

Surface antigen one (Sao) protein is a bacterial surface protein identified in the important zoonotic pathogen Streptococcus suis serotype 2 (S. suis 2) during an extensive search for functional proteins. The Sao protein is anchored to the bacterial cell wall by the LPVTG motif and is widely distributed in many S. suis serotypes. In this paper, we present the immunodominant epitope peptide of the Sao protein that is recognized by BALB/c antibodies against the Sao protein: 355SEKQMPSVVNENAVTPEKQMTNKENDNIET384 (location Sao355-384). To determine the core epitope recognized by antibodies, we prepared truncation peptide libraries. Analyses of the immunoreactivity of truncation peptides with anti-Sao355-384 serum revealed that the most immunoreactive sequence was 355SEKQMPSVVNENAVTPEK372 (location Sao355-372). Moreover, we observed that this core epitope also showed good specificity based on the ratio of reactivity with serum from S. suis-positive patients compared to serum from S. suis-negative patients. Our results point to the potential of using the Sao355-372 peptide in diagnostic assays to determine S. suis infection in humans.

Inactivation of the htpsA gene affects capsule development and pathogenicity of Streptococcus suis.

STREPTOCOCCUS SUIS: serotype 2 (S. suis 2) is an important swine pathogen and also an emerging zoonotic agent. HtpsA has been reported as an immunogenic cell surface protein on the bacterium. In the present study, we constructed an isogenic mutant strain of htpsA, namely ΔhtpsA, to study its role in the development and virulence of S. suis 2. Our results showed that the mutant strain lost its typical encapsulated structure with decreased concentrations of sialic acid. Furthermore, the survival rate in whole blood, the anti-phagocytosis by RAW264.7 murine macrophage, and the adherence ability to HEp-2 cells were all significantly affected in the ΔhtpsA. In addition, the deletion of htpsA sharply attenuated the virulence of S. suis 2 in an infection model of mouse. RNA-seq analysis revealed that 126 genes were differentially expressed between the ΔhtpsA and the wild-type strains, including 28 upregulated and 98 downregulated genes. Among the downregulated genes, many were involved in carbohydrate metabolism and synthesis of virulence-associated factors. Taken together, htpsA was demonstrated to play a role in the morphological development and pathogenesis of the highly virulent S. suis 2 05ZYH33 strain.

Genetic Diversity of Listeria monocytogenes Isolates from Invasive Listeriosis in China.

Listeria monocytogenes is a deadly foodborne pathogen, and infections can result in meningoencephalitis and sepsis with mortality rates of up to 30%. In this study, we performed comparative whole-genome analysis of 30 clinical isolates sequenced together with 32 previously sequenced clinical and food isolates from China. The data indicate that L. monocytogenes isolates belonging to the clonal complexes (CC) -1, -8, -9, -87, -121, and -155 are present in human clinical cases. The majority of isolates are from CC-87, 9, and 8 and overlap with those CCs previously reported on the basis of multilocus sequence typing for isolates from Chinese food products. Detailed genome analysis of isolates, representative of CCs in clinical and food products, revealed strong similarities both in their core- and accessory genomes indicating that they are highly related. When compared to genome sequences of isolates of a given CC worldwide, clinical isolates of China were distinct and clustered in unified clades. Our data indicate that epidemic clones of L. monocytogenes (CC-87, 9, and 8) with unusually high occurrence of plasmids are unique to China and suggest that common populations of L. monocytogenes clones are present in both clinical and food products in China.

Streptococcus suis DivIVA Protein Is a Substrate of Ser/Thr Kinase STK and Involved in Cell Division Regulation.

Streptococcus suis serotype 2 is an important swine pathogen and an emerging zoonotic agent that causes severe infections. Recent studies have reported a eukaryotic-like Ser/Thr protein kinase (STK) gene and characterized its role in the growth and virulence of different S. suis 2 strains. In the present study, phosphoproteomic analysis was adopted to identify substrates of the STK protein. Seven proteins that were annotated to participate in different cell processes were identified as potential substrates, which suggests the pleiotropic effects of stk on S. suis 2 by targeting multiple pathways. Among them, a protein characterized as cell division initiation protein (DivIVA) was further investigated. In vitro analysis demonstrated that the recombinant STK protein directly phosphorylates threonine at amino acid position 199 (Thr-199) of DivIVA. This effect could be completely abolished by the T199A mutation. To determine the specific role of DivIVA in growth and division, a divIVA mutant was constructed. The ΔdivIVA strain exhibited impaired growth and division, including lower viability, enlarged cell mass, asymmetrical division caused by aberrant septum, and extremely weak pathogenicity in a mouse infection model. Collectively, our results reveal that STK regulates the cell growth and virulence of S. suis 2 by targeting substrates that are involved in different biological pathways. The inactivation of DivIVA leads to severe defects in cell division and strongly attenuates pathogenicity, thereby indicating its potential as a molecular drug target against S. suis.

Identification of oligopeptide-binding protein (OppA) and its role in the virulence of Streptococcus suis serotype 2.

The oligopeptide permease (Opp) cassette, an oligopeptide transport system belongs to the superfamily of ATP-binding cassette (ABC) transporter, is widely distributed in bacteria, including Streptococcus suis (S. suis). It is encoded by the opp operon containing oppA, oppB, oppC, oppD, and oppF. In addition to the uptake of peptide, the oppA gene also plays an important role in virulence of many pathogens. In this study, an oppA homologue from the highly virulent S. suis serotype 2 (S. suis 2) strain 05ZYH33 was identified. Flow cytometry and Western blot confirmed that OppA is a surface immunogenic protein and is expressed during S. suis 2 infection. To explore the role of oppA in S. suis 2 growth and pathogenicity, an isogenic 05ZYH33 mutant of oppA (△oppA) was obtained by homologous recombination. Although the complementary strain was not obtained due to the △oppA strain is not transformable, the current data revealed that deletion of the oppA gene in S. suis 2 has greatly affected its growth and virulence. Our data revealed that the growth rate is significantly slow for the △oppA. Adherence of the △oppA strain to human epithelial cells is greatly reduced comparing to the wild strain. Mouse infection experiment showed that inactivation of oppA greatly attenuated the high pathogenicity of S. suis 2. The observed results suggest that OppA is a surface-exposed protein and plays important roles in the growth and pathogenicity of S. suis 2.

The type II histidine triad protein HtpsC is a novel adhesion with the involvement of Streptococcus suis virulence.

Streptococcal histidine triad proteins HTPs are widely distributed within the Streptococcus genus. Based on the phylogenetic relationship and domain composition, HTPs are classified into type I and type II subfamilies. Previous studies revealed that several pathogenic streptococci contain more than one htp gene. We found that the highly virulent strain of Streptococcus suis 2 (S. suis 2), 05ZYH33 encodes 3 HTPs, designated HtpsA (previously described as HtpS), HtpsB, and HtpsC. Among them, HtpsC is the only member that contains leucine-rich repeat (LRR) domains at the C-terminal. In this study, we demonstrated that the recombinant HtpsC could bind to 2 different components of human ECM complex laminin and fibronectin in vitro, suggesting that it is a novel adhesin of S. suis 2. Having constructed an htpsC mutant, we evaluated its role in the pathogenesis of the highly virulent S. suis 2 strain 05ZYH33. Our data showed that inactivation of htpsC significantly affected adherence of S. suis 2 to Hep-2 cells and shortened the survival of the bacteria in whole blood. Furthermore, deletion of htpsC significantly attenuated the virulence of S. suis 2 in mice. These results demonstrated that htpsC was involved in the pathogenesis of the highly virulent S. suis 2 strain 05ZYH33. In line with the observation, immunization with HtpsC significantly prolonged mice's survival after S. suis 05ZYH33 challenge, indicating its potential use in the vaccine development against S. suis.

Development of reverse transcription loop-mediated isothermal amplification assays to detect Hantaan virus and Seoul virus.

We developed two assays based on one-step reverse transcription loop-mediated isothermal amplification (RT-LAMP) to identify Hantaan virus (HTNV) and Seoul virus (SEOV), members of the Hantavirus genus that cause hemorrhagic fever with renal syndrome (HFRS). Our results showed that these assays can be conducted within 30min under isothermal conditions. The detection limit for HTNV was around 10 copies per reaction, similar to detection levels for quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays. The detection limit for SEOV was 100 copies per reaction, a sensitivity that was 10-fold lower than that for qRT-PCR assays but 10-fold higher than that for RT-PCR assays. The method we developed was specific for both HTNV and SEOV without any cross-reaction with other pathogens. We conclude that RT-LAMP assays could be useful for the rapid and direct detection of HTNV and SEOV clinically, and for the epidemiological investigation of HFRS.

Isolation and characterization of a native avirulent strain of Streptococcus suis serotype 2: a perspective for vaccine development.

Streptococcus suis, an emerging infectious pathogen, is the cause of two large-scale outbreaks of human streptococcal toxic shock syndrome in China, and has attracted much attention from the scientific community. The genetic basis of its pathogenesis remains enigmatic, and no effective prevention measures have been established. To better understand the virulence differentiation of S. suis and develop a promising vaccine, we isolated and sequenced a native avirulent S. suis strain (05HAS68). Animal experiments revealed that 05HAS68 is an avirulent strain and could protect piglets from the attack of virulent strains. Comparative genomics analyses demonstrated the genetic basis for the lack of virulence in 05HAS68, which is characterized by the absence of some important virulence-associated factors and the intact 89K pathogenicity island. Lack of virulence was also illustrated by reduced survival of 05HAS68 compared to a virulent strain in pig whole blood. Further investigations revealed a large-scale genomic rearrangement in 05HAS68, which was proposed to be mediated by transposase genes and/or prophages. This genomic rearrangement may have caused the genomic diversity of S. suis, and resulted in biological discrepancies between 05HAS68 and highly virulent S. suis strains.

The ß-galactosidase (BgaC) of the zoonotic pathogen Streptococcus suis is a surface protein without the involvement of bacterial virulence.

Streptococcal pathogens have evolved to express exoglycosidases, one of which is BgaC ß-galactosidase, to deglycosidate host surface glycolconjucates with exposure of the polysaccharide receptor for bacterial adherence. The paradigm BgaC protein is the bgaC product of Streptococcus, a bacterial surface-exposed ß-galactosidase. Here we report the functional definition of the BgaC homologue from an epidemic Chinese strain 05ZYH33 of the zoonotic pathogen Streptococcus suis. Bioinformatics analyses revealed that S. suis BgaC shared the conserved active sites (W240, W243 and Y454). The recombinant BgaC protein of S. suis was purified to homogeneity. Enzymatic assays confirmed its activity of ß-galactosidase. Also, the hydrolysis activity was found to be region-specific and sugar-specific for the Gal ß-1,3-GlcNAc moiety of oligosaccharides. Flow cytometry analyses combined with immune electron microscopy demonstrated that S. suis BgaC is an atypical surface-anchored protein in that it lacks the "LPXTG" motif for typical surface proteins. Integrative evidence from cell lines and mice-based experiments showed that an inactivation of bgaC does not significantly impair the ability of neither adherence nor anti-phagocytosis, and consequently failed to attenuate bacterial virulence, which is somewhat similar to the scenario seen with S. pneumoniae. Therefore we concluded that S. suis BgaC is an atypical surface-exposed protein without the involvement of bacterial virulence.

Prevalent distribution and conservation of Streptococcus suis Lmb protein and its protective capacity against the Chinese highly virulent strain infection.

Streptococcus suis (S. suis) is an important zoonotic pathogen that causes multiple diseases in both pigs and humans. Many studies suggest that Streptococcus utilizes host extracellular matrix proteins, including laminin, for adhesion and invasion of host cells. Recently, we identified a putative Lmb protein (CDS 0330) of a highly virulent strain of S. suis (serotype 2). In this study, we characterized the ability of CDS 0330 to bind human laminin, and evaluated the protective efficacy of a recombinant protein vaccine. Bioinformatic analysis revealed that both the amino acid sequence and tertiary structure of CDS 0330 were similar to Lmb proteins in other Streptococcus. In addition, the sequence of CDS 0330 was present in the genomes of 26 of the 38 sequenced streptococci species, indicating an early origin and conservation of this gene. Particularly, all 17 sequenced S. suis genomes, regardless of serotype or geographic origin, contained CDS 0330 gene in their genome with a minimum pair-wise amino acid identity of 92%. PCR amplification revealed that CDS 0330 gene is distributed throughout 35 S. suis serotypes in the lmb-htp format. Flow cytometry analysis confirmed that CDS 0330 was expressed on the cell surface of S. suis, and ELISA revealed the recombinant CDS 0330 protein could bind laminin in vitro. Finally, vaccinating mice with recombinant CDS 0330 protein significantly prolonged survival after S. suis infection. Together, these data reveal that CDS 0330 is a laminin binding protein of S. suis 2, and open new avenues for preventing S. suis 2 infection.

Rapid visual detection of highly pathogenic Streptococcus suis serotype 2 isolates by use of loop-mediated isothermal amplification.

Streptococcus suis serotype 2 (S. suis 2) is an important zoonotic pathogen that causes considerable economic losses to the pig industry and significantly threatens public health worldwide. The highly pathogenic S. suis 2, which contains the 89K pathogenicity island (PAI), has caused large-scale outbreaks of infections in humans, resulting in high mortality rates. In this study, we established two loop-mediated isothermal amplification (LAMP)-based assays that can rapidly detect S. suis 2 and the 89K PAI and can be performed simultaneously under the same conditions. Further, based on the findings of these two LAMP assays and using the same set of serially diluted DNA samples, we compared the sensitivities of different LAMP product detection methods, including SYBR green detection, gel electrophoresis, turbidimetry, calcein assays, and hydroxynaphthol blue detection. The results suggest that target genes can be amplified and detected within 48 min under 63°C isothermal conditions. The sensitivity of tests for S. suis 2 detection varies between detection methods and reaction systems, indicating that for each LAMP reaction system, multiple detection methods should be performed to select the optimal one. The sensitivities of the optimized methods (7.16 copies/reaction) in the present study were identical to those of the real-time PCR assay, and the test results for reference strains and clinical samples showed that these LAMP systems have high specificities. Thus, since the LAMP systems established in this study are simple, fast, and sensitive, they may have good clinical potential for detecting the highly pathogenic S. suis 2.

Genetic diversity and evolutionary characterization of Chinese porcine reproductive and respiratory syndrome viruses based on NSP2 and ORF5.

To more fully understand the extent of genetic diversity of PRRSV in China, we analyzed the Nsp2 and ORF5 gene sequences of 35 representative PRRSV isolates from 2008 to 2012. Sequence analysis revealed that the Nsp2 and ORF5 genes have undergone genetic variation. Furthermore, the isolate FJLYDX04 contains five insertions at positions 599 to 603 and is the first isolate from China reported to have an insertion in Nsp2. Our results suggest that the highly pathogenic PRRSV has become the dominant strain in China and that Chinese PRRSV has undergone rapid evolution and can circumvent immune responses induced by currently used vaccines.

Insight into the evolution of the histidine triad protein (HTP) family in Streptococcus.

The Histidine Triad Proteins (HTPs), also known as Pht proteins in Streptococcus pneumoniae, constitute a family of surface-exposed proteins that exist in many pathogenic streptococcal species. Although many studies have revealed the importance of HTPs in streptococcal physiology and pathogenicity, little is known about their origin and evolution. In this study, after identifying all htp homologs from 105 streptococcal genomes representing 38 different species/subspecies, we analyzed their domain structures, positions in genome, and most importantly, their evolutionary histories. By further projecting this information onto the streptococcal phylogeny, we made several major findings. First, htp genes originated earlier than the Streptococcus genus and gene-loss events have occurred among three streptococcal groups, resulting in the absence of the htp gene in the Bovis, Mutans and Salivarius groups. Second, the copy number of htp genes in other groups of Streptococcus is variable, ranging from one to four functional copies. Third, both phylogenetic evidence and domain structure analyses support the division of two htp subfamilies, designated as htp I and htp II. Although present mainly in the pyogenic group and in Streptococcus suis, htp II members are distinct from htp I due to the presence of an additional leucine-rich-repeat domain at the C-terminus. Finally, htp genes exhibit a faster nucleotide substitution rate than do housekeeping genes. Specifically, the regions outside the HTP domains are under strong positive selection. This distinct evolutionary pattern likely helped Streptococcus to easily escape from recognition by host immunity.

Attenuation of Streptococcus suis virulence by the alteration of bacterial surface architecture.

NeuB, a sialic acid synthase catalyzes the last committed step of the de novo biosynthetic pathway of sialic acid, a major element of bacterial surface structure. Here we report a functional NeuB homologue of Streptococcus suis, a zoonotic agent, and systematically address its molecular and immunological role in bacterial virulence. Disruption of neuB led to thinner capsules and more susceptibility to pH, and cps2B inactivation resulted in complete absence of capsular polysaccharides. These two mutants both exhibited increased adhesion and invasion to Hep-2 cells and improved sensibility to phagocytosis. Not only do they retain the capability of inducing the release of host pro-inflammatory cytokines, but also result in the faster secretion of IL-8. Easier cleaning up of the mutant strains in whole blood is consistent with virulence attenuation seen with experimental infections of both mice and SPF-piglets. Therefore we concluded that altered architecture of S. suis surface attenuates its virulence.

[Capsular saliva acid of Streptococcus suis 2 influences virulence and host inflammatory responses].

OBJECTIVE: We clarified the pathogenic influence of the absence of Streptococcus suis type 2 capsular saliva acid on BLAB/c mice. METHODS: The virulence of the experimental strains were compared; the distribution of strains in vivo was determined by quantitative plating. Histopathological analysis was used to qualitatively compare the different pathogenicity of wild strain and knockout strains. ELISA was used to test the levels of cytokine in whole blood cells for the stimulation of strains. RESULTS: The virulence of mutant strains was significantly reduced, and when the genes were restored, toxicity levels were recovered to that of the wild type strain. The distribution in blood and in the brain between wild strain and knock out strains has significant difference, and Streptococcus suis type 2 strains can cause different degrees of brain damage. During the in vitro test, the mutant strains can stimulate the whole blood cells to secrete higher levels of MCP-1 and IL-6. CONCLUSION: Capsular saliva acid affects bacterial virulence and host cell inflammation response. As an important virulence factor of Streptococcus suis type 2, it can damage the blood brain barrier and cause meningitis.

Functional definition of LuxS, an autoinducer-2 (AI-2) synthase and its role in full virulence of Streptococcus suis serotype 2.

Quorum sensing is a widespread chemical communication in response to fluctuation of bacterial population density, and has been implicated into bacterial biofilm formation and regulation of expression of virulence factors. The luxS gene product, S-ribosylhomocysteinase, catalizes the last committed step in biosynthetic pathway of autoinducer 2 (AI-2), a signaling molecule for inter-species quorum sensing. We found a luxS homologue in 05ZYH33, an epidemic strain of Streptococcus suis serotype 2 (SS2) in China. A luxS null mutant (ΔluxS) of 05ZYH33 strain was obtained using an approach of homologous recombination. LuxS was determined to be required for AI-2 production in 05ZYH33 strain of S. suis 2. Inactivation of luxS gene led to a wide range of phenotypic changes including thinner capsular walls, increased tolerance to H(2)O(2), reduced adherence capacity to epithelial cells, etc. In particular, loss of LuxS impaired dramatically its full virulence of SS2 in experimental model of piglets, and functional complementation restored it nearly to the level of parent strain. Genome-wide transcriptome analyses suggested that some known virulence factors such as CPS are down-regulated in the ΔluxS mutant, which might in part explain virulence attenuation by luxS deletion. Similarly, 29 of 71 genes with different expression level were proposed to be targets candidate regulated by LuxS/AI-2-dependent quorum sensing.

[Construction and in vitro assay of the sortase BCD geneknock-out mutant of Streptococcus suis 2].

OBJECTIVE: Streptococcus suis 2 is an emerging zoonotic pathogen responsible for a wide range of life-threatening diseases in pigs and humans. In this study, we investigated the functionality of one of Streptococcus suis 2 sortases, known as the srtBCD. METHODS: To obtain the isogenic mutant srtBCD, the competent cells of 05ZYH33 were subjected to electrotrans formation with recombinant plasmid based on the principle of homologous recombination. The resulting mutant strains was further confirmed by a series of PCR and reverse transcription PCR. To better assess the role of srtBCD gene in the virulence of 05ZYH33, cell adherence assays and experimental infection of mice was adopted. RESULTS: A SrtBCD defective mutant of 05ZYH33 was found to be associated with growth curve upon cultivation in standard laboratory used in our in vitro assays. Furthermore, abolishment of the expression of srtBCD result in impaired interactions of S. suis with human laryngeal epithelial cell line. However, there is no differences when infection mice by the WT and mutant strain. CONCLUSION: These results suggest that srtBCD are critical for the pathogen-host interaction of S. suis 2, but abolishment of srtBCD does not impair the full virulence of 05ZYH33. It is to expect that future study carried out with S. suis 2 to verification the conclusions.