Characterization of a novel streptococcal heme-binding protein SntA and its interaction with host antioxidant protein AOP2

Wan, Yun; Zhang, Sihua; Li, Lü; Chen, Huanchun; Zhou, Rui

doi:10.1016/j.micpath.2017.08.018

Cited by 9 publications

(17 citation statements)

References 32 publications

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“…The sntA -deleted strain Δ sntA was constructed in our previous study ( 24 ). To construct sntA complementary strain, a DNA fragment containing the entire sntA coding sequence and its promoter and terminator was amplified by using primers CΔ sntA _F/CΔ sntA _R.…”

Section: Methodsmentioning

confidence: 99%

“…Proteins transferred onto PVDF membrane (Millipore, 0.45 µm). Mouse SntA polyclonal antibody ( 24 ) was used for SntA immunodetection, and chemiluminescence detection (Bio-Rad, USA) with HRP-conjugate goat anti-mouse IgG (Antgene, Wuhan, China) by MF-Chemi BIS 3.2 (DNR, Israel).…”

Section: Methodsmentioning

confidence: 99%

“…Recombinant SntA protein (Protein ID: WP_012027972.1) was expressed and purified as our previous report ( 24 ). To obtain the recombinant proteins of the complement C1q subunits, the cDNAs of C1qA, C1qB, and C1qC were amplified from the total cDNA of porcine lung tissue with primers C1qA_F/R, C1qB_F/R, C1qC_F/R, respectively (Table 1 ).…”

Section: Methodsmentioning

confidence: 99%

“…In our previous study, surface protein SntA of S. suis without any unknown function has been characterized to be a heme-binding protein which involved in the pathogenesis of S. suis in pigs. SntA can interact with the host antioxidant protein AOP2 and consequently inhibit its antioxidant activity ( 24 ). Complement C1q is identified as another interacting partner of SntA when we screen the SntA binding proteins in the host.…”

Section: Introductionmentioning

confidence: 99%

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The Surface-Exposed Protein SntA Contributes to Complement Evasion in Zoonotic Streptococcus suis

Deng

Fang

et al. 2018

Front. Immunol.

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Streptococcus suis is an emerging zoonotic pathogen causing streptococcal toxic shock like syndrome (STSLS), meningitis, septicemia, and even sudden death in human and pigs. Serious septicemia indicates this bacterium can evade the host complement surveillance. In our previous study, a functionally unknown protein SntA of S. suis has been identified as a heme-binding protein, and contributes to virulence in pigs. SntA can interact with the host antioxidant protein AOP2 and consequently inhibit its antioxidant activity. In the present study, SntA is identified as a cell wall anchored protein that functions as an important player in S. suis complement evasion. The C3 deposition and membrane attack complex (MAC) formation on the surface of sntA-deleted mutant strain ΔsntA are demonstrated to be significantly higher than the parental strain SC-19 and the complementary strain CΔsntA. The abilities of anti-phagocytosis, survival in blood, and in vivo colonization of ΔsntA are obviously reduced. SntA can interact with C1q and inhibit hemolytic activity via the classical pathway. Complement activation assays reveal that SntA can also directly activate classical and lectin pathways, resulting in complement consumption. These two complement evasion strategies may be crucial for the pathogenesis of this zoonotic pathogen. Concerning that SntA is a bifunctional 2′,3′-cyclic nucleotide 2′-phosphodiesterase/3′-nucleotidase in many species of Gram-positive bacteria, these complement evasion strategies may have common biological significance.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Surface-Exposed Protein SntA Contributes to Complement Evasion in Zoonotic Streptococcus suis

Deng

Fang

et al. 2018

Front. Immunol.

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“…[67] identified a novel SP1 protein which is secreted by S. suis type 2 and interacts with the host's peptidoglycan recognition protein (PGLYRP-1), inhibiting the PGLYRP-1-mediated bacteriostatic effect. Wan et al [68] described a novel SntA protein localized in the cell wall of S. suis type 2 that binds to heme, thus acquiring iron for the bacterium from the host's haemoglobin and other haemoproteins. Moreover, SntA protein can interact with the host antioxidant protein and inhibit its activity.…”

Section: Other Virulence Factorsmentioning

confidence: 99%

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part II – Pathogenesis

Dutkiewicz

Zając

Sroka

et al. 2018

Ann Agric Environ Med.

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Streptococcus suis is a re-emerging zoonotic pathogen that may cause severe disease, mostly meningitis, in pigs and in humans having occupational contact with pigs and pork, such as farmers, slaughterhose workers and butchers. The first stage of the pathogenic process, similar in pigs and humans, is adherence to and colonisation of mucosal and/or epithelial surface(s) of the host. The second stage is invasion into deeper tissue and extracellular translocation of bacterium in the bloodstream, either free in circulation or attached to the surface of monocytes. If S. suis present in blood fails to cause fatal septicaemia, it is able to progress into the third stage comprising penetration into host's organs, mostly by crossing the blood-brain barrier and/or blood-cerebrospinal fluid barrier to gain access to the central nervous system (CNS) and cause meningitis. The fourth stage is inflammation that plays a key role in the pathogen esis of both systemic and CNS infections caused by S. suis. The pathogen may induce the overproduction of pro-inflammatory cytokines that cause septic shock and/or the recruitment and activation of different leukocyte populations, causing acute inflammation of the CNS. Streptococcus suis can also evoke - through activation of microglial cells, astrocytes and possibly other cell types - a fulminant inflammatory reaction of the brain which leads to intracranial complications, including brain oedema, increased intracranial pressure, cerebrovascular insults, and deafness, as a result of cochlear sepsis. In all stages of the pathogenic process, S. suis interacts with many types of immunocompetent host's cells, such as polymorphonuclear leukocytes, mononuclear macrophages, lymphocytes, dendritic cells and microglia, using a range of versatile virulence factors for evasion of the innate and adaptive immune defence of the host, and for overcoming environmental stress. It is estimated that S. suis produces more than 100 different virulence factors that could be classified into 4 groups: surface components or secreted elements, enzymes, transcription factors or regulatory systems and transporter factors or secretion systems. A major virulence factor is capsular polysaccharide (CPS) that protects bacteria from phagocytosis. However, it hampers adhesion to and invasion of host's cells, release of inflammatory cytokines and formation of the resistant biofilm which, in many cases, is vital for the persistence of bacteria. It has been demonstrated that the arising by mutation unencapsulated S. suis clones, which are more successful in penetration to and propagation within the host's cells, may coexist in the organism of a single host together with those that are encapsulated. Both 'complementary' clones assist each other in the successful colonization of host's tissues and persistence therein. S. suis has an open pan-genome characterized by a frequent gene transfer and a large diversity. Of the genetic determinants of S. suis pathogenicity, t...

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Streptococcus suis pathogenesis—A diverse array of virulence factors for a zoonotic lifestyle

Tram

Jennings

Blackall

et al. 2021

Advances in Microbial Physiology

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Characterization of a novel streptococcal heme-binding protein SntA and its interaction with host antioxidant protein AOP2

Cited by 9 publications

References 32 publications

The Surface-Exposed Protein SntA Contributes to Complement Evasion in Zoonotic Streptococcus suis

The Surface-Exposed Protein SntA Contributes to Complement Evasion in Zoonotic Streptococcus suis

Streptococcus suis: a re-emerging pathogen associated with occupational exposure to pigs or pork products. Part II – Pathogenesis

Streptococcus suis pathogenesis—A diverse array of virulence factors for a zoonotic lifestyle

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