Trigger factor of Streptococcus suis is involved in stress tolerance and virulence

Wu, Tao; Zhao, Zhanqin; Wang, Qisheng; Ma, Hongwei; Lu, Ka; Ren, Wen; Liu, Zhengya; Chang, Haitao; Bei, Weicheng; Qiu, Yinsheng; Chen, Huanchun

doi:10.1016/j.micpath.2010.10.001

Cited by 31 publications

(20 citation statements)

References 41 publications

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“…The results demonstrated that the Δ stk mutants showed defects in their ability to grow at various stress conditions, such as high temperature, low pH, oxidative stress and high osmolarity, compared with the wild-type strain. Similar results have been reported for SS2 for trigger factor mutants [58].The significantly decreased stress tolerance pattern of Δ stk mutant strain may be due to the down-regulation of some stress response genes sodA, ad and oppuABC (decreased by 22%–43%)(Fig.10). It has been demonstrated that the SodA and AD were involved in oxidative stress and acidic pH stress in S. suis , respectively [50], [53].…”

Section: Discussionsupporting

confidence: 82%

Contribution of Eukaryotic-Type Serine/Threonine Kinase to Stress Response and Virulence of Streptococcus suis

Zhu

Zhou

et al. 2014

PLoS ONE

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Streptococcus suis serotype 2 (SS2) is an important swine and human pathogen responsible for septicemia and meningitis. The bacterial homologues of eukaryotic-type serine/threonine kinases (ESTKs) have been reported to play critical roles in various cellular processes. To investigate the role of STK in SS2, an isogenic stk mutant strain (Δstk) and a complemented strain (CΔstk) were constructed. The Δstk showed a significant decrease in adherence to HEp-2 cells, compared with the wild-type strain, and a reduced survival ratio in whole blood. In addition, the Δstk exhibited a notable reduced tolerance of environmental stresses including high temperature, acidic pH, oxidative stress, and high osmolarity. More importantly, the Δstk was attenuated in both the CD1 mouse and piglet models of infection. The results of quantitative reverse transcription-PCR (qRT-PCR) analysis indicated that the expressions of a few genes involving in adherence, stress response and virulence were clearly decreased in the Δstk mutant strain. Our data suggest that SsSTK is required for virulence and stress response in SS2.

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Section: Discussionsupporting

confidence: 82%

Contribution of Eukaryotic-Type Serine/Threonine Kinase to Stress Response and Virulence of Streptococcus suis

Zhu

Zhou

et al. 2014

PLoS ONE

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“…We used a well-established intraperitoneal mouse infection model (4,9,50) to assess virulence of the ⌬troA mutant. This demonstrated that TroA is required to cause systemic disease in mice.…”

Section: Discussionmentioning

confidence: 99%

“…To test the virulence of the ⌬troA mutant bacteria in systemic infection, we used a murine infection model broadly used to assess virulence of S. suis mutants (4,9,50). Ten CD1 mice were inoculated intraperitoneally with 10 9 CFU of wild-type or ⌬troA mutant bacteria.…”

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confidence: 99%

TroA of Streptococcus suis Is Required for Manganese Acquisition and Full Virulence

et al. 2011

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Streptococcus suis causes infections in pigs and occasionally in humans, resulting in manifestations as meningitis, sepsis, arthritis, and septic shock. For survival within the host, S. suis requires numerous nutrients including trace metals. Little is known about the specific proteins involved in metal scavenging in S. suis. In this study we evaluated the role of the putative high-affinity metal binding lipoprotein TroA in metal acquisition and virulence. A mutant strain deficient in the expression of TroA (⌬troA mutant) was constructed. Growth of the ⌬troA mutant in Todd-Hewitt broth was similar to wild-type growth; however, growth of the ⌬troA mutant in cation-deprived Todd-Hewitt broth and in porcine serum was strongly reduced compared to growth of wild-type bacteria. Supplementing the medium with extra manganese but not with magnesium, zinc, copper, nickel, or iron restored growth to wild-type levels, indicating that TroA is specifically required for growth in environments low in manganese. The ⌬troA mutant also showed increased susceptibility to H 2 O 2 , suggesting that TroA is involved in counteracting oxidative stress. Furthermore, the expression of the troA gene was subject to environmental regulation at the transcript level. In a murine S. suis infection model, the ⌬troA mutant displayed a nonvirulent phenotype. These data indicate that S. suis TroA is involved in manganese acquisition and is required for full virulence in mice.Streptococcus suis is an important pathogen of pigs and may cause meningitis, sepsis, arthritis, and septic shock. Occasionally, S. suis is able to infect humans. Infected humans may show symptoms similar to those in pigs (1,5,11,32). Although human infections are exceptional, a large outbreak in humans was reported in 2005 in China, with 215 cases and 39 deaths (52). Of the 33 known S. suis serotypes, serotype 2 is most frequently isolated from diseased pigs and humans. However, serotype 9 infections are emerging in pigs, especially in Europe (7,35,48). Current control measures are insufficient and mainly rely on antibiotic treatment and vaccination with homologous bacterins. Increased antibiotic resistance has been reported for S. suis (17, 49), and bacterin-based vaccines do not provide protection against multiple serotypes (6).For growth and function, bacteria have to acquire numerous nutrients from their surrounding environment. For pathogenic bacteria, an important group of essential nutrients are the trace metals. Metals such as iron, zinc, and manganese have been shown to be essential structural and catalytic cofactors for several bacterial proteins (2). However, the concentration of free available trace metals within an infected host is relatively low compared to the metal concentrations in medium usually applied for in vitro growth. Within the host, several trace metals are sequestered; for instance, iron binds to hemoglobin, and zinc and manganese bind to the S100 family of proteins produced by neutrophils (14,15). This recruitment of trace metals by host proteins ha...

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“…The trigger factor protein, a ribosome-associated molecular chaperone functioning in cooperation with the DnaK and GroEL chaperones, has been associated with stress tolerance in different streptococcal species (491)(492)(493). For the zoonotic pathogen S. suis, a trigger factor-deficient strain was attenuated in a mouse peritonitis model (493).…”

Section: General Stress Responses and Virulencementioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

540

404

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SUMMARYLactic acid bacteria (LAB) are important starter, commensal, or pathogenic microorganisms. The stress physiology of LAB has been studied in depth for over 2 decades, fueled mostly by the technological implications of LAB robustness in the food industry. Survival of probiotic LAB in the host and the potential relatedness of LAB virulence to their stress resilience have intensified interest in the field. Thus, a wealth of information concerning stress responses exists today for strains as diverse as starter (e.g.,Lactococcus lactis), probiotic (e.g., severalLactobacillusspp.), and pathogenic (e.g.,EnterococcusandStreptococcusspp.) LAB. Here we present the state of the art for LAB stress behavior. We describe the multitude of stresses that LAB are confronted with, and we present the experimental context used to study the stress responses of LAB, focusing on adaptation, habituation, and cross-protection as well as on self-induced multistress resistance in stationary phase, biofilms, and dormancy. We also consider stress responses at the population and single-cell levels. Subsequently, we concentrate on the stress defense mechanisms that have been reported to date, grouping them according to their direct participation in preserving cell energy, defending macromolecules, and protecting the cell envelope. Stress-induced responses of probiotic LAB and commensal/pathogenic LAB are highlighted separately due to the complexity of the peculiar multistress conditions to which these bacteria are subjected in their hosts. Induction of prophages under environmental stresses is then discussed. Finally, we present systems-based strategies to characterize the “stressome” of LAB and to engineer new food-related and probiotic LAB with improved stress tolerance.

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Trigger factor of Streptococcus suis is involved in stress tolerance and virulence

Cited by 31 publications

References 41 publications

Contribution of Eukaryotic-Type Serine/Threonine Kinase to Stress Response and Virulence of Streptococcus suis

Contribution of Eukaryotic-Type Serine/Threonine Kinase to Stress Response and Virulence of Streptococcus suis

TroA of Streptococcus suis Is Required for Manganese Acquisition and Full Virulence

Stress Physiology of Lactic Acid Bacteria

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