Stress-triggered signaling affecting survival or suicide of Streptococcus pneumoniae

Cortes, Paulo R.; Piñas, Germán E.; Cian, Melina B.; Yandar, Nubia; Echenique, José

doi:10.1016/j.ijmm.2014.12.002

Cited by 26 publications

(50 citation statements)

References 63 publications

(87 reference statements)

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“…We hypothesized that pneumococcal two-component systems (TCSs) sense physiological changes induced by IAV-infection of pneumocytes and mediate adaptative responses that lead to increased intracellular bacterial survival. Next, we considered that the intracellular changes induced by IAV-infection generate stress conditions sensed by S. pneumoniae via TCSs other than ComE and CiaR [15, 16]. From a previous systematic screening of insertion-duplication histidine kinase ( hk ) mutants of S. pneumoniae [15] (Table S1), we focused the search on hk mutations that were null for pneumococcal intracellular survival in the absence of IAV infection.…”

Section: Resultsmentioning

confidence: 99%

“…Next, we considered that the intracellular changes induced by IAV-infection generate stress conditions sensed by S. pneumoniae via TCSs other than ComE and CiaR [15, 16]. From a previous systematic screening of insertion-duplication histidine kinase ( hk ) mutants of S. pneumoniae [15] (Table S1), we focused the search on hk mutations that were null for pneumococcal intracellular survival in the absence of IAV infection. When non-IAV infected A549 pneumocytes were inoculated with the S. pneumoniae hk mutants, most of them showed no changes in intracellular survival compared to the wt strain, including the hk01::ery mutant (Fig S2).…”

Section: Resultsmentioning

confidence: 99%

“…S. pneumoniae needs an acidic stress response for intracellular survival in pneumocytes [15, 16] and survives in acidic autophagic vesicles of Detroit 562 human nasopharyngeal epithelial cells and in mouse embryonic fibroblasts (MEFs) [14]. In IAV-infected cells, S. pneumoniae is likely to survive in acidic autophagic vesicles, which implies exposure to the acidic environment and increased ROS production induced by IAV [14].…”

Section: Resultsmentioning

confidence: 99%

“…The same work also showed that the bacterial protein Ply, a cholesterol-binding, thiol-activated cytolysin, provides advantages for the bacteria to escape from endosomal elimination at early stages of infection. We previously reported that the two-component systems (TCSs) ComDE and CiaRH are involved in the pneumococcal stress response to acidic conditions and in the intracellular survival of S. pneumoniae in pneumocytes [15]. In addition, we recently reported that the crosstalk signaling between the serine/threonine kinase StkP and ComE controls H 2 O 2 production in S. pneumoniae modulating its intracellular survival in pneumocytes [16].…”

Section: Introductionmentioning

confidence: 99%

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The pneumococcal two-component system VisRH is linked to enhanced intracellular survival ofStreptococcus pneumoniaein influenza-infected pneumocytes

Reinoso-Vizcaíno

Cian

Cortes

et al. 2019

Preprint

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The virus-bacterial synergism implicated in secondary bacterial infections caused by Streptococcus pneumoniae following infection with epidemic or pandemic influenza A virus (IAV) is well documented. However, the molecular mechanisms behind such synergism remain largely ill-defined. In pneumocytes infected with influenza A virus, subsequent infection with S. pneumoniae leads to enhanced pneumococcal intracellular survival. The pneumococcal two-component system VisRH appears essential for such enhanced survival. Through comparative transcriptomic analysis between the ΔvisR and wt strains, a list of 179 differentially expressed genes was defined. Among those, the clpL protein chaperone gene and the psaB Mn+2 transporter gene, which are involved in the stress response, are important in enhancing S. pneumoniae survival in influenza-infected cells. The ΔvisR, ΔclpL and ΔpsaB deletion mutants display increased susceptibility to acidic and oxidative stress and no enhancement of intracellular survival in IAV-infected pneumocyte cells. These results suggest that the VisRH two-component system senses IAV-induced stress conditions and controls adaptive responses that allow survival of S. pneumoniae in IAV-infected pneumocytes.Author summaryS. pneumoniae is an inhabitant of the human nasopharynx that is capable of causing a variety of infections contributing to an estimated 1.6 million deaths each year. Many of these deaths occur as result of secondary S. pneumoniae infections following seasonal or pandemic influenza. Although S. pneumoniae is considered a typical extracellular pathogen, an intracellular survival mechanism has been more recently recognized as significant in bacterial pathogenesis. The synergistic effects between influenza A and S. pneumoniae in secondary bacterial infection are well documented; however, the effects of influenza infections on intracellular survival of S. pneumoniae are ill-defined. Here, we provide evidence that influenza infection increases S. pneumoniae intracellular survival in pneumocytes. We demonstrate that the poorly understood VisRH signal transduction system in pneumococcus controls the expression of genes involved in the stress response that S. pneumoniae needs to increase intracellular survival in influenza A-infected pneumocytes. These findings have important implications for understanding secondary bacterial pathogenesis following influenza and for the treatment of such infections in influenza-stricken patients.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The pneumococcal two-component system VisRH is linked to enhanced intracellular survival ofStreptococcus pneumoniaein influenza-infected pneumocytes

Reinoso-Vizcaíno

Cian

Cortes

et al. 2019

Preprint

Self Cite

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“…The transition from asymptomatic carriage to a pathogenic phenotype is dependent on a complex array of biochemical environmental cues that can influence the growth characteristics of S. pneumoniae (Cortes et al, 2015). Previous studies have demonstrated that changes in environments can modulate numerous proteins and carbohydrates that modify cell attachment, colonization and invasion that dictate biofilm formation and persistence in host (Allegrucci et al, 2006; Sanchez et al, 2011; Allan et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro

Ndjom

Kantor

Jones

2017

Front. Cell. Infect. Microbiol.

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Sepsis is a life-threatening health condition caused by infectious pathogens of the respiratory tract, and accounts for 28–50% of annual deaths in the US alone. Current treatment regimen advocates the use of corticosteroids as adjunct treatment with antibiotics, for their broad inhibitory effect on the activity and production of pro-inflammatory mediators. However, despite their use, corticosteroids have not proven to be able to reverse the death incidence among septic patients. We have previously demonstrated the potential for neuroendocrine factors to directly influence Streptococcus pneumoniae virulence, which may in turn mediate disease outcome leading to sepsis and septic shock. The current study investigated the role of Corticotropin-releasing hormone (CRH) in mediating key markers of pneumococcal virulence as important phenotypic determinants of sepsis and septic shock risks. In vitro cultures of serotype 1 pneumococcal strain with CRH promoted growth rate, increased capsule thickness and penicillin resistance, as well as induced pneumolysin gene expression. These results thus provide significant insights of CRH–pathogen interactions useful in understanding the underlying mechanisms of neuroendocrine factor's role in the onset of community acquired pneumonias (CAP), sepsis and septic shock.

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Importance of protein Ser/Thr/Tyr phosphorylation for bacterial pathogenesis

et al. 2020

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Protein phosphorylation regulates a large variety of biological processes in all living cells. In pathogenic bacteria, the study of serine, threonine, and tyrosine (Ser/Thr/Tyr) phosphorylation has shed light on the course of infectious diseases, from adherence to host cells to pathogen virulence, replication, and persistence. Mass spectrometry (MS)-based phosphoproteomics has provided global maps of Ser/Thr/Tyr phosphosites in bacterial pathogens. Despite recent developments, a quantitative and dynamic view of phosphorylation events that occur during bacterial pathogenesis is currently lacking. Temporal, spatial, and subpopulation resolution of phosphorylation data is required to identify key regulatory nodes underlying bacterial pathogenesis. Herein, we discuss how technological improvements in sample handling, MS instrumentation, data processing, and machine learning should improve bacterial phosphoproteomic datasets and the information extracted from them. Such information is expected to significantly extend the current knowledge of Ser/ Thr/Tyr phosphorylation in pathogenic bacteria and should ultimately contribute to the design of novel strategies to combat bacterial infections.

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Stress-triggered signaling affecting survival or suicide of Streptococcus pneumoniae

Cited by 26 publications

References 63 publications

The pneumococcal two-component system VisRH is linked to enhanced intracellular survival ofStreptococcus pneumoniaein influenza-infected pneumocytes

The pneumococcal two-component system VisRH is linked to enhanced intracellular survival ofStreptococcus pneumoniaein influenza-infected pneumocytes

CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro

Importance of protein Ser/Thr/Tyr phosphorylation for bacterial pathogenesis

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