<i>Staphylococcus aureus</i>
            triggers a shift from influenza virus–induced apoptosis to necrotic cell death

Krüchten, Andre van; Wilden, Janine J.; Niemann, Silke; Peters, Georg; Löffler, Bettina; Ludwig, Stephan; Ehrhardt, Christina

doi:10.1096/fj.201701006r

Cited by 11 publications

(9 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In another study, the filtered supernatant from S. aureus failed to induce apoptosis when applied to endothelial cell monolayers, thereby excluding any effect from the preformed α-toxin or other soluble bacterial factors [ 51 ]. Also, van Kruchten, Wilden [ 52 ] showed that human alveolar basal epithelial cell line (A549), bronchial epithelial cell line (Calu-3), primary human umbilical vein endothelial cells (HUVECs) and human bronchial epithelial cells (HBEpCs) infected with S. aureus alone displayed no apoptosis. Heat treating of S. haemolyticus markedly interfered with the bacterial cytotoxic potential on the PHSF cells.…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of Staphylococcus haemolyticus on primary human skin fibroblast cells

et al. 2020

View full text Add to dashboard Cite

Staphylococcus haemolyticus ( S. haemolyticus ) is one of the Coagulase-negative staphylococci (CoNS) that inhabits the skin as a commensal. It is increasingly implicated in opportunistic infections, including diabetic foot ulcer (DFU) infections. In contrast to the abundance of information available for S. aureus and S. epidermidis , little is known about the pathogenicity of S. haemolyticus , despite the increased prevalence of this pathogen in hospitalized patients. We described, for the first time, the pathogenesis of different clinical isolates of S. haemolyticus isolated from DFU on primary human skin fibroblast (PHSF) cells. Virulence-related genes were investigated, adhesion and invasion assays were carried out using Giemsa stain, transmission electron microscopy (TEM), MTT and flowcytometry assays. Our results showed that most S. haemolyticus carried different sets of virulence-related genes. S. haemolyticus adhered to the PHSF cells to variable degrees. TEM showed that the bacteria were engulfed in a zipper-like mechanism into a vacuole inside the cell. Bacterial internalization was confirmed using flowcytometry and achieved high intracellular levels. PHSF cells infected with S.haemolyticus suffered from amarked decrease in viability and increased apoptosis when treated with whole bacterial suspensions or cell-free supernatants but not with heat-treated cells. After co-culture with PBMCs, S. haemolyticus induced high levels of pro-inflammatory cytokines. This study highlights the significant development of S. haemolyticus , which was previously considered a contaminant when detected in cultures of clinical samples. Their high ability to adhere, invade and kill the PHSF cells illustrate the severe damage associated with DFU infections. Abbreviations CoNS, coagulase-negative staphylococci; DFU, diabetic foot ulcer; DM, diabetes mellitus; DMEM, Dulbecco’s Modified Eagle Medium; MTT, 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide; PBMCs,peripheral blood mononuclear cells; PHSF, primary human skin fibroblast; CFU, colony-forming unit.

show abstract

Section: Discussionmentioning

confidence: 99%

Pathogenesis of Staphylococcus haemolyticus on primary human skin fibroblast cells

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Intrinsic BAX/BAK-dependent apoptosis or caspase-9 cleavage has been reported following H5N1 and seasonal H1N1 infection of human primary type I-like alveolar epithelial cells [74], as well as PR8 infection of A549 cells [75,76], primary murine tracheal cells [77] and H7N9-infection of human blood-derived monocytes [83] (Table 2). Mechanistically, the 2009 pandemic H1N1 infection of A549 cells has been shown to promote apoptosis by downregulation of pro-survival BCL-XL [117].…”

Section: Intrinsic "Mitochondrial-dependent" Apoptosis In Iav Infectionmentioning

confidence: 99%

Die Another Way: Interplay between Influenza A Virus, Inflammation and Cell Death

Laghlali

Lawlor

Tate

2020

Viruses

View full text Add to dashboard Cite

Influenza A virus (IAV) is a major concern to human health due to the ongoing global threat of a pandemic. Inflammatory and cell death signalling pathways play important roles in host defence against IAV infection. However, severe IAV infections in humans are characterised by excessive inflammation and tissue damage, often leading to fatal disease. While the molecular mechanisms involved in the induction of inflammation during IAV infection have been well studied, the pathways involved in IAV-induced cell death and their impact on immunopathology have not been fully elucidated. There is increasing evidence of significant crosstalk between cell death and inflammatory pathways and a greater understanding of their role in host defence and disease may facilitate the design of new treatments for IAV infection.

show abstract

“…21 Research focused on the pathogenesis of S. aureus infection secondary to IAV has accumulated for these years. 9,14,18,[22][23][24][25][26][27][28][29] However, there is much less information available on MRSA pneumonia secondary to IAV infection. 30 Blyth et al 10 concluded that coinfection of IAV and bacteria synergistically aggravated inflammatory injury to the host.…”

Section: Introductionmentioning

confidence: 99%

Aggravated MRSA pneumonia secondary to influenza A virus infection is derived from decreased expression of IL‐1β

Shi

Liang

et al. 2020

Journal of Medical Virology

View full text Add to dashboard Cite

Secondary methicillin‐resistant Staphylococcus aureus (MRSA) infection is a cause of severe pneumonia with high mortality during influenza A virus (IAV) pandemics. Alveolar macrophages (AMs) mount cellular defenses against IAV and MRSA infection, which occurs via the nucleotide‐binding domain‐like receptor protein 3 (NLRP3) inflammasome. However, the activity and function of the NLRP3 inflammasome in MRSA pneumonia secondary to IAV infection remain unclear. To clarify this, we studied MRSA infection secondary to IAV both in vitro and in mouse model. The expression of the NLRP3 inflammasome was evaluated by quantitative reverse transcription polymerase chain reaction, immunofluorescence, Western blot, and enzyme‐linked immunosorbent assay. The lung pathology and the rate of weight change were observed. We found that IAV infection for 1 week activated NLRP3 inflammasome. The enhanced expression of NLRP3, caspase‐1, and cleaved caspase‐1 was associated with MRSA infection secondary to IAV, but the expression of interleukin (IL)‐1β decreased in superinfection with MRSA both in vitro and in vivo. The aggravated inflammatory pathology in MRSA pneumonia secondary to IAV infection was associated with decreased expression of IL‐1β. And increased weight loss in MRSA pneumonia secondary to IAV infection was related to decreased concentration of IL‐1β in serum. It infers that superinfection with MRSA reduces expression of IL‐1β someway, and decreased expression of IL‐1β impairs the host immunity and leads to aggravated pneumonia. These results contributed to our understanding of the detailed activity of the NLRP3 inflammasome, IL‐1β, and their relationship with aggravation of MRSA pneumonia secondary to IAV infection. Immunotherapy targeting the IL‐1β signaling pathway could be possible therapeutic strategy for secondary MRSA pneumonia.

show abstract

Staphylococcus aureus triggers a shift from influenza virus–induced apoptosis to necrotic cell death

Cited by 11 publications

References 67 publications

Pathogenesis of Staphylococcus haemolyticus on primary human skin fibroblast cells

Pathogenesis of Staphylococcus haemolyticus on primary human skin fibroblast cells

Die Another Way: Interplay between Influenza A Virus, Inflammation and Cell Death

Aggravated MRSA pneumonia secondary to influenza A virus infection is derived from decreased expression of IL‐1β

Contact Info

Product

Resources

About