The rise and rise of<i>Staphylococcus aureus</i>: laughing in the face of granulocytes

Anwar, Sadia; Prince, Lynne R.; Foster, Simon J.; Whyte, Moira K. B.; Sabroe, Ian

doi:10.1111/j.1365-2249.2009.03950.x

Cited by 61 publications

(52 citation statements)

References 112 publications

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“…This was unexpected, since we predicted that neutrophil challenge would enhance bacterial virulence factor expression to interfere with recognition/killing mechanisms. While recent studies have demonstrated the ability of S. aureus to survive intracellularly within neutrophils and, to a lesser extent, macrophages, one would expect this adaptation to necessitate large-scale transcriptional changes (39). One possibility to explain the discrepancy between macrophages and neutrophils in regulating biofilm transcriptional responses is that neutrophils were added to biofilms at a 10-fold-lower density than macrophages.…”

Section: Discussionmentioning

confidence: 99%

Global Transcriptome Analysis of Staphylococcus aureus Biofilms in Response to Innate Immune Cells

et al. 2013

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bThe potent phagocytic and microbicidal activities of neutrophils and macrophages are among the first lines of defense against bacterial infections. Yet Staphylococcus aureus is often resistant to innate immune defense mechanisms, especially when organized as a biofilm. To investigate how S. aureus biofilms respond to macrophages and neutrophils, gene expression patterns were profiled using Affymetrix microarrays. The addition of macrophages to S. aureus static biofilms led to a global suppression of the biofilm transcriptome with a wide variety of genes downregulated. Notably, genes involved in metabolism, cell wall synthesis/structure, and transcription/translation/replication were among the most highly downregulated, which was most dramatic at 1 h compared to 24 h following macrophage addition to biofilms. Unexpectedly, few genes were enhanced in biofilms after macrophage challenge. Unlike coculture with macrophages, coculture of S. aureus static biofilms with neutrophils did not greatly influence the biofilm transcriptome. Collectively, these experiments demonstrate that S. aureus biofilms differentially modify their gene expression patterns depending on the leukocyte subset encountered.

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Section: Discussionmentioning

confidence: 99%

Global Transcriptome Analysis of Staphylococcus aureus Biofilms in Response to Innate Immune Cells

et al. 2013

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“…S taphylococcus aureus can act as a peaceful colonizer of the skin and the nostrils or as an aggressive pathogen causing invasive diseases and sepsis. Intracellular survival of S. aureus, abscess formation, as well as the emergence of methicillin-resistant strains complicate the treatment of serious infections (1). S. aureus also produces virulence factors such as hemolytic and leucolytic toxins and C-targeting factors that contribute to immune evasion (2).…”

mentioning

confidence: 99%

TLR8 Senses Staphylococcus aureus RNA in Human Primary Monocytes and Macrophages and Induces IFN-β Production via a TAK1–IKKβ–IRF5 Signaling Pathway

Bergstrøm

Aune

Awuh

et al. 2015

The Journal of Immunology

124

162

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Staphylococcus aureus may cause serious infections and is one of the most lethal and common causes of sepsis. TLR2 has been described as the main pattern recognition receptor that senses S. aureus and elicits production of proinflammatory cytokines via MyD88–NF-κB signaling. S. aureus can also induce the production of IFN-β, a cytokine that requires IFN regulatory factors (IRFs) for its transcription, but the signaling mechanism for IFN-β induction by S. aureus are unclear. Surprisingly, we demonstrate that activation of TLR2 by lipoproteins does not contribute to IFN-β production but instead can suppress the induction of IFN-β in human primary monocytes and monocyte-derived macrophages. The production of IFN-β was induced by TLR8-mediated sensing of S. aureus RNA, which triggered IRF5 nuclear accumulation, and this could be antagonized by concomitant TLR2 signaling. The TLR8-mediated activation of IRF5 was dependent on TAK1 and IκB kinase (IKK)β, which thus reveals a physiological role of the recently described IRF5-activating function of IKKβ. TLR8–IRF5 signaling was necessary for induction of IFN-β and IL-12 by S. aureus, and it also contributed to the induction of TNF. In conclusion, our study demonstrates a physiological role of TLR8 in the sensing of entire S. aureus in human primary phagocytes, including the induction of IFN-β and IL-12 production via a TAK1–IKKβ–IRF5 pathway that can be inhibited by TLR2 signaling.

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“…Additionally, quorum sensing molecules control neutrophil ROS response and penetration into P. aeruginosa bioilms [60]. Similarly, Aggregatibacter actinomycetemcomitans and S. aureus produce bacterial toxins that induce neutrophils lysis and degranulation [61][62][63]. In addition to directly atacking neutrophils, dysbiotic microbiota in bioilms can render themselves resistant to neutrophil-mediated killing by disguising their immunogenicity.…”

Section: Dysbiotic Bacteriamentioning

confidence: 99%

“…For example, P. aeruginosa bioilms produce bacterial surfactants that induce rapid neutrophil death [59], and Aggregatibacter actinomycetemcomitans and S. aureus produce bacterial toxins that induce neutrophil lysis and degranulation [61][62][63]. These bacterial products could be neutralized with antibodies or novel pharmaceutical drugs to prevent their negative efects on neutrophils.…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Neutrophil Role in Periodontal Disease

Rosales¹,

Uribe‐Querol²

2017

Role of Neutrophils in Disease Pathogenesis

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Oral tissues are constantly exposed to damage from the mechanical efort of eating and from the invasion of foreign microorganisms such as bacteria, fungi, and virus. In healthy oral tissues, there is a balance between symbiotic bacteria and cells from the innate immune system, mainly neutrophils. When this balance is broken, inlammation appears and more immune cells are recruited to the gingiva. Neutrophils form a barrier against dysbiotic bacteria. However, when neutrophils are insuicient, bacteria thrive causing periodontitis, a chronic inlammatory disease that destroys the tooth-supporting tissues or periodontium. Damage of periodontal tissues leads to tooth loss, and in severe cases, it can also afect systemic health by increasing a person's risk for atherosclerosis, rheumatoid arthritis, diabetes, and even cancer. The mechanisms neutrophil employ to keep a balance with bacteria in order to maintain healthy oral tissues is the focus of this chapter. We discuss how neutrophil antimicrobial functions keep bacteria at check and how some dysbiotic bacteria block neutrophils to promote an inlammatory state. Also, novel therapeutic approaches for periodontitis are discussed.

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The rise and rise ofStaphylococcus aureus: laughing in the face of granulocytes

Cited by 61 publications

References 112 publications

Global Transcriptome Analysis of Staphylococcus aureus Biofilms in Response to Innate Immune Cells

Global Transcriptome Analysis of Staphylococcus aureus Biofilms in Response to Innate Immune Cells

TLR8 Senses Staphylococcus aureus RNA in Human Primary Monocytes and Macrophages and Induces IFN-β Production via a TAK1–IKKβ–IRF5 Signaling Pathway

Neutrophil Role in Periodontal Disease

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