Staphylococcus aureus host cell invasion and post-invasion events

Sinha, Bhanu; Fraunholz, Martin

doi:10.1016/j.ijmm.2009.08.019

Cited by 128 publications

(108 citation statements)

References 56 publications

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“…Also S. aureus is able to survive the autophagic pathway, but details in terms of S. aureus and autophagy are controversial in literature. 5,6,20 Here we show the intracellular fate of S. aureus from evasion of the autophagic machinery to intracellular replication in nonprofessional phagocytes, namely murine fibroblasts and human keratinocytes, in detail. We further show the enclosure process of intracellular S. aureus by the phagophore membrane in real time.…”

Section: Discussionmentioning

confidence: 91%

“…However, the intracellular fate of S. aureus is an ongoing controversial discussion. 5,6 A fundamental process in eukaryotic cells is macroautophagy (hereafter referred to as autophagy), a catabolic pathway, that degrades damaged or unnecessary cytosolic components to supply metabolic pathways with nutrients and to maintain ATP production and macromolecular synthesis. 7 Autophagy is evolutionarily conserved in all eukaryotic cells and controlled by essential key regulators, known as autophagy-related (ATG) proteins.…”

Section: Introductionmentioning

confidence: 99%

“…[16][17][18][19] Nevertheless, mechanisms of autophagic escape are still relatively unknown. 6,8 S. aureus has been connected to autophagy before, but the molecular mechanisms for autophagosome formation, autophagosomal escape and intracellular survival of S. aureus are controversial. For instance Schnaith et al report that S. aureus use autophagosomes as a replicative niche, whereas Mestre et al observe replication of S. aureus in the cytosol.…”

Section: Introductionmentioning

confidence: 99%

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Intracellular Staphylococcus aureus eludes selective autophagy by activating a host cell kinase

et al. 2016

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Autophagy, a catabolic pathway of lysosomal degradation, acts not only as an efficient recycle and survival mechanism during cellular stress, but also as an anti-infective machinery. The human pathogen Staphylococcus aureus (S. aureus) was originally considered solely as an extracellular bacterium, but is now recognized additionally to invade host cells, which might be crucial for persistence. However, the intracellular fate of S. aureus is incompletely understood. Here, we show for the first time induction of selective autophagy by S. aureus infection, its escape from autophagosomes and proliferation in the cytoplasm using live cell imaging. After invasion, S. aureus becomes ubiquitinated and recognized by receptor proteins such as SQSTM1/p62 leading to phagophore recruitment. Yet, S. aureus evades phagophores and prevents further degradation by a MAPK14/p38a MAP kinase-mediated blockade of autophagy. Our study demonstrates a novel bacterial strategy to block autophagy and secure survival inside the host cell.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Intracellular Staphylococcus aureus eludes selective autophagy by activating a host cell kinase

et al. 2016

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“…Furthermore, S. aureus co-infections are a major complication contributing to high morbidity and mortality during both pandemic and seasonal influenza virus pneumonia (2). S. aureus deploys a combination of virulence factors, including adhesins, toxins, and immunomodulatory molecules, that facilitate infection of different host tissues (3,4).…”

mentioning

confidence: 99%

“…Surfactant protein A (SP-A) 3 is a crucial component of the pulmonary innate immune system in the alveolar spaces (5,6). SP-A is the major protein constituent of pulmonary surfactant; it is involved in organization of large aggregate surfactant phospholipids lining the alveolar surface and acts as an opsonin for pathogens (7).…”

mentioning

confidence: 99%

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

Sever-Chroneos

Krupa

Davis

et al. 2011

Journal of Biological Chemistry

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There is limited knowledge about host factors that facilitate eradication of Staphylococcus aureus infection in the lung. Methicillin-resistant S. aureus has remained a major cause of hospital-and health care-associated pneumonia since its appearance over 40 years ago and has recently become a more prominent etiology in community acquired pneumonia. Colonization of nasal epithelium with S. aureus, a normal occurrence in over 20% of the population, increases the risk for the development of staphylococcal pneumonia (1). Furthermore, S. aureus co-infections are a major complication contributing to high morbidity and mortality during both pandemic and seasonal influenza virus pneumonia (2). S. aureus deploys a combination of virulence factors, including adhesins, toxins, and immunomodulatory molecules, that facilitate infection of different host tissues (3, 4).Surfactant protein A (SP-A) 3 is a crucial component of the pulmonary innate immune system in the alveolar spaces (5, 6). SP-A is the major protein constituent of pulmonary surfactant; it is involved in organization of large aggregate surfactant phospholipids lining the alveolar surface and acts as an opsonin for pathogens (7). SP-A is incorporated in the tubular myelin fraction of pulmonary surfactant that covers the alveolar lining fluid of the distal airway epithelium. The presence of pathogen-derived molecules may trigger reorganization of surfactant lipids (8 -11) and exposure of SP-A to bind pathogens at points of entry on the surfactant interface. Alveolar macrophages in the aqueous hypophase may then patrol areas of disturbance on the surfactant layer binding SP-A-opsonized bacteria. SP-A binds pathogens via a carboxyl-terminal carbohydrate recognition domain in a calcium-dependent manner. Amino-terminal collagen-like and coiled-coil do-

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Detection of methicillin‐resistant Staphylococcus aureus persistence in osteoblasts using imaging flow cytometry

et al. 2020

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Methicillin‐resistant S. aureus has been reported as the main pathogen involved in chronic infections, osteomyelitis, and prosthetic joint infections. The host/pathogen interaction is dynamic and requires several changes to promote bacterial survival. Here, we focused on the internalization and persistence behavior of well‐characterized Staphylococcus aureus invasive strains belonging to the main ST‐MRSA‐SCCmec clones. To overcome the limitations of the cell culture method, we comparatively analyzed the ability of internalization within human MG‐63 osteoblasts with imaging flow cytometry (IFC). After evaluation by cell culture assay, the MRSA clones in the study were all able to readily internalize at 3h postinfection, the persistence of intracellular bacteria was evaluated at 24h both by routine cell culture and IFC assay, after vancomycin‐BODIPY staining. A statistical difference of persistence was found in ST5‐SCCmecII (26.59%), ST228‐SCCmecI (20.25%), ST8‐SCCmecIV (19.52%), ST239‐SCCmecIII (47.82%), and ST22‐SCCmecIVh (50.55%) showing the same ability to internalize as ATCC12598 (51%), the invasive isolate used as control strain for invasion and persistence assays. We demonstrated that the intracellular persistence process depends on the total number of infected cells. Comparing our data obtained by IFC with those of the cell culture assay, we obtained greater reproducibility rates and a number of intracellular bacteria, with the advantage of analyzing live host cells. Moreover, with some limitations related to the lack of whole‐genome sequencing analysis, we validated the different proclivities to persist in the main Italian HA‐MRSA invasive isolates and our results highlighted the heterogeneity of the different clones to persist during cell infection.

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Staphylococcus aureus host cell invasion and post-invasion events

Cited by 128 publications

References 56 publications

Intracellular Staphylococcus aureus eludes selective autophagy by activating a host cell kinase

Intracellular Staphylococcus aureus eludes selective autophagy by activating a host cell kinase

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

Detection of methicillin‐resistant Staphylococcus aureus persistence in osteoblasts using imaging flow cytometry

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