Apoptosis of human keratinocytes after bacterial invasion

Nuzzo, I.; Sanges, M.R; Folgore, A; Carratelli, Caterina Romano

doi:10.1111/j.1574-695x.2000.tb01435.x

Cited by 61 publications

(40 citation statements)

References 32 publications

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“…While S. aureus is not generally considered an intracellular pathogen, many host cells, including corneal epithelial cells, internalize S. aureus (19). Furthermore, internalization of S. aureus can induce apoptosis in many cell types, including epithelial cells, endothelial cells, and keratinoyctes (3,20,29,35). If retinal cells internalize S. aureus, bacterial toxins and the proteases could be released through pores in a phagocytic vacuole, potentially making the cell more vulnerable to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis

et al. 2008

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Bacterial infections of the eye highlight a dilemma that is central to all immune-privileged sites. On the one hand, immune privilege limits inflammation to prevent bystander destruction of normal tissue and loss of vision. On the other hand, bacterial infections require a robust inflammatory response for rapid clearance of the pathogen. We demonstrate that the retina handles this dilemma, in part, by activation of a protective heat shock protein. During Staphylococcus aureus-induced endophthalmitis, the small heat shock protein ␣B-crystallin is upregulated in the retina and prevents apoptosis during immune clearance of the bacteria. In the absence of ␣B-crystallin, mice display increased retinal apoptosis and retinal damage. We found that S. aureus produces a protease capable of cleaving ␣B-crystallin to a form that coincides with increased retinal apoptosis and tissue destruction. We conclude that ␣B-crystallin is important in protecting sensitive retinal tissue during destructive inflammation that occurs during bacterial endophthalmitis.

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Section: Discussionmentioning

confidence: 99%

αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis

et al. 2008

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“…In epithelial cells, keratinocytes, or osteoblasts, S. aureus-induced apoptosis may require internalization of the bacteria (26,27,30,32,33). Conversely, Bantel et al (16) showed that S. aureus α-toxin does not require bacterial internalization to induce apoptosis.…”

Section: Figurementioning

confidence: 99%

Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils

Genestier

Michallet²,

Prévost³

et al. 2005

J. Clin. Invest.

349

274

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Panton-Valentine leukocidin (PVL) is a pore-forming toxin secreted by Staphylococcus aureus that has recently been associated with necrotizing pneumonia. In the present study, we report that in vitro, PVL induces polymorphonuclear cell death by necrosis or by apoptosis, depending on the PVL concentration. PVL-induced apoptosis was associated with a rapid disruption of mitochondrial homeostasis and activation of caspase-9 and caspase-3, suggesting that PVL-induced apoptosis is preferentially mediated by the mitochondrial pathway. Polymorphonuclear cell exposure to PVL leads to mitochondrial localization of the toxin, whereas Bax, 1 of the 2 essential proapoptotic members of the Bcl-2 family, was still localized in the cytosol. Addition of PVL to isolated mitochondria induced the release of the apoptogenic proteins cytochrome c and Smac/ DIABLO. Therefore, we suggest that PVL, which belongs to the pore-forming toxin family, could act at the mitochondrion level by creating pores in the mitochondrial outer membrane. Furthermore, LukS-PV, 1 of the 2 components of PVL, was detected in lung sections of patients with necrotizing pneumonia together with DNA fragmentation, suggesting that PVL induces apoptosis in vivo and thereby is directly involved in the pathophysiology of necrotizing pneumonia.

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“…Similarly, internalization has been reported to be a prerequisite for inducing apoptosis in cells infected with Staphylococcus aureus (Nuzzo et al, 2000;Kahl et al, 2000;Menzies & Kourteva, 1998;Bayles et al, 1998), suggesting that the induction of programmed cell death by facultative intracellular bacteria is a common occurrence in host cellbacterium interactions. Tsai et al (1999) reported that 11-13 % of HEp-2 cells showed indications of apoptosis at 20 h following GAS infection, and that about 40 % of the cells exhibited membrane injury.…”

Section: Hep-2 Cell Damage Is Caused By Programmed Cell Deathmentioning

confidence: 99%

Fate of Streptococcus pyogenes and epithelial cells following internalization

Marouni

Sela

2004

Journal of Medical Microbiology

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The fate of GAS and epithelial cells following internalization was determined in this study. HEp-2 cells harbouring intracellular bacteria were treated with antibiotics to kill extracellular adherent bacteria, washed, and the fate of bacteria and epithelial cells was assessed up to 24 h post-infection. In the absence of antibiotics, massive bacterial growth was apparent in the cell medium, accompanied by extensive cell death, suggesting that intracellular bacteria had multiplied and damaged the monolayer. Addition of the internalization inhibitor, cytochalasin D, either pre-or post-internalization prevented bacterial growth and cell injury; post-internalization treatment with chloramphenicol had the same effect. Analysis of three apoptotic markers in HEp-2 cells -chromatin condensation, DNA laddering and translocation of phosphatidylserine onto the cell-surface membrane -indicated that HEp-2 cells underwent apoptosis. Taken together, the data presented here support a model in which intenalized bacteria can induce their own externalization into the medium by a process that requires both an intact host-cell cytoskeleton and de novo synthesis of bacterial proteins. Concomitantly, intracellular and, apparently, extracellular free bacteria induce apoptosis through their cytotoxic activity, and release essential nutrients required for their growth.

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Apoptosis of human keratinocytes after bacterial invasion

Cited by 61 publications

References 32 publications

αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis

αB-Crystallin Protects Retinal Tissue during Staphylococcus aureus - Induced Endophthalmitis

Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils

Fate of Streptococcus pyogenes and epithelial cells following internalization

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