Salmonella-induced cell death: apoptosis, necrosis or programmed cell death?

Boise, Lawrence H.; Collins, Carleen

doi:10.1016/s0966-842x(00)01937-5

Cited by 142 publications

(105 citation statements)

References 26 publications

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“…A similar situation has also been noted in Salmonella-induced macrophage cell death (21,22), and the morphological features of infected macrophages have been shown to be both necrotic and apoptotic; cell death occurred in Salmonella infection (21,23,24). Salmonella infection of macrophages mediated by Salmonella pathogenicity island 1 (SPI-1) TTSS is capable of inducing both caspase-1-dependent and -independent cell death (25,26), whereas the cell death mediated by SPI-2 TTSS is partly dependent on caspase-1 (27).…”

supporting

confidence: 78%

A Novel Caspase-1/Toll-like Receptor 4-independent Pathway of Cell Death Induced by Cytosolic Shigella in Infected Macrophages

Suzuki

Nakanishi

Tsutsui

et al. 2005

Journal of Biological Chemistry

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Shigella-induced macrophage cell death is an important step in the induction of acute inflammatory responses that ultimately lead to bacillary dysentery. Cell death was previously reported to be dependent upon the activation of caspase-1 via interaction with IpaB secreted by intracellular Shigella, but in this study, we show that Shigella infection of macrophages can also induce cell death independent of caspase-1 or IpaB activity. Time-lapse imaging and electron microscopic analyses indicated that caspase-1-dependent and -independent cell death is morphologically indistinguishable and that both resemble necrosis. Analyses of Shigella mutants or Escherichia coli using co-infection with Listeria suggested that a component common to Gram-negative bacteria is involved in inducing caspase-1-independent cell death. Further studies revealed that translocation of bacterial lipid A into the cytosol of macrophages potentially mediates cell death. Notably, cell death induced by cytosolic bacteria was TLR4-independent. These results identify a novel cell death pathway induced by intracellular Gram-negative bacteria that may play a role in microbial-host interactions and inflammatory responses.

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supporting

confidence: 78%

A Novel Caspase-1/Toll-like Receptor 4-independent Pathway of Cell Death Induced by Cytosolic Shigella in Infected Macrophages

Suzuki

Nakanishi

Tsutsui

et al. 2005

Journal of Biological Chemistry

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“…A variety of bacterial pathogens induce cell death in macrophages (16), but the mechanisms by which cell death is induced seem to be manifold and there exists considerable controversy; i.e., combinations of different types of macrophage cells and bacteria have been reported to induce different modes of cell death in bacterial-infected macrophages, with some exhibiting apoptotic or autophagic cell death and others exhibiting necrosis or oncosis (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26). The mode of cell death in LM-infected J774 cells has been shown to be nonapoptotic (Ref.…”

Section: Discussionmentioning

confidence: 99%

“…Intracellular bacterial pathogens evade the macrophage killing mechanisms that eliminate intracellular pathogens, and thus they can survive and replicate inside macrophages (12)(13)(14)(15). In addition, a variety of bacterial pathogens are known to induce cell death in macrophages (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26). However, the biological significance of the pathogen-induced cell death in macrophages is not fully defined with respect to the host-parasite relationship and it may differ with individual pathogens; viz, the macrophage cell death may be one evasion mechanisms of bacteria from killing by macrophages, or it may constitute a host defense response to the incoming pathogen to halt its survival within macrophages and/or to present Ags to the adaptive immune system through bystander dendritic cells (27,28), or it may be the result of a bacterial strategy to promote disease through activation of caspase-1 which can cleave the proforms of the inflammatory cytokines IL-1␤ and IL-18 (18 -20).…”

mentioning

confidence: 99%

A Novel Functional T Cell Hybridoma Recognizes Macrophage Cell Death Induced by Bacteria: A Possible Role for Innate Lymphocytes in Bacterial Infection

Kubota

2006

The Journal of Immunology

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We have established a novel TCRαβ (TCRVβ6)+CD4−CD8− T cell hybridoma designated B6HO3. When the B6HO3 cells were cocultured with bacterial-infected J774 macrophage-like cells, IFN-γ production by B6HO3 cells was triggered through direct cell-cell contact with dying J774 cells infected with Listeria monocytogenes (LM), Shigella flexneri, or Salmonella typhimurium that expressed the type III secretion system, but not with intact J774 cells infected with heat-killed LM, nonhemolytic lysteriolysin O-deficient (Hly−) LM, plasmid-cured Shigella, or stationary-phase Salmonella. However, the triggering of B6HO3 cells for IFN-γ production involved neither dying hepatoma cells infected with LM nor dying J774 cells caused by gliotoxin treatment or freeze thawing. Cycloheximide and Abs to H-2Kd, H-2Dd, Iad, CD1d, TCRVβ6, and IL-12 did not inhibit the contact-dependent IFN-γ response, indicating that this IFN-γ response did not require de novo protein synthesis in bacterial-infected J774 cells and was TCR and IL-12 independent. Thus, in an as yet undefined way, B6HO3 hybridoma recognizes a specialized form of macrophage cell death resulting from bacterial infection and consequently produces IFN-γ. Moreover, contact-dependent interaction of minor subsets of splenic αβ T cells, including NKT cells with dying LM-infected J774 and bone marrow-derived macrophage (BMM) cells, proved to provide an IFN-γ-productive stimulus for these minor T cell populations, to which the parental T cell of the B6HO3 hybridoma appeared to belong. Unexpectedly, subsets of γδ T and NK cells similarly responded to dying LM-infected macrophage cells. These results propose that innate lymphocytes may possess a recognition system sensing macrophage cell “danger” resulting from bacterial infection.

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“…Up-regulation of cas-1 expression by Shigella and Salmonella sp. is known to induce macrophage apoptosis (46). Similar activation of apoptosis by cas-1-inducing doses of LPS or IL-18 may allow bacteria to multiply unchecked.…”

Section: Discussionmentioning

confidence: 99%

IL-18 Levels and the Outcome of Innate Immune Response to Lipopolysaccharide: Importance of a Positive Feedback Loop with Caspase-1 in IL-18 Expression

Joshi

Kalvakolanu

Hasday

et al. 2002

The Journal of Immunology

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LPS enhanced antibacterial host defenses (ABHD) when given at low (75 μg) doses (16 of 19 mice survived 3× LD50 Escherichia coli vs 3 of 19 LPS-naive mice; p = 0.0001), but induced lethal inflammation at high (500 μg) doses (5 of 5 died). Differences in the cytokine profiles induced by these LPS doses may provide insight into the mechanism(s) of transition from beneficial to lethal LPS responses. The 75 μg LPS induced 5.9 ± 0.9 ng/ml serum IL-18 at 8 h, which decreased to 2.3 ± 0.4 ng/ml by 24 h, whereas 500 μg LPS induced 11.1 ± 1.6 ng/ml serum IL-18 levels at 8 h, which increased until death. Compared with 75 μg, higher but sublethal (150 μg) doses of LPS induced greater serum IL-18 levels and less effectively induced ABHD (3 of 8 survived). Reduction of serum IL-18 with neutralizing Ab improved the ABHD induced by 150 μg, but reduced that produced by 75 μg LPS, suggesting an optimal range of serum IL-18 level was essential for efficient ABHD. Increased expression of caspase-1 mRNA in response to the higher IL-18 levels induced at the 150 and 500 μg, but not at the 75 μg doses of LPS may represent a positive feedback regulatory loop leading to sustained serum IL-18 levels. We conclude that the regulation of serum IL-18 expression is critical to the outcome of innate immune responses to LPS.

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Salmonella-induced cell death: apoptosis, necrosis or programmed cell death?

Cited by 142 publications

References 26 publications

A Novel Caspase-1/Toll-like Receptor 4-independent Pathway of Cell Death Induced by Cytosolic Shigella in Infected Macrophages

A Novel Caspase-1/Toll-like Receptor 4-independent Pathway of Cell Death Induced by Cytosolic Shigella in Infected Macrophages

A Novel Functional T Cell Hybridoma Recognizes Macrophage Cell Death Induced by Bacteria: A Possible Role for Innate Lymphocytes in Bacterial Infection

IL-18 Levels and the Outcome of Innate Immune Response to Lipopolysaccharide: Importance of a Positive Feedback Loop with Caspase-1 in IL-18 Expression

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