Apoptotic Effect of Outer-Membrane Proteins from Campylobacter jejuni on Chicken Lymphocytes

Zhu, Jianbo; Meinersmann, Richard J.; Hiett, Kelli L.; Evans, Donald L.

doi:10.1007/pl00006795

Cited by 17 publications

(16 citation statements)

References 34 publications

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“…The enteric bacteria cause more than 50% of cell death within a few hours. In contrast, H. pylori induced only up to 25% of host cell death in 24 h. In Pseudomonas aeruginosa (12) and Campylobacter jejuni (77), apoptotic activities of the outer membrane porins have been identified. Incubation of the porins purified from these organisms with the host cell causes a rather small degree of apoptosis (12,77), which is comparable to that of H. pylori.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, H. pylori induced only up to 25% of host cell death in 24 h. In Pseudomonas aeruginosa (12) and Campylobacter jejuni (77), apoptotic activities of the outer membrane porins have been identified. Incubation of the porins purified from these organisms with the host cell causes a rather small degree of apoptosis (12,77), which is comparable to that of H. pylori. In this mechanism, by interacting with the plasma membranes of the host cells, porins become embedded as hydrophilic pores in the phospholipid bilayer, damaging the structure and function of this part of the host cell architecture and leading to the activation of apoptotic signaling pathways (12).…”

Section: Discussionmentioning

confidence: 99%

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Apoptotic Signaling Pathway Activated by Helicobacter pylori Infection and Increase of Apoptosis-Inducing Activity under Serum-Starved Conditions

et al. 2001

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The enhanced gastric epithelial cell apoptosis observed during infection with Helicobacter pylori has been suggested to be of significance in the etiology of gastritis, peptic ulcers, and neoplasia. To investigate the cell death signaling induced by H. pylori infection, human gastric epithelial cells were incubated with H. pylori for up to 72 h. H. pylori infection induced the activation of caspase -8, -9, and -3 and the expression of the proapoptotic Bcl-2 family proteins Bad and Bid. The peak of the activity of the caspases occurred at 24 h. At this time, the inhibition of caspase-8 or -9 almost completely suppressed H. pylori-induced apoptosis. Inhibition of caspase-8 suppressed the expression of Bad and Bid and the subsequent activation of caspase-9 and -3. These observations indicate that H. pylori induces apoptosis through a pathway involving the sequential induction of apical caspase-8 activity, the proapoptotic proteins Bad and Bid, caspase-9 activity, and effector caspase-3 activity. Activation of the pathway was independent of CagA or vacuolating toxin. A membrane fraction of H. pylori was sufficient to activate this pathway, and treatment with proteinase K eliminated the activity. Apoptotic activity of the membrane fraction was significantly increased by incubating the bacteria under serum-starved conditions for 24 h. These observations suggest that environmental conditions in the human stomach could induce H. pylori-mediated pathogenesis, leading to a variety of clinical outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Apoptotic Signaling Pathway Activated by Helicobacter pylori Infection and Increase of Apoptosis-Inducing Activity under Serum-Starved Conditions

et al. 2001

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“…Both previous reports of induction of apoptosis by C. jejuni in either chicken lymphocytes (24) or human monocytes (20) indicated that PCD was independent of CjCDT, although limited data were presented. Siegesmund et al (20) reported that apoptosis of THP-1 monocytes required, instead, secretion of the Cia (campylobacter invasion antigen) proteins that are secreted through the flagellar secretion apparatus (10,11,18).…”

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confidence: 93%

“…CDTs from other bacteria are also known to target immune cells and ultimately induce apoptosis (3,19,21). There have been two reports of apoptotic responses to C. jejuni (20,24), and both suggested that mechanisms independent of CDT were responsible. Here, we confirm earlier observations of long-term campylobacter survival and replication within monocytes and the induction of apoptosis.…”

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confidence: 99%

Intracellular Survival of Campylobacter jejuni in Human Monocytic Cells and Induction of Apoptotic Death by Cytholethal Distending Toxin

2005

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Campylobacter jejuni 81-176 is capable of extensive replication within human monocytic cell vacuoles and induces apoptotic death via cytolethal distending toxin.Our understanding of the interaction of Campylobacter jejuni with immune effector cells is limited. C. jejuni can survive phagocytosis by human mononuclear cells and remain viable for extended periods (9), induce secretion of chemokines (8), and mediate apoptosis (20). C. jejuni elaborates a well-characterized toxin, cytolethal distending toxin (CjCDT), that induces cell cycle arrest and interleukin 8 (IL-8) secretion from intestinal epithelial cells in culture (2,7,13,22). CDTs from other bacteria are also known to target immune cells and ultimately induce apoptosis (3,19,21). There have been two reports of apoptotic responses to C. jejuni (20,24), and both suggested that mechanisms independent of CDT were responsible. Here, we confirm earlier observations of long-term campylobacter survival and replication within monocytes and the induction of apoptosis. Since CDTs of other pathogens induce apoptosis of lymphocytes (1,3,17,19,21), we reexamined the effect of CjCDT on human monocytes in culture.Growth of C. jejuni in human 28SC monocyte cultures. The human monocyte line 28SC was infected with 81-176 at a multiplicity of infection (MOI) of 100:1 for 2 h. Extracellular bacteria were killed with 100 g/ml gentamicin for an additional 2-h incubation. The cells were washed and reincubated, and bacterial counts were enumerated at various times. Peak levels of 81-176 were recovered from 48-hour cultures (Fig. 1), representing an approximate 3-log-unit increase in bacterial counts (from approximately 10 4 CFU/ml following gentamicin treatment to 10 7 CFU/ml after 48 h). Viable campylobacters were recovered up to day 7, consistent with the results of Kiehlbauch et al. (9). In contrast, in the absence of monocytes, 81-176 viability dropped rapidly, and no bacteria could be cultured after 72 h. Thus, replication of C. jejuni within monocytes was more extensive than the limited replication following internalization into epithelial cells (12).Green fluorescent protein (GFP)-tagged 81-176 was imaged within 28SC cells using fluorescence microscopy. Generalized fluorescence (Fig. 2B) could be seen intracellularly within enlarged and irregularly shaped areas of cells ( Fig. 2A). Using live/dead staining, the C. jejuni organisms appeared to be localized within vacuoles, either as single or multiple bacteria (Fig. 2C and D). The bacteria appeared motile within the vacuoles, consistent with expression of GFP under the control of the 28 promoter of the major flagellin (5). Induction of chemokines from 28SC cells is independent of CDT. Viable campylobacters mediated chemokine responses from 28SC cells in 24-h cultures (Fig. 3A). 81-176 induced 1,689 Ϯ 848 pg/ml IL-6 and 1,231 Ϯ 479 pg/ml IL-8 in nine independent experiments. Since CDT is localized to bacterial membranes and is known to induce IL-8 secretion from intestinal epithelial cells (7), we compared the abilities of pu...

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“…A cytotoxicnecrotizing-factor-producing strain of E. coli also with CDT activity, BM2-1, induces apoptotic cell death (De Rycke et al, 1996). It is also noteworthy that C. jejuni outer-membrane proteins cause apoptosis of chicken lymphocytes (Zhu et al, 1999). Furthermore, H. ducreyi CDT is responsible for apoptosis in Jurkat cells (Gelfanova et al, 1999), and A. actinomycetemcomitans causes murine macrophage apoptosis (Kato et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Campylobacter upsaliensis exerts a cytolethal distending toxin effect on HeLa cells and T lymphocytes

et al. 2001

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Campylobacter upsaliensis is an emerging human enteropathogen. However, little is known about the pathogenesis of C. upsaliensis infection. In this study the authors demonstrate that C. upsaliensis whole-cell preparations and extracts produce a cytolethal distending toxin (CDT)-like effect on HeLa cells characterized by progressive distension and nuclear fragmentation culminating in cell death over 5 d. To further delineate the nature of this toxic effect in relation to CDT from other pathogens, the effect of C. upsaliensis on cellular events in epithelial cells and immunocytes was investigated. C. upsaliensis lysate-treated HeLa cells subjected to FACScan analysis using carboxyfluorescein diacetete succinimidyl ester (CFDA-SE) as a cell tracer demonstrated cell division arrest. Propidium iodide (PI) staining of HeLa cells revealed that cell cycle arrest occurred in G 2 /M. Human T lymphocytes exposed to C. upsaliensis lysates also showed cell cycle arrest in G 2 /M. Using a combination of Annexin V/PI staining and TUNEL assay, cytodistended HeLa cells were shown to undergo apoptotic cell death. These data provide the first insights into the virulence mechanisms of this novel enteropathogen.

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Apoptotic Effect of Outer-Membrane Proteins from Campylobacter jejuni on Chicken Lymphocytes

Cited by 17 publications

References 34 publications

Apoptotic Signaling Pathway Activated by Helicobacter pylori Infection and Increase of Apoptosis-Inducing Activity under Serum-Starved Conditions

Apoptotic Signaling Pathway Activated by Helicobacter pylori Infection and Increase of Apoptosis-Inducing Activity under Serum-Starved Conditions

Intracellular Survival of Campylobacter jejuni in Human Monocytic Cells and Induction of Apoptotic Death by Cytholethal Distending Toxin

Campylobacter upsaliensis exerts a cytolethal distending toxin effect on HeLa cells and T lymphocytes

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