Induction of Apoptotic Cell Death in Peripheral Blood Mononuclear and Polymorphonuclear Cells by an Oral Bacterium,<i>Fusobacterium nucleatum</i>

Jewett, Anahid; Hume, W.R.; Le, Ho; Huynh, Tri N.; Han, Yiping W.; Cheng, Genhong; Shi, Wenyuan

doi:10.1128/iai.68.4.1893-1898.2000

Cited by 94 publications

(76 citation statements)

References 35 publications

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“…Indeed, IL-2-treated NK cells have decreased amounts of InB in their cell lysates (22). Moreover, we have shown previously that expression of superrepressor of InB, which inhibits nuclear factor-nB in NK cells, increases cell death of NK and T cells (22,31).…”

Section: Discussionmentioning

confidence: 99%

Coengagement of CD16 and CD94 Receptors Mediates Secretion of Chemokines and Induces Apoptotic Death of Naive Natural Killer Cells

Jewett

Cacalano

Head

et al. 2006

Clinical Cancer Research

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Down-modulation of CD16 (FcgRIII) receptors and loss of natural killer (NK) cell function have been observed in oral cancer patients. However, neither the mechanisms nor the significance of the decrease in CD16 receptors have been fully understood. The cytotoxic activity and survival of NK cells are negatively regulated by antibodies directed against CD16 surface receptor. The addition of anti-CD94 antibody in combination with either F(abV ) 2 fragment or intact anti-CD16 antibody to NK cells resulted in significant inhibition of NK cell cytotoxic function and induction of apoptosis in resting human peripheral blood NK cells. Addition of interleukin-2 to anti-CD16 and/or anti-CD94 antibody-treated NK cells significantly inhibited apoptosis and increased the function of NK cells. There was a significant increase in tumor necrosis factor-a (TNF-a) but not IFN-g secretion in NK cells treated either with anti-CD16 antibody alone or in combination with anti-CD94 antibodies. Consequently, the addition of anti-TNF-a antibody partially inhibited apoptosis of NK cells mediated by the combination of anti-CD94 and anti-CD16 antibodies. Increase in apoptotic death of NK cells also correlated with an increase in type 2 inflammatory cytokines and in the induction of chemokines. Thus, we conclude that binding of antibodies to CD16 and CD94 NK cell receptors induces death of the NK cells and signals for the release of chemokines.

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Section: Discussionmentioning

confidence: 99%

Coengagement of CD16 and CD94 Receptors Mediates Secretion of Chemokines and Induces Apoptotic Death of Naive Natural Killer Cells

Jewett

Cacalano

Head

et al. 2006

Clinical Cancer Research

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“…However, the Fas/Fas-L pathway is primarily used to regulate lymphocyte activation (Shresta et al, 1998) and granulocyte reactivity (Jewett et al, 2000;Gamonal et al, 2001) and to prevent over-reactivity in both cell types. This process, although not presently wellunderstood, may be a potentially important step in the protection of periodontal tissues from damage due to microbial infection and associated inflammation (Gamonal et al, 2001).…”

Section: (4):237-252 (2003)mentioning

confidence: 99%

The Role of Acquired Immunity and Periodontal Disease Progression

Teng

2003

Critical Reviews in Oral Biology & Medicine

142

128

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Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response-in particular, CD4 + T-cells-plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction. In particular, studies of the pathogen-specific CD4 + T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) microorganism-triggered periodontal CD4 + T-cell-mediated osteoclastogenic factor, 'RANK-L', which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8 + T-cells, and CD4 + T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications.Abbreviations used in the paper are as follows:

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“…Microbial pathogens such as Escherichia coli (20) and Candida albicans (21) were found to induce apoptosis of PMN. Induction of apoptotic death of both mononuclear and polymorphonuclear leukocytes by Fusobacterium nucleatum was suggested to mediate immunosuppression in periodontal disease (22). In contrast, inhibition of apoptosis of host cells by intracellular pathogens such as Theileria (23), Toxoplasma (24), or the agents of human granulocytic ehrlichiosis (HGE) (25) can provide an intracellular niche for the pathogens by extending the life span of the host cells.…”

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Inhibition of the Spontaneous Apoptosis of Neutrophil Granulocytes by the Intracellular Parasite Leishmania major

Aga

Katschinski

Zandbergen

et al. 2002

The Journal of Immunology

250

240

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Macrophages are the major target cell population of the obligate intracellular parasites Leishmania. Although polymorphonuclear neutrophil granulocytes (PMN) are able to internalize Leishmania promastigotes, these cells have not been considered to date as host cells for the parasites, primarily due to their short life span. In vitro coincubation experiments were conducted to investigate whether Leishmania can modify the spontaneous apoptosis of human PMN. Coincubation of PMN with Leishmania major promastigotes resulted in a significant decrease in the ratio of apoptotic neutrophils as detected by morphological analysis of cell nuclei, TUNEL assay, gel electrophoresis of low m.w. DNA fragments, and annexin V staining. The observed antiapoptotic effect was found to be associated with a significant reduction of caspase-3 activity in PMN. The inhibition of PMN apoptosis depended on viable parasites because killed Leishmania or a lysate of the parasites did not have antiapoptotic effect. L. major did not block, but rather delayed the programmed cell death of neutrophils by ∼24 h. The antiapoptotic effect of the parasites could not be transferred by the supernatants, despite secretion of IL-8 by PMN upon coculture with L. major. In vivo, intact parasites were found intracellularly in PMN collected from the skin of mice 3 days after s.c. infection. This finding strongly suggests that infection with Leishmania prolongs the survival time of neutrophils also in vivo. These data indicate that Leishmania induce an increased survival of neutrophil granulocytes both in vitro and in vivo.

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Induction of Apoptotic Cell Death in Peripheral Blood Mononuclear and Polymorphonuclear Cells by an Oral Bacterium,Fusobacterium nucleatum

Cited by 94 publications

References 35 publications

Coengagement of CD16 and CD94 Receptors Mediates Secretion of Chemokines and Induces Apoptotic Death of Naive Natural Killer Cells

Coengagement of CD16 and CD94 Receptors Mediates Secretion of Chemokines and Induces Apoptotic Death of Naive Natural Killer Cells

The Role of Acquired Immunity and Periodontal Disease Progression

Inhibition of the Spontaneous Apoptosis of Neutrophil Granulocytes by the Intracellular Parasite Leishmania major

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