Apoptosis and in vivo distribution and clearance of eosinophils in normal and <i>Trichinella spiralis</i>-infected rats

Gon, Songi; Saito, Susumu; Takeda, Yuji; Miyata, Hiroaki; Takatsu, Kiyoshi; Sendo, Fujiro

doi:10.1002/jlb.62.3.309

Cited by 15 publications

(10 citation statements)

References 14 publications

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“…Gon et al [36] demonstrated that a considerable percentage of eosinophils in non-infected rats undergo apoptosis within a few hours, whereas the apoptosis rate of eosinophils from Trichinella-infected rats is notably lower. The inhibition of eosinophil apoptosis during the later stages of a Trichinella infection is related to the presence of IL-5.…”

Section: Apoptosis Of Eosinophilsmentioning

confidence: 99%

Eosinophils and Trichinella infection: toxic for the parasite and the host?

Bruschi

Korenaga

Watanabe

2008

Trends in Parasitology

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Section: Apoptosis Of Eosinophilsmentioning

confidence: 99%

Eosinophils and Trichinella infection: toxic for the parasite and the host?

Bruschi

Korenaga

Watanabe

2008

Trends in Parasitology

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“…In certain situations, anti-apoptotic members of the Bcl-2 family such as inhibitor of apoptosis protein (IAP) may be involved in delaying apoptosis [16]. Although normal eosinophils are sensitive to apoptosis, Trichinella spiralis-infected eosinophils show resistance to apoptotic cell death [17]. Therefore, apoptosis may regulate pathogenesis of several infectious diseases [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

Kim

Lee

et al. 2010

Eur J Immunol

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Although Helicobacter pylori infections of the gastric mucosa are characterized by the infiltration of inflammatory cells such as eosinophils, the responses of eosinophils to H. pylori vacuolating cytotoxin (VacA) have not been fully elucidated. This study investigates the role of VacA in the apoptosis of human eosinophils. We treated human eosinophils with purified H. pylori VacA and observed that induction of apoptosis is a relatively late event. Expression of cellular inhibitor of apoptosis protein (c-IAP)-2 was upregulated during the early period of VacA stimulation, and transfection with c-IAP2 siRNA augmented apoptotic cell death. VacA caused the translocation of cytoplasmic Bax to the mitochondria and increased cytochrome c release from mitochondria in eosinophils. Transfection of an EoL-1 eosinophil cell line with Bax siRNA decreased the release of cytochrome c and DNA fragmentation. Furthermore, apoptosis facilitated by Bax and cytochrome c was primarily regulated by p38 MAPK in VacA-treated eosinophils. These results suggest that the exposure of human eosinophils to H. pylori VacA induces the early upregulation of c-IAP2 and a relatively late apoptotic response, with the apoptosis progressing through a sequential pathway that includes p38 MAPK activation, Bax translocation, and cytochrome c release.

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“…During the late phase of infection, in the presence of an anti-IL-5 antibody, this inhibitory effect on apoptosis was lost. This suggests an involvement of this cytokine which, however, is not involved in the induction of eosinophilia observed in the early infection period [60]. In consideration of these results, it has been hypothesized that eosinophilia could be due to a reduced eosinophil apoptosis, favoured by increased levels of IL-5 and other protective cytokines such as granulocyte-macrophage colonystimulating factor (GM-CSF) or IL-3, which would determine an accumulation of these cells in the blood and tissues [61].…”

Section: The Role Of Eosinophilsmentioning

confidence: 67%

The Immune Response to the Parasitic Nematode Trichinella and the Ways to Escape it. From Experimental Studies to Implications for Human Infection

Bruschi

2002

curr drug targets immune endocr metabol disord

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The review describes different aspects of the host immune response to Trichinella, not only at the intestinal level on which most of the studies have focused until now, but also in the muscles which represent the final target of host invasion. The role of antibodies, T cells, mast cells, eosinophils and neutrophils, respectively, in immune reaction to this nematode is considered, in the light of the recent data derived from experimental models, both "in vivo" and more recently "in vitro" and when available, from clinical observations. A section is also devoted to the principal escape mechanisms from host immune responses, described in Trichinella, which are in part common to other parasites, in part peculiar. Two groups of mechanisms are described: antigen-dependent, such as anatomic seclusion, antigen stage-specificity, shedding and renewal and molecular mimicry, and those directly affecting the host immune response. Of the latter, some act at central level like immune suppression, polyclonal activation and eosinophilia induction, others interfere with effector functions as in the case of host leukocyte modification, immune complex accumulation, blocking antibody production or complement assembly blocking. The antigenic composition of the different stages is the subject of another section which has the aim to give an overview of the principal antigens described up to now, without giving too many biochemical details, but just illustrating the candidates for possible vaccines. Finally, the perspectives for vaccination are described. Most of the results described are derived from the experimental studies, but their implications in human infection are relevant.

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Apoptosis and in vivo distribution and clearance of eosinophils in normal and Trichinella spiralis-infected rats

Cited by 15 publications

References 14 publications

Eosinophils and Trichinella infection: toxic for the parasite and the host?

Eosinophils and Trichinella infection: toxic for the parasite and the host?

Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

The Immune Response to the Parasitic Nematode Trichinella and the Ways to Escape it. From Experimental Studies to Implications for Human Infection

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