The nitric oxide donors, azide and hydroxylamine, inhibit the programmed cell death of cytokine‐deprived human eosinophils

Beauvais, Francis; Michel, Laurence; Dubertret, Louis

doi:10.1016/0014-5793(95)00188-f

Cited by 118 publications

(82 citation statements)

References 26 publications

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“…Thus, NO might be critically involved in eosinophil apoptosis. However, our data are in contrast to previously published work indicating that NO acts as a survival factor for eosinophils (47)(48)(49). A recent report also showed that LPS administration in OVA-immunized and -challenged rats drastically decreased an established airway eosinophilia but in conflict to our results, this suppression was associated with a decreased activity of NOS2 (50).…”

Section: Discussioncontrasting

confidence: 99%

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Rodríguez

Keller

Faquim-Mauro

et al. 2003

The Journal of Immunology

152

153

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Asthma results from an intrapulmonary allergen-driven Th2 response and is characterized by intermittent airway obstruction, airway hyperreactivity, and airway inflammation. An inverse association between allergic asthma and microbial infections has been observed. Microbial infections could prevent allergic responses by inducing the secretion of the type 1 cytokines, IL-12 and IFN-γ. In this study, we examined whether administration of bacterial LPS, a prototypic bacterial product that activates innate immune cells via the Toll-like receptor 4 (TLR4) could suppress early and late allergic responses in a murine model of asthma. We report that LPS administration suppresses the IgE-mediated and mast cell-dependent passive cutaneous anaphylaxis, pulmonary inflammation, airway eosinophilia, mucus production, and airway hyperactivity. The suppression of asthma-like responses was not due to Th1 shift as it persisted in IL-12−/− or IFN-γ−/− mice. However, the suppressive effect of LPS was not observed in TLR4- or NO synthase 2-deficient mice. Our findings demonstrate, for the first time, that LPS suppresses Th2 responses in vivo via the TLR4-dependent pathway that triggers NO synthase 2 activity.

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Section: Discussioncontrasting

confidence: 99%

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Rodríguez

Keller

Faquim-Mauro

et al. 2003

The Journal of Immunology

152

153

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show abstract

“…Although studies have shown that NO or related molecules can exert either pro-or anti-apoptotic effects depending on the cell type and stimulus (39,(43)(44)(45)(46)(47)(48)(49), the emerging picture is one where the predominant physiologic effect of NOS is inhibition of apoptosis. For instance, NO inhibits apoptosis in murine splenic B cells, human B cell lines, rat ovarian follicles, and human eosinophils (39,(47)(48)(49). The cellular factors and target proteins that are responsible for the specificity of NO-related effects on apoptosis remain to be determined.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibits Fas-induced Apoptosis

Mannick¹,

Miao²,

Stamler³

1997

Journal of Biological Chemistry

298

168

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“…NO dependent generation of intracellular cGMP has been shown to protect against apoptosis in lymphocytes (Genaro et al, 1995), eosinophils (Beauvais et al, 1995), embryonic motor neurons (Estevez et al, 1998), PC12 cells (Kim et al, 1999) and ovarian follicles (Chun et al, 1995). Exactly how cGMP protects against apoptosis is at present unclear.…”

Section: Cgmp Dependent Mechanismsmentioning

confidence: 99%