Flt-3 Ligand Reverses Late Allergic Response and Airway Hyper-Responsiveness in a Mouse Model of Allergic Inflammation

Edwan, Jehad H.; Perry, Greg A.; Talmadge, James E.; Agrawal, Devendra K.

doi:10.4049/jimmunol.172.8.5016

Cited by 64 publications

(54 citation statements)

References 70 publications

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“…Following immune excitation, memory/effector CD4 + Th2 cells then leave the draining lymph nodes and extravasate at sites of inflammation during the challenge phase. Once in the tissues, Th2 cells interact with IgE-bearing local DC to increase IL-4, IL-5, IL-9, and IL-13 production [90][91][92][96][97][98][99][100][101][102]. These cytokines are important for inducing tissue eosinophilia, airway hyperreactivity, and the production of chemokines that attract further inflammatory cells.…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

View full text Add to dashboard Cite

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“…Animal experimentation is authorised by the Government in the Decree Law 116/92, according to the European Economical Community (CEE) guidelines number 609/86. The experimental asthmatic state was induced in animals referring to previously described models [15][16][17][18]. In brief, mice (n=5/group) were immunized by i.p.…”

Section: Experimental Asthma Model Inductionmentioning

confidence: 99%

Low dose oral administration of cytokines for treatment of allergic asthma

Gariboldi

Palazzo

Zanobbio

et al. 2009

Pulmonary Pharmacology & Therapeutics

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Many inflammatory diseases are characterized by an imbalance among lymphocyte populations, in particular Th1, Th2 and the recently described Th17 cells. The Th1/Th2 imbalance is linked to many factors, but certainly the role of cytokines is essential.In Th2 diseases IL-4 expression is predominant, while Th1 pathologies are characterized by high expression of IFN-γ and IL-12. Though today the therapeutical proposal for many inflammatory diseases aims to re-establish normal levels of Th1/Th2 cytokines, the pharmacological use of cytokines, which are very active molecules, is limited by the possible collateral effects. Therefore, our study aims to determine, in a murine model of allergic asthma, the possible therapeutic activity of low dose cytokines solutions, mechanically activated. We found that oral administration of low doses IL-12 plus IFN-γ is able to solve the bronchial hyperresponsiveness condition of mice, establishing normal cytokine levels. The anti-asthma activity was confirmed by histological analysis of lungs and bronchoalveolar lavage fluid cell count. Serum ovalbumin-specific IgE was also significantly inhibited by treatment with low-dose activated cytokines solution. These findings may suggest a novel approach to diseases which involve a Th1/Th2 imbalance.

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“…A single-chamber whole-body plethysmograph (Buxco Electronics, Troy, NY) without the use of anesthesia or restraint was used to measure pulmonary functions (Agrawal et al, 2001;Edwan et al, 2004). Mice were challenged with increasing doses of methacholine (SigmaAldrich) to measure AHR.…”

Section: Noninvasive Methods For Measuring Pulmonary Functionmentioning

confidence: 99%

“…We have previously reported that FL protects against (Agrawal et al, 2001) and reverses (Edwan et al, 2004(Edwan et al, , 2005(Edwan et al, , 2006 airway hyperresponsiveness (AHR) and allergic airway inflammation in murine model of asthma. FL treatment increased the total number of DCs in the lungs together with a reduction in AHR to methacholine.…”

Section: Introductionmentioning

confidence: 99%

Flt3 ligand generates morphologically distinct semimature dendritic cells in ovalbumin-sensitized mice

Bharadwaj

Agrawal

2007

Experimental and Molecular Pathology

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Dendritic cells (DCs) are unique antigen presenting cells that are immature prior to their encounter with an antigen. Exposure to allergens induces the maturation of DCs with changes in morphology and presence of dendrites. Here, we demonstrate that the DCs in the lungs of ovalbumin (OVA)-sensitized and challenged mice are more mature owing to their pronounced dendrites than the DCs in the lungs and spleen of PBS-treated mice, which are immature and possess cytoplasmic veils. Intermediate to these two groups are the DCs in the Flt3 ligand-treated group that exhibit comparatively fewer dendrites and cytoplasmic veils and hence are classified as semimature. Presence of large numbers of well developed mitochondria and rough endoplasmic reticulum in myeloid DCs from both lungs and spleen of OVA-sensitized and challenged mice indicate greater functional activity. Additionally, DCs from the OVA-sensitized and challenged mice also exhibit fat and glycogen stores, which are indicative of a mature population. In addition, treatment of the animals with Flt3 ligand attenuated airway hyperresponsiveness to methacholine in OVA-sensitized and challenged mice. These data suggest that morphological features could be indicative of the maturation and distinct functional state of DCs, and this could be associated with underlying mechanisms of Flt3 ligand-induced immunomodulation in allergic asthma.

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Flt-3 Ligand Reverses Late Allergic Response and Airway Hyper-Responsiveness in a Mouse Model of Allergic Inflammation

Cited by 64 publications

References 70 publications

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Low dose oral administration of cytokines for treatment of allergic asthma

Flt3 ligand generates morphologically distinct semimature dendritic cells in ovalbumin-sensitized mice

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