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Find video protocols related to scientific articles indexed in Pubmed.
Leptin has a priming effect on eotaxin-induced human eosinophil chemotaxis.
Int. Arch. Allergy Immunol.
PUBLISHED: 02-22-2011
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Tissue eosinophilia is one of the hallmarks of allergic diseases and Th2-type immune responses including asthma. Systemic inflammation caused by adipose tissue in obesity via production of adipokines such as leptin has been attracting attention recently as a contributor to exacerbation of allergic immune reactions. In this study, we examined whether leptin might affect eosinophil chemotactic responses.
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The opposing role of two prostaglandin D2 receptors, DP and CRTH2, in human eosinophil migration.
Ann. Allergy Asthma Immunol.
PUBLISHED: 01-21-2011
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Prostaglandin D2 (PGD2) regulates various immunological responses via two distinct PGD2 receptors, prostaglandin D receptor (DP), and chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). Recent studies have demonstrated that PGD2 induces the migration of eosinophils through CRTH2. Although human eosinophils express both DP and CRTH2, it is unclear whether the function of DP is involved in eosinophil migration.
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The pathophysiological roles of PI3Ks and therapeutic potential of selective inhibitors in allergic inflammation.
Int. Arch. Allergy Immunol.
PUBLISHED: 06-04-2010
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Phosphoinositide 3-kinases (PI3Ks) are known to be involved in a variety of cellular responses such as cell survival, proliferation, differentiation and cell migration. Recently, PI3Ks have been associated with the pathogenesis of asthma because various immune cells regulate allergic responses. Among the three classes of PI3Ks, the roles of PI3K gamma and PI3K delta in allergic responses have attracted particular attention. In a previous report, allergic airway hyperresponsiveness (AHR), inflammation and airway remodeling in an ovalbumin-induced asthma model were decreased in PI3K gamma-deficient mice compared with wild-type mice. In addition, AHR and inflammation were attenuated by administration of a selective PI3K delta inhibitor in a murine model of asthma. These results indicate that PI3K gamma and PI3K delta may be new therapeutic targets for asthma. However, PI3K gamma and PI3K delta may differ in terms of the mechanism of regulation. In this review, we focus on the roles of PI3K gamma and PI3K delta in the pathogenesis of asthma and discuss the mechanistic differences between PI3K gamma and PI3K delta.
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15-Deoxy-Delta(12,14)-prostaglandin J2 induces IL-8 and GM-CSF in a human airway epithelial cell line (NCI-H292).
Int. Arch. Allergy Immunol.
PUBLISHED: 06-03-2009
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15-Deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2), a major prostanoid metabolized from prostaglandin D2 (PGD2), plays an important role in various biological processes including inflammatory responses. 15d-PGJ2 exerts its effects through two major receptors, chemoattractant receptor- homologous molecule expressed on Th2 cells (CRTH2) and peroxisome proliferator-activated receptor-gamma (PPARgamma). The 15d-PGJ2/PPARgamma system, in particular, regulates numerous biological processes including adipogenesis, apoptosis, and inflammation. Although our studies have shown that PGD2 (metabolic precursor of 15d-PGJ2) induces IL-8 and GM-CSF production, the role of 15d-PGJ2 (metabolite of PGD2) is unknown in human bronchial epithelial cells. In this study, we investigated the function of 15d-PGJ2 on a human airway epithelial cell line: NCI-H292.
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Regulation of peroxisome proliferator-activated receptor-gamma expression in human eosinophils by estradiol.
Int. Arch. Allergy Immunol.
PUBLISHED: 06-03-2009
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Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor that regulates not only adipogenesis but also immune reaction. We previously demonstrated that human eosinophils expressed functional PPARgamma, although the modulator of PPARgamma expression is less well understood. Because clinical studies have shown that the efficacy of PPARgamma agonists as insulin sensitizers is stronger in women than in men, we investigated whether sex hormones caused any changes in eosinophil PPARgamma expression levels.
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Allergic airway hyperresponsiveness, inflammation, and remodeling do not develop in phosphoinositide 3-kinase gamma-deficient mice.
J. Allergy Clin. Immunol.
PUBLISHED: 02-20-2009
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Bronchial asthma is characterized by chronic airway inflammation caused by inflammatory cells. Phosphoinositide 3-kinases (PI3Ks) are known to play a prominent role in fundamental cellular responses of various inflammatory cells, including proliferation, differentiation, and cell migration. PI3Ks therefore are expected to have therapeutic potential for asthma. Although some investigations of the involvement between the pathogenesis of asthma and PI3K have been performed, it is unknown whether PI3Kgamma, a PI3K isoform, is involved in the pathogenesis of asthma.
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Obesity and eosinophilic inflammation: does leptin play a role.
Int. Arch. Allergy Immunol.
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It has been pointed out that obesity is a risk factor for, and is involved in the exacerbation of asthma. Mounting evidence about adipose tissue-derived proteins (adipokines) gave rise to the current understanding of obesity as a systemic inflammatory disorder. In this review, we summarized the involvement of leptin, focusing on eosinophil functions. Several studies have indicated that leptin can restrain eosinophil apoptosis, enhance migration, increase adhesion molecules and induce cytokine production. Since leptin also acts on a variety of immune cells related to allergic response, increased leptin in obese individuals potentially explains the mechanism by which obesity leads to an exacerbation of asthma. Further studies targeting adipokines will delineate the association between obesity and eosinophil-associated diseases.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.