T cell cytokine profiles in childhood asthma

Brown, Vanessa; Warke, T.J.; Shields, Michael; Ennis, Madeleine

doi:10.1136/thorax.58.4.311

Cited by 57 publications

(55 citation statements)

References 57 publications

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“…Increased eosinophil numbers in BALF of asthmatic subjects were not related to disease severity, whereas neutrophilic inflammation was often correlated with disease severity [36][37][38]. Increase in interferon-cproducing cells [39] and in interferon-c concentrations [40] were found in BALF of asthmatic children. Furthermore, young asthmatic children had increased activated macrophages that released pro-inflammatory mediators (e.g.…”

Section: Balfmentioning

confidence: 81%

Update on the roles of distal airways in asthma

Burgel¹,

Blic²,

Chanez³

et al. 2009

European Respiratory Review

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The present review is the summary of an expert workshop that took place in Vence (France) in 2007 on the role of distal airways in asthma. The evidence showing inflammation and remodelling in distal airways, and their possible involvement in asthma control and natural history, was reviewed. The usefulness and limitations of various techniques used for assessing distal airways were also evaluated, including pulmonary function tests and imaging. Finally, the available data studying the benefit of treatment better targeting distal airways in asthma was examined. It was concluded that both proximal and distal airways were involved in asthma and that distal airways were the major determinant of airflow obstruction. Inflammation in distal airways appeared more intense in severe and uncontrolled asthma. Distal airways were poorly attained by conventional aerosol of asthma medications owing to their granulometry, being composed of 3-5 mm particles. Both proximal and distal airways might be targeted either by delivering medications systemically or by aerosol of extra-fine particles. Extra-fine aerosols of long-acting b-agonists, inhaled corticosteroids or inhaled corticosteroid/long-acting b-agonist combinations have been shown in short-term studies to be not inferior to non-extra-fine aerosols of comparators. However, available studies have not yet demonstrated that extra-fine inhaled medications offer increased benefit compared with usual aerosols in asthmatic patients.

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Section: Balfmentioning

confidence: 81%

Update on the roles of distal airways in asthma

Burgel¹,

Blic²,

Chanez³

et al. 2009

European Respiratory Review

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“…In humans, it has been shown that expression of IL-4 and its receptor correlates with asthma [24,25]. Furthermore, murine studies demonstrate a role for IL-4 in BAL and lung eosinophil accumulation [26,27], and mice deficient in IL-4 are not hyperreactive when sensitized and challenged to OVA [28].…”

Section: Discussionmentioning

confidence: 99%

CD8+ T cell contributions to allergen induced pulmonary inflammation and airway hyperreactivity

et al. 2005

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The pathogenesis of asthma has been linked to the production of type 2 cytokines, which can be expressed by several cell types in the lung. These studies investigated CD8 + T cell responses in a murine cockroach antigen (CRA) model of asthma. The results from these present studies show that depletion of CD8 + T cells after allergen sensitization to CRA significantly reduces airway hyperreactivity, airway eosinophilia and pulmonary type 2 cytokine levels. The data demonstrate that CD8 + T cells from CRA-sensitized mice can produce type 2 cytokines IL-4, IL-5 and IL-13 upon antigen challenge, and that the transfer of these cells into naive mice will cause airway hyperreactivity when exposed to CRA. We found that the transferred airway response is dependent on both IL-4 and IL-13 from CD8 + T cells using cytokine knockout mice. Compared to CD4 + T cells, CD8 + T cells were not as numerous in the lungs of sensitized and challenged mice, but were as efficacious in the transfer of airway disease. The most severe airway response was observed when both CD4 + and CD8 + T cells were transferred at the same time. Altogether, these studies highlight a role for CD8 + T lymphocytes in the development of allergen-induced airway responses.

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“…It stimulates antigen presenting cells and major histocompatibility complex (MHC) class II molecule expression, driving specific immune responses through antigen recognition and antibody production. In the lung, IFN-␥ signaling has been implicated in viral infections, sarcoidosis, mycobacterial infections, cystic fibrosis, and hypersensitivity pneumonitis (8,(23)(24)(25)39). IFN-␥ may play a role as a modifier of cytokine/ chemokine production and may influence cellular recruitment into inflammatory lesions.…”

mentioning

confidence: 99%

Influence of IFN-γ on gene expression in normal human bronchial epithelial cells: modulation of IFN-γ effects by dexamethasone

Pawliczak¹,

Logun²,

Madara³

et al. 2005

Physiological Genomics

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-Interferon gamma (IFN-␥) plays a role in a variety of lung inflammatory responses, and corticosteroids are frequently employed as a treatment in these conditions. Therefore, the effect of IFN-␥, of the corticosteroid dexamethasone (Dex), or of both on gene expression was studied in normal human bronchial epithelial (NHBE) cells. NHBE cells were exposed to medium alone, IFN-␥ (300 U/ml), Dex (10 Ϫ7 M), or both IFN-␥ and Dex for 8 or 24 h. Gene expression was examined using oligonucleotide microarrays. A principal components analysis demonstrated that the IFN-␥ treatment effect was the primary source of differences in the data. With a 5% false discovery rate, of the 66 genes upregulated by IFN-␥ by twofold or greater at 8 h and 287 genes upregulated at 24 h, coincubation with Dex inhibited the expression of 2 genes at 8 h and 45 genes at 24 h. Prominent among these were cytokines and secreted proteins. Dex cotreatment increased expression of 65 of the 376 genes that were inhibited by IFN-␥ by 50% at 24 h. The majority of these genes encode cell cycle or nuclear proteins. Dex alone increased the expression of only 22 genes and inhibited the expression of 7 genes compared with controls at 24 h. The effect of Dex on IFN-␥-induced changes suggests a specific, targeted effect on IFN-␥ responses that is substantially greater than the effect of Dex alone. Dex had little effect on the immediate early response to IFN-␥ but a significant effect on the late responses.

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T cell cytokine profiles in childhood asthma

Cited by 57 publications

References 57 publications

Update on the roles of distal airways in asthma

Update on the roles of distal airways in asthma

CD8+ T cell contributions to allergen induced pulmonary inflammation and airway hyperreactivity

Influence of IFN-γ on gene expression in normal human bronchial epithelial cells: modulation of IFN-γ effects by dexamethasone

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