Assessment of T lymphocyte cytokine production in induced sputum from asthmatics: a flow cytometry study

Boniface, S.; Koscher, V.; Mamessier, Émilie; Biaze, M. El; Dupuy, P; Lorec, Anne-Marie; Guillot, Caroline; Badier, M; Bongrand, Pierre; Vervloët, D.; Magnan, A.

doi:10.1046/j.1365-2222.2003.01762.x

Cited by 54 publications

(36 citation statements)

References 32 publications

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“…The present authors cultured sputum inflammatory cells of asthmatic and normal subjects. In the few studies that tried to keep sputum cells in culture to evaluate the inflammatory characteristics of asthma, sputum cells were cultured without fractionation [18][19][20][21][22]. The cells were separated into two fractions, adherent and nonadherent, and cytokines, chemokines and cell composition were evaluated in each fraction.…”

Section: Discussionmentioning

confidence: 99%

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Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Scheicher¹,

Teixeira²,

Cunha³

et al. 2007

European Respiratory Journal

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The aim of the present study was to elucidate whether the culture of cells recovered from induced sputum may represent a suitable model to evaluate cytokine and chemokine production by airway inflammatory cells.Sputum induction was performed in 21 normal subjects and 30 asthmatic patients. A total of 21 out of the 30 asthmatic patients were taking inhaled corticosteroids, while the remaining nine were steroid-naive asthmatics. The steroid-naive group was evaluated before and after a 14-day treatment with oral prednisone (40 mg?day -1). The supernatant of lysed and centrifuged sputum and the supernatant of sputum cell culture were analysed. Tumour necrosis factor-a, interleukin (IL)-8 (CXCL8), IL-1b, IL-13 and eotaxin-2 (CCL24) concentrations were determined by specific ELISA.Eotaxin-2 production by cell culture was higher in the asthma group (131¡108 pg?mL) than in the control group (36¡41 pg?mL -1 ) and treatment with oral corticosteroids eliminated this difference. In addition, reduction of eotaxin-2 levels by corticosteroid treatment was greater in cell culture (81.3% reduction) than in sputum (26.4%). There was correlation between the decrease in eotaxin-2 production and the decrease in blood eosinophil number and between eotaxin-2 and eosinophils in sputum.Eotaxin-2 may play an important role in asthma and the response to corticosteroid treatment suggests that analysis of sputum cell culture is relevant as an inflammatory parameter.

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Section: Discussionmentioning

confidence: 99%

“…Several studies [15][16][17] have used the culture of blood cells to examine asthma pathophysiology and the responsiveness to treatment. However, very few studies have employed the culture of sputum cells [18][19][20][21][22]. It is likely that cells from the airways provide better information due to their proximity to the site of asthmatic inflammation.…”

mentioning

confidence: 99%

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Scheicher¹,

Teixeira²,

Cunha³

et al. 2007

European Respiratory Journal

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“…No real consensus exists in the literature about IFN-␥ expression in asthma (5,7,10,35,44,54,55,66,75), since published data show that levels of this cytokine are either increased, decreased, or unchanged in asthma and upregulated in subjects treated with corticosteroids (4,5,66,75). Airways exposed to increased TNF-␣ and decreased IFN-␥ concentrations could thus favor IL-17BR expression in vivo by smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

TNF-α and IFN-γ inversely modulate expression of the IL-17E receptor in airway smooth muscle cells

Lajoie-Kadoch

Joubert

Létuvé

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Our data indicate that TNF-␣ upregulates IL-17BR mainly through nuclear factor-B as assessed with the IB kinase 2 inhibitor AS-602868. In addition, both IFN-␥ and dexamethasone are able to antagonize a TNF-␣-induced IL-17BR increase in mRNA expression. The mitogen-activated protein kinase kinase inhibitor U0126 totally reversed the inhibition observed with IFN-␥, suggesting the involvement of the extracellular signal-regulated kinase pathway in this effect. In addition, on stimulation with IL-17E, airway smooth muscle cells increase their expression of ECM components, namely procollagen-␣I and lumican mRNA. Furthermore, immunohistochemical analysis of biopsies from asthmatic subjects reveals that this receptor is abundant in smooth muscle layers. This is the first report showing IL-17BR receptor in structural cells of the airways. Our results suggest a potential proremodeling effect of IL-17E on airway smooth muscle cells through the induction of ECM and that its receptor is upregulated by proinflammatory conditions.

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“…Meta-analysis: Forest plot and pooled RR of the association between any allergy and pancreatic cancer using the random-effects model. (66)(67)(68). These data suggest that the hypersensitivity found in allergic responses may lead to a broader activation of the immune system and to increased immune surveillance against tumors.…”

Section: Discussionmentioning

confidence: 99%

Allergies and the Risk of Pancreatic Cancer: A Meta-analysis with Review of Epidemiology and Biological Mechanisms

Gandini

Lowenfels

Jaffee

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

111

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Previous reports suggest that allergic disorders may protect against various types of cancer, but the association between history of allergy and pancreatic cancer risk has not been well studied. We did a systematic review and meta-analysis of published studies to evaluate the association of any type, and specific types, of allergy and the risk of pancreatic cancer. We did a comprehensive literature search using MEDLINE, PUBMED, and the ISI Web of Science databases to identify potential relevant case-control and cohort studies. Pooled relative risks (RR) and 95% confidence intervals (95% CI) were calculated using the fixed-and random-effects model. Fourteen population-based studies (4 cohort and 10 case-control studies) with a total of 3,040 pancreatic cancer cases fulfilled our inclusion criteria. A history of allergy was associated with a reduced risk of pancreatic cancer (RR, 0.82; 95% CI, 0.68-0.99). The risk reduction was stronger for allergies related to atopy (RR, 0.71; 95% CI, 0.64-0.80), but not for asthma (RR, 1.01; 95% CI, 0.77-1.31). There was no association between allergies related to food or drugs and pancreatic cancer (RR, 1.08; 95% CI, 0.74-1.58). Overall, there was no evidence of publication bias. Allergies, in particular those related to atopy, seem to be associated with a decreased risk of pancreatic cancer. The hyperactive immune system of allergic individuals may, therefore, in some way lead to increased surveillance and protect against pancreatic cancer development. (Cancer Epidemiol Biomarkers Prev 2005;14(8):1908 -16)

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Assessment of T lymphocyte cytokine production in induced sputum from asthmatics: a flow cytometry study

Abstract: IS T cell cytokine production indicates a basic Th2 bias in asthma, accompanied during symptoms by a Th1-like activation. These results open the field for longitudinal studies of the variation of T cell activation in asthma.

Cited by 54 publications

References 32 publications

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation

TNF-α and IFN-γ inversely modulate expression of the IL-17E receptor in airway smooth muscle cells

Allergies and the Risk of Pancreatic Cancer: A Meta-analysis with Review of Epidemiology and Biological Mechanisms

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