Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-<i>γ</i>, IL-4, IL-10 and IL-13) in patients with allergic asthma

Wong, Chun‐Kwok; Ho, C. Y.; Ko, Fanny W.S.; Chan, Cora; Ho, Alice; Hui, David S.; Lam, C. W. K.

doi:10.1046/j.1365-2249.2001.01602.x

Cited by 405 publications

(329 citation statements)

References 47 publications

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“…Aberrant increases in proinflammatory cytokine and chemokine secretion in allergic asthmatic patients were reported in clinical studies. 35,36 We found that allergic rhinitis patients showed higher plasma IL-33 median concentration than normal controls (33.6 versus 9.8 pg/ ml). It has been reported that CCL2 concentration in bronchoalveolar lavage fluid was found to be elevated in allergic asthmatic patients.…”

Section: Il-33 Activates Eosinophilsmentioning

confidence: 81%

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

et al. 2009

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The novel interleukin (IL)-1 family cytokine IL-33 has been shown to activate T helper 2 (Th2) lymphocytes, mast cells and basophils to produce an array of proinflammatory cytokines, as well as to mediate blood eosinophilia, IgE secretion and hypertrophy of airway epithelium in mice. In the present study, we characterized the activation of human eosinophils by IL-33, and investigated the underlying intracellular signaling mechanisms. IL-33 markedly enhanced eosinophil survival and upregulated cell surface expression of the adhesion molecule intercellular adhesion molecule (ICAM)-1 on eosinophils, but it suppressed that of ICAM-3 and L-selectin. In addition, IL-33 mediates significant release of the proinflammatory cytokine IL-6 and the chemokines CXCL8 and CCL2. We found that IL-33-mediated enhancement of survival, induction of adhesion molecules, and release of cytokines and chemokines were differentially regulated by activation of the nuclear factor (NF)-kB, p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathways. Furthermore, we compared the above IL-33 activities with two structurally and functionally related cytokines, IL-1b and IL-18. IL-1b, but not IL-18, markedly upregulated cell surface expression of ICAM-1. IL-1b and IL-18 also significantly enhanced eosinophil survival, and induced the release of IL-6 and chemokines CXCL8 and CCL2 via the activation of the NF-kB, p38 MAPK and ERK pathways. Synergistic effects on the release of IL-6 were also observed in combined treatment with IL-1b, IL-18 and IL-33. Taken together, our findings provide insight into IL-33-mediated activation of eosinophils via differential intracellular signaling cascades in the immunopathogenesis of allergic inflammation.

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Section: Il-33 Activates Eosinophilsmentioning

confidence: 81%

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

et al. 2009

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“…[32][33][34][35][36] IL-17A also plays a role in human asthmatic patients and in airways of allergic animals. 18,28,30,[37][38][39] Studies have found that in patients with moderate-to-severe asthma, neutrophils are found to be more abundant than eosinophils in the bronchoalveolar lavage fluid. 30,31,40 IL-17A can promote neutrophil recruitment, which might contribute to certain asthmatic phenotypes characterized by both high neutrophil counts and IL-17A expression.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of IL-19 expression in airway epithelia by IL-17A and IL-4/IL-13: Important implications in asthma

Huang

Wachi

Thai

et al. 2008

Journal of Allergy and Clinical Immunology

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“…However, it is worth mentioning here that work in human subjects both has suggested that neutrophils may be potentially important contributors to airway pathology in certain subsets of patients with asthma, [41][42][43][44][45][46][47][48] and has identified IL-17 expression in the lungs of some subjects with this disorder. 32,[49][50][51][52][53] Therefore, it will be of interest to attempt to investigate whether the mechanisms that contribute to the mast cell-dependent enhancement of IL-17-dependent airway neutrophilia that have been revealed in our analyses of OTII mice have any bearing on the regulation of neutrophil recruitment that can occur in human asthma.…”

Section: Discussionmentioning

confidence: 99%

Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

Nakae

Suto

Berry

et al. 2006

Blood

142

124

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IntroductionSeveral proinflammatory cytokines, including TNF, IL-1, and IL-17, can directly induce neutrophil recruitment. For example, inhalation of recombinant TNF, IL-1, or IL-17 can provoke neutrophil infiltration into the airways. [1][2][3] These cytokines can also play important roles in the pulmonary neutrophilia induced by infection with the Gram-negative bacteria Klebsiella pneumoniae, and can contribute to bacterial clearance. [4][5][6] However, both the roles of these proinflammatory cytokines, and the most important cellular sources of their production, can vary according to the models of inflammation analyzed. For example, in mice, mast cell-derived TNF has been reported to contribute importantly to neutrophil recruitment and host defense against K. pneumoniae. 7 By contrast, it has been reported that 8,9 but neither TNF nor IL-1, 10 is important for the pulmonary neutrophilia induced by LPS, a component of Gram-negative bacteria.To date, no reports have investigated the possible role of mast cells in the development of T helper 17 (Th17) cell-dependent, neutrophil-rich inflammatory responses, either in the airways or in other anatomical sites. To address this question, we decided to use a model of protein antigen (Ag) (ovalbumin [OVA])-induced neutrophil-predominant airway inflammation in OVA-specific T-cell receptor (TCR)-expressing mice. We took this approach because of reports indicating that OVA challenge can induce neutrophil-rich airway inflammation in OVA-specific TCR-expressing BALB/c-DO11.10 mice, 11,12 and that IL-17 is required for the induction of airway hyperreactivity (AHR) in this model. 13 However, we elected to use OVA-specific TCR-expressing C57BL/6-OTII mice, 14 instead of BALB/c-DO11.10 mice, for the work reported herein. C57BL/6-OTII mice are on the same strain background as mice that are either profoundly deficient in mast cells, lack the FcR␥ chain (that is required for the activation of mast cells via either the Fc⑀RI or Fc␥RIII that are expressed on their surface 15,16 ), or lack IL-17 or any of several other specific cytokines or cytokine receptors. Therefore, by working with C57BL/6-OTII mice, we were able to use a genetic approach to investigate in detail the importance of each of these candidate elements in the airway neutrophil infiltration elicited by OVA challenge in this model. Materials and methods Experimental approachWe first established and characterized a model of OVA-induced neutrophilrich airway inflammation in OVA-specific TCR-expressing C57BL/6-OTII mice. We then used a combination of pharmacologic and genetic approaches to investigate the potential roles of individual mediators, cytokines, and chemoattractants in the development of the neutrophil-rich airway inflammation induced by Ag challenge in this model. Finally, we used a genetic approach to investigate the roles of FcR␥, mast cells, and mast cell-derived TNF in this model of Ag-and Th17 cell-dependent, neutrophil-rich airway inflammation. The online version of this article contains a data supplement...

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Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-γ, IL-4, IL-10 and IL-13) in patients with allergic asthma

Cited by 405 publications

References 47 publications

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

Intracellular signaling mechanisms regulating the activation of human eosinophils by the novel Th2 cytokine IL-33: implications for allergic inflammation

Potentiation of IL-19 expression in airway epithelia by IL-17A and IL-4/IL-13: Important implications in asthma

Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice

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