Serum Levels of Interleukins (IL)-4, IL-5, IL-13, and Interferon-γ in Acute Asthma

Lee, Yong Chul; Lee, Kyung Hun; Lee, Heung Bum; Rhee, Yang Keun

doi:10.1081/jas-100107544

Cited by 80 publications

(58 citation statements)

References 31 publications

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“…IL-4, IL-5 and IL-13 are detectable in the serum (1-50 pg/ ml range) of asthma patients in an acute episode (79). However, once recruited to the local tissue, T cells are more likely to reflect changes in immunopathology.…”

Section: T-cell-associated Biomarkersmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

106

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Diagnosis early in life, sensitization, asthma endotypes, monitoring of disease and treatment progression are key motivations for the exploration of biomarkers for allergic rhinitis and allergic asthma. The number of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic genes have not yet entered clinical application. We hypothesize that the combination of multiple genes may generate biomarkers with prognostic potential. The current review attempts to group more than 161 different potential biomarkers involved in respiratory inflammation to pave the way for future classifiers. The potential biomarkers are categorized into either epithelial or infiltrate-derived or mixed origin, epithelial biomarkers. Furthermore, surface markers were grouped into cell-typespecific categories. The current literature provides multiple biomarkers for potential asthma endotypes that are related to T-cell phenotypes such as Th1, Th2, Th9, Th17, Th22 and Tregs and their lead cytokines. Eosinophilic and neutrophilic asthma endotypes are also classified by epithelium-derived CCL-26 and osteopontin, respectively. There are currently about 20 epithelium-derived biomarkers exclusively derived from epithelium, which are likely to innovate biomarker panels as they are easy to sample. This article systematically reviews and categorizes genes and collects current evidence that may promote these biomarkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.

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Section: T-cell-associated Biomarkersmentioning

confidence: 99%

Current and future biomarkers in allergic asthma

Zissler

Bieren

Jakwerth

et al. 2016

Allergy

106

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“…Alternatively, IL-13 may participate in asthma pathogenesis using pathways independent of IL-5 [36]. Higher levels of serum IL-5, but not IL-13, are associated with severe airway obstruction in asthmatics [37]. …”

Section: Discussionmentioning

confidence: 99%

Azithromycin Inhibits IL-5 Production of T Helper Type 2 Cells from Asthmatic Children

Lin

Lee

Liang

et al. 2011

Int Arch Allergy Immunol

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Background: Childhood asthma is a type 2 helper T (Th2) cell-driven inflammatory airway disease characterized by recurrent episodes of airway obstruction. Azithromycin (AZM), a macrolide antibiotic exhibiting anti-inflammatory activity aside from its antibacterial effect, may prove beneficial for asthmatic children. This study aimed to determine the effect of AZM on Th2 cells from atopic asthmatic children and non-atopic controls. Methods: CD4+ cells were isolated from peripheral blood mononuclear cells of 9 patients with asthma and 9 non-atopic individuals. Cells were activated as Th0 and differentiated into Th2 cells. The effect of AZM on activated CD4+ cells was evaluated with respective cell proliferation and cytokine production. Results: Th0 and Th2 CD4+ T cells from atopic asthmatic children produced greater interleukin (IL)-5 (Th2 cytokine) but lower interferon (IFN)-γ (Th1 cytokine) compared to the non-atopic controls, respectively. AZM inhibited IL-5 production of Th0 and Th2 cells from atopic asthmatics in a dose-dependent fashion, without significantly affecting their IL-13 and IFN-γ production. A similar effect was observed in non-atopic controls except that AZM did inhibit IFN-γ production of their Th0 cells. AZM at a higher dose decreased cell viability by inhibiting CD4+ T cell proliferation and enhanced their apoptosis, an effect similarly observed in Th0 and Th2 cells, and did not differ between asthmatic children and controls. Conclusion: Our finding that AZM preferentially downregulates IL-5 production suggests its therapeutic potentials in controlling childhood asthma.

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“…TRE-Tight-IL-22 mice were identified and crossbred with the CC10-rtTA or SPC-rtTA transgenic mice [31,32] (kind gifts from Dr. Jeffrey Whitsett, the University of Cincinnati) to produce CC10-rtTA-IL-22 or SPC-rtTA-IL-22 double Tg(+) mice. Tg (2) or wild type (WT) littermates were used as controls. In this study terms Tg(2) and WT are interchangeable.…”

Section: Methodsmentioning

confidence: 99%

“…Th2 cytokines, IL-4 and IL-13, play a central role in orchestrating these responses, whereas Th1 cytokine IFN-c may have opposing effects [1][2][3][4]. Furthermore, the Th17 cytokine IL-17A is critical in the pathogenesis of severe asthma [4,5].…”

Section: Introductionmentioning

confidence: 99%

Immune Modulatory Effects of IL-22 On Allergen-Induced Pulmonary Inflammation

Fang¹

2013

Journal of Allergy and Clinical Immunology

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IL-22 is a Th17/Th22 cytokine that is increased in asthma. However, recent animal studies showed controversial findings in the effects of IL-22 in allergic asthma. To determine the role of IL-22 in ovalbumin-induced allergic inflammation we generated inducible lung-specific IL-22 transgenic mice. Transgenic IL-22 expression and signaling activity in the lung were determined. Ovalbumin (OVA)-induced pulmonary inflammation, immune responses, and airway hyperresponsiveness (AHR) were examined and compared between IL-22 transgenic mice and wild type controls. Following doxycycline (Dox) induction, IL-22 protein was readily detected in the large (CC10 promoter) and small (SPC promoter) airway epithelial cells. IL-22 signaling was evidenced by phosphorylated STAT3. After OVA sensitization and challenge, compared to wild type littermates, IL-22 transgenic mice showed decreased eosinophils in the bronchoalveolar lavage (BAL), and in lung tissue, decreased mucus metaplasia in the airways, and reduced AHR. Among the cytokines and chemokines examined, IL-13 levels were reduced in the BAL fluid as well as in lymphocytes from local draining lymph nodes of IL-22 transgenic mice. No effect was seen on the levels of serum total or OVA-specific IgE or IgG. These findings indicate that IL-22 has immune modulatory effects on pulmonary inflammatory responses in allergen-induced asthma.

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Serum Levels of Interleukins (IL)-4, IL-5, IL-13, and Interferon-γ in Acute Asthma

Cited by 80 publications

References 31 publications

Current and future biomarkers in allergic asthma

Current and future biomarkers in allergic asthma

Azithromycin Inhibits IL-5 Production of T Helper Type 2 Cells from Asthmatic Children

Immune Modulatory Effects of IL-22 On Allergen-Induced Pulmonary Inflammation

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