IL-18 might reflect disease activity in mild and moderate asthma exacerbation

Tanaka, Hiroshi; N, Miyazaki; Oashi, Kensuke; Teramoto, S; Shiratori, Masanori; Hashimoto, Midori; Ohmichi, Mitsuhide; Abe, Shosaku

doi:10.1067/mai.2001.112275

Cited by 130 publications

(97 citation statements)

References 28 publications

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“…Serum levels of IL-18 are elevated in patients with bronchial asthma (SI Fig. 10), and a significant correlation between IL-18 serum levels and the disease severity of bronchial asthma has been reported (38).…”

Section: Discussionmentioning

confidence: 99%

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

Hayashi¹,

Yoshimoto²,

Izuhara

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

128

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We previously reported that ovalbumin (OVA) and IL-18 nasally administered act on memory type T helper (Th)1 cells to induce airway hyperresponsiveness (AHR) and inflammation, which is characterized by peribronchial infiltration with neutrophils and eosinophils. Here, we report this administration also induces lung fibrosis in an IL-13-dependent manner. bronchial asthma ͉ LPS ͉ periostin ͉ hydroxy proline ͉ airway inflammation

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Section: Discussionmentioning

confidence: 99%

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

Hayashi¹,

Yoshimoto²,

Izuhara

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

128

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“…Taken together, these experiments show that IL-18 has both allergy-promoting and antiallergic functions (20). A surfeit of IL-18 was recently found in allergic patients with atopic dermatitis or asthma (21)(22)(23)(24)(25). However, IL-18 was also raised in patients with other diseases in which dominant Th1 cells play a key role of immunity (26)(27)(28)(29)(30).…”

Section: Introductionmentioning

confidence: 94%

“…In recent studies, several individual investigations related the functions of IL-18 expression and serum levels in allergic diseases have been published. Raised serum IL-18 levels were studied in the patients with allergic asthma (22) and acute asthma (21), atopic dermatitis (40), and allergic rhinitis (41). In the procedure of Th2 differentiation, IL-18 and T-cell receptormediated stimulation was induced by allergens such as house dust mites, which could trigger naive CD4…”

Section: Discussionmentioning

confidence: 99%

Association of interleukin‐18 gene polymorphism with asthma in Chinese patients

Lee

Lin

Wan

et al. 2008

Clinical Laboratory Analysis

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Like other allergic diseases, asthma results from multiple conditions. Asthmatic beginning and severity are mediated by both environmental and genetic factors. In asthma studies, important work is realization of the genetic background and identification of genetic factors resulting in asthma development and phenomena. Here, we investigated whether interleukin (IL)-18 single nucleotide polymorphisms (SNPs) are involved in Chinese asthma patients. IL-18 (IL-18) SNP was detected by polymerase chain reaction (PCR)-based restriction analysis in 201 patients with asthma and 60 normal controls. Significant differences were found in the genotype distribution of IL-18 SNP between asthma patients and controls (P 5 0.000003). Allelic frequency of the IL-18 gene distinguished asthma patients from controls (P 5 0.000066). The results revealed a significant difference between asthma patients and normal controls in IL-18 SNP and a statistical correlation between IL-18 polymorphisms (105A/C) and asthma formation. We concluded that Chinese who carry the C/C homozygote of the IL-18-105A/C gene polymorphism in coding regions may have a higher risk of developing asthma.

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“…In a murine bronchial asthma model with Ag-specific Th1 cells, administration of IL-18 induced asthma symptoms (11). Furthermore, IL-18 sera levels are elevated in atopic dermatitis patients as well as in asthmatics (12,13). IL-33 is an important mediator of allergy by its induction of Th2 cytokines (9,14,15) and has been associated with development of severe asthma, with high plasma and bronchial levels of IL-33 located in epithelial and smooth muscle cells (16)(17)(18).…”

Section: D4mentioning

confidence: 99%

IL-1 Family Members IL-18 and IL-33 Upregulate the Inflammatory Potential of Differentiated Human Th1 and Th2 Cultures

Blom

Poulsen

2012

The Journal of Immunology

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The IL-1 family members IL-1β, IL-18, and IL-33 are potent cytokines in relationship to amplifying the CD4+ T cell cytokine production. To evaluate their impact on in vitro-differentiated human Th1 and Th2 cultures, such cultures were established from naive T cells, purified from healthy blood donors, and reactivated in the presence of IL-1β, IL-18, or IL-33. Interestingly, we observe modifying responses in Th1 and Th2 cultures induced by IL-18 or IL-33 but not by IL-1β, both contributing to amplify production of IL-5, IL-13, and IFN-γ. IL-18 or IL-33 stimulation of Th1 cultures resulted in increased IFN-γ and IL-13 production concurrent with reduced IL-10 gene transcription and secretion even though Th1 cultures, in contrast to IL-18Rα, had low ST2L expression. Furthermore, adding IL-18 to Th1 cultures promoted Tbet mRNA expression and production. Th2 cultures stimulated with IL-18 or IL-33 had an increased IL-5 secretion. Interestingly, E4BP4 gene expression and the percentage of E4BP4+ cells of the recently shown IL-10 transcriptional regulator E4BP4 correlated with IL-10 gene expression and protein secretion in Th1 cultures. Taken together, we report that the IL-1 family “alarmins” IL-18 and IL-33 in addition to amplifying both Th1- and Th2-associated cytokines block production of the regulatory cytokine IL-10 in Th1 cultures.

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IL-18 might reflect disease activity in mild and moderate asthma exacerbation

Cited by 130 publications

References 28 publications

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

T helper 1 cells stimulated with ovalbumin and IL-18 induce airway hyperresponsiveness and lung fibrosis by IFN-γ and IL-13 production

Association of interleukin‐18 gene polymorphism with asthma in Chinese patients

IL-1 Family Members IL-18 and IL-33 Upregulate the Inflammatory Potential of Differentiated Human Th1 and Th2 Cultures

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