TH2 and TH1 lung inflammation induced by airway allergen sensitization with low and high doses of double-stranded RNA

Jeon, Seong Gyu; Oh, Sun Young; Park, Hye Kyung; Kim, You Sun; Shim, Eun Jin; Lee, Hyun Seung; Oh, Min Hee; Bang, Bo-Ram; Chun, Eunyoung; Kim, Sang Heon; Gho, Yong Song; Zhu, Zhou; Kim, You Young

doi:10.1016/j.jaci.2007.05.030

Cited by 67 publications

(93 citation statements)

References 29 publications

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“…These data confirm that poly(I:C), similar to LPS, can induce sensitization to an allergen, which, after re-exposure, leads to an inflammatory environment supporting the development of allergic airway disease. Moreover, they confirm and expand the observations of Kim and colleagues (51), which demonstrated a Th2-inducing role of low doses of intranasally applied poly(I:C) on the development of an allergic airway disease. Additionally, we show that application of R848 failed to induce an inflammatory cytokine profile.…”

Section: Discussionsupporting

confidence: 89%

TLR3 but Not TLR7/8 Ligand Induces Allergic Sensitization to Inhaled Allergen

Reuter¹,

Dehzad²,

Martin³

et al. 2012

The Journal of Immunology

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Epidemiological studies suggest that viral infections during childhood are a risk factor for the development of asthma. However, the role of virus-specific pattern recognition receptors in this process is not well defined. In the current study, we compare the effects of the inhaled viral TLR ligands polyinosinic-polycytidylic acid (TLR3) and resiquimod (TLR7/8) on sensitization to a model allergen (OVA) in a murine model. Both compounds enhance the migration, activation, and Ag-processing of myeloid dendritic cells from the lung to the draining lymph nodes comparable to the effects of LPS. Application of polyinosinic-polycytidylic acid [poly(I:C)] or LPS induces production of allergen-specific IgE and IgG1, whereas resiquimod (R848) had no effect. In addition, rechallenge of mice with OVA resulted in airway inflammation and mucus production in animals that received either poly(I:C) or LPS but not after application of R848. In summary, these results show that activation of TLR3 in combination with inhaled allergen results in induction of dendritic cell activation and migration similar to the effects of LPS. This leads to the development of allergic airway disease after allergen rechallenge, whereas mice treated with R848 did not develop allergic airway disease. These findings give further insight into the effects of stimulation of different TLRs on the development of asthma.

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Section: Discussionsupporting

confidence: 89%

TLR3 but Not TLR7/8 Ligand Induces Allergic Sensitization to Inhaled Allergen

Reuter¹,

Dehzad²,

Martin³

et al. 2012

The Journal of Immunology

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“…Much clinical evidence indicates that neutrophilic inflammation in the airways is related to asthma severity (1). Neutrophilic inflammation is also important in the pathogenesis of COPD (5).…”

Section: Discussionmentioning

confidence: 99%

“…Cellularity in bronchoalveolar lavage (BAL) fluid was analyzed, as described previously (1). Briefly, after counting the total number of cells in the BAL samples, the cell were stained by Diff-Quik solution and were classified as macrophages, lymphocytes, neutrophils, or eosinophils.…”

Section: The Evaluation Of Copd Phenotypesmentioning

confidence: 99%

“…iological contaminants in indoor air can induce immune dysregulation in the lung, resulting in inflammatory pulmonary disorders, such as asthma and chronic obstructive pulmonary disease (COPD) (1). In terms of the immunopathogenesis of airway inflammation, the eosinophilic subtype represents inflammation induced by IL-4-and IL-13-secreting Th2 cells, whereas the neutrophilic subtype is related to both IFN-g-and IL-17-dependent Th1 and Th17 inflammation (2)(3)(4).…”

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confidence: 99%

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Extracellular Vesicles Derived from Gram-Negative Bacteria, such asEscherichia coli, Induce Emphysema Mainly via IL-17A–Mediated Neutrophilic Inflammation

Kim

Lee

Choi

et al. 2015

The Journal of Immunology

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Recent evidence indicates that Gram-negative bacteria–derived extracellular vesicles (EVs) in indoor dust can evoke neutrophilic pulmonary inflammation, which is a key pathology of chronic obstructive pulmonary disease (COPD). Escherichia coli is a ubiquitous bacterium present in indoor dust and secretes nanometer-sized vesicles into the extracellular milieu. In the current study, we evaluated the role of E. coli–derived EVs on the development of COPD, such as emphysema. E. coli EVs were prepared by sequential ultrafiltration and ultracentrifugation. COPD phenotypes and immune responses were evaluated in C57BL/6 wild-type (WT), IFN-γ–deficient, or IL-17A–deficient mice after airway exposure to E. coli EVs. The present study showed that indoor dust from a bed mattress harbors E. coli EVs. Airway exposure to E. coli EVs increased the production of proinflammatory cytokines, such as TNF-α and IL-6. In addition, the repeated inhalation of E. coli EVs for 4 wk induced neutrophilic inflammation and emphysema, which are associated with enhanced elastase activity. Emphysema and elastase activity enhanced by E. coli EVs were reversed by the absence of IFN-γ or IL-17A genes. In addition, during the early period, lung inflammation is dependent on IL-17A and TNF-α, but not on IFN-γ, and also on TLR4. Moreover, the production of IFN-γ is eliminated by the absence of IL-17A, whereas IL-17A production is not abolished by IFN-γ absence. Taken together, the present data suggest that E. coli–derived EVs induce IL-17A–dependent neutrophilic inflammation and thereby emphysema, possibly via upregulation of elastase activity.

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“…For example, the number of patients with Th1 diseases such as Crohn's disease and rheumatoid arthritis have also increased recently, and Th2, but not Th1, is induced by a stimulus of a low concentration of toll-like receptor 3 (TLR3), which forms a complex with double-stranded RNA. 10) Furthermore, immune T cells other than Th1 and Th2 have been found to exhibit a close relationship with the recent increase in autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

Participation of Th17 and Treg Cells in Pediatric Bronchial Asthma

Yamamoto

Negoro

Wakagi

et al. 2010

JOURNAL OF HEALTH SCIENCE

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The immune response plays an important role in the development of allergic diseases. It is established that a complex network of various immunocytes such as Th2, non-Th2 (Th17), and regulatory T (Treg) participate in allergic reactions. In this study, we examined the frequencies of Th17 cells (IL-17-positive cells) and Treg cells (FOXP3-positive cells) in the peripheral blood and elucidated their participation in pediatric allergic diseases such as bronchial asthma and food allergies. Our study included 35 subjects, 27 with allergic diseases (19 with asthma and 8 with food allergies) and 8 were controls (without any allergic diseases); their age ranged from 1 to 13 years. The frequency of Th17 cells (IL-17-positive cells) among the CD4 + T cells in the peripheral blood was 2.33 ± 1.29% in patients with bronchial asthma, 1.53 ± 1.34% in those with food allergies, and 1.50 ± 0.809% in controls. These results indicated that only the patients with bronchial asthma had a trend towards a higher frequency of Th17 cells (p = 0.1558). The ratio of Th17 cells to Treg cells did not show any statistical correlation among the patients with bronchial asthma. However, when we excluded the patients with a severe type of asthma, we could obtain an inverse trend between the ratio of Th17 cells to Treg cells (p = 0.1655). This study suggested that Th17 cells and Treg cells participate in pediatric allergic reactions such as bronchial asthma.

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TH2 and TH1 lung inflammation induced by airway allergen sensitization with low and high doses of double-stranded RNA

Cited by 67 publications

References 29 publications

TLR3 but Not TLR7/8 Ligand Induces Allergic Sensitization to Inhaled Allergen

TLR3 but Not TLR7/8 Ligand Induces Allergic Sensitization to Inhaled Allergen

Extracellular Vesicles Derived from Gram-Negative Bacteria, such asEscherichia coli, Induce Emphysema Mainly via IL-17A–Mediated Neutrophilic Inflammation

Participation of Th17 and Treg Cells in Pediatric Bronchial Asthma

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