Y.-K. Kim

Extracellular vesicles derived from Staphylococcus aureus induce atopic dermatitis‐like skin inflammation

To cite this article: Hong S‐W, Kim M‐R, Lee E‐Y, Kim JH, Kim Y‐S, Jeon SG, Yang J‐M, Lee B‐J, Pyun B‐Y, Gho YS, Kim Y‐K. Extracellular vesicles derived from Staphylococcus aureus induce atopic dermatitis‐like skin inflammation. Allergy 2011; 66: 351–359.

Staphylococcus aureus-derived extracellular vesicles induce neutrophilic pulmonary inflammation via both Th1 and Th17 cell responses.

Recent evidence indicates that Staphylococcus aureus, one of the most important human pathogens, secretes vesicles into the extracellular milieu.

Decreased diversity of nasal microbiota and their secreted extracellular vesicles in patients with chronic rhinosinusitis based on a metagenomic analysis

Chronic rhinosinusitis (CRS) is an inflammatory process in the nasal cavity and paranasal sinuses, and bacteria have been considered to be a cause. Indeed, recent evidence indicates that bacteria‐derived extracellular vesicles (EV) appear to be an important causative agent of inflammatory diseases. Here, we aimed to evaluate the diversity of nasal microbiota and their secreted EV in patients with CRS.

Extracellular vesicles, especially derived from Gram-negative bacteria, in indoor dust induce neutrophilic pulmonary inflammation associated with both Th1 and Th17 cell responses

Many bacterial components in indoor dust can evoke inflammatory pulmonary diseases. Bacteria secrete nanometre‐sized vesicles into the extracellular milieu, but it remains to be determined whether bacteria‐derived extracellular vesicles in indoor dust are pathophysiologically related to inflammatory pulmonary diseases.

Immunomodulating effects of endotoxin in mouse models of allergic asthma.

Endotoxin or lipopolysaccharide (LPS) is a cell wall component of Gram‐negative bacteria. Like aeroallergens, LPS is ubiquitous in our living environment. Epidemiology studies in young children have found that LPS exposure at home is inversely correlated with the development of atopic diseases, thus the ‘hygiene hypothesis’ for allergic diseases. However, positive association has also been found between indoor LPS exposure and the development of wheezing or asthma in children. In humans, experimental exposure to LPS in the airways can cause inflammatory responses and lung function changes directly or modulate responses to allergens indirectly, particularly in those with asthma. In animal studies, experimental exposure to LPS has generated some conflicting, sometimes opposite, results in host responses to allergen stimulation. In this article, we will review recent advances in our understanding of the immunomodulating effects of LPS on allergen‐induced responses and analyse some of the possible reasons for the inconsistent findings.

A viral PAMP double-stranded RNA induces allergen-specific Th17 cell response in the airways which is dependent on VEGF and IL-6.

To cite this article: Choi J‐P, Kim Y‐S, Tae Y‐M, Choi E‐J, Hong B‐S, Jeon SG, Gho YS, Zhu Z, Kim Y‐K. A viral PAMP double‐stranded RNA induces allergen‐specific Th17 cell response in the airways which is dependent on VEGF and IL‐6. Allergy 2010; 65: 1322–1330.

Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung.

To cite this article: Moon H‐G, Tae Y‐M, Kim Y‐S, Gyu Jeon S, Oh S‐Y, Song Gho Y, Zhu Z, Kim Y‐K. Conversion of Th17‐type into Th2‐type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung. Allergy 2010; 65: 1093–1103.

15‐lipoxygenase metabolites play an important role in the development of a T‐helper type 1 allergic inflammation induced by double‐stranded RNA

Background We recently demonstrated that the T‐helper type 1 (Th1) immune response plays an important role in the development of non‐eosinophilic inflammation induced by airway exposure of an allergen plus double‐stranded RNA (dsRNA). However, the role of lipoxygenase (LO) metabolites in the development of Th1 inflammation is poorly understood.

TNF-alpha is a key mediator in the development of Th2 cell response to inhaled allergens induced by a viral PAMP double-stranded RNA

Viral pathogen–associated molecular patterns, such as dsRNA, disrupt airway tolerance to inhaled allergens. Specifically, the Th2 and Th17 cell responses are induced by low‐dose dsRNA and the Th1‐dominant response by high‐dose dsRNA.

Association and functional relevance of E237G, a polymorphism of the high‐affinity immunoglobulin E‐receptor β chain gene, to airway hyper‐responsiveness

Background The hyper‐sensitivity reaction of IgE, with its high‐affinity receptors (FcɛRI), is central to the phenomenon of atopic diseases.