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

Kim, Y.-S.; Choi, Eun Jung; Lee, Won Hee; Choi, Sang Joon; Roh, Tae-Young; Park, J.; Jee, Young Koo; Zhu, Zhaohui; Koh, Young Yull; Gho, Yong Song; Kim, Y.-K.

doi:10.1111/cea.12085

Cited by 78 publications

(87 citation statements)

References 34 publications

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“…In contrast, repeated airway administration of LPS mEV isolated from indoor house dust to mice led to neutrophilic pulmonary inflammation with infiltration of Th1 and Th17 cells [143]. The vesicles were internalized by airway epithelial cells and alveolar macrophages.…”

Section: Role Of Bacterial Mev Of Dust In Airway Remodeling During Atmentioning

confidence: 99%

Functions of Exosomes and Microbial Extracellular Vesicles in Allergy and Contact and Delayed-Type Hypersensitivity

Nazimek

Bryniarski²,

Askenase³

2016

Int Arch Allergy Immunol

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Extracellular vesicles, such as exosomes, are newly recognized intercellular conveyors of functional molecular mechanisms. Notably, they transfer RNAs and proteins between different cells that can then participate in the complex pathogenesis of allergic and related hypersensitivity responses and disease mechanisms, as described herein. This review highlights this important new appreciation of the in vivo participation of such extracellular vesicles in the interactions between allergy-mediating cells. We take into account paracrine epigenetic exchanges mediated by surrounding stromal cells and the endocrine receipt of exosomes from distant cells via the circulation. Exosomes are natural ancient nanoparticles of life. They are made by all cells and in some form by all species down to fungi and bacteria, and are present in all fluids. Besides a new focus on their role in the transmission of genetic regulation, exosome transfer of allergens was recently shown to induce allergic inflammation. Importantly, regulatory and tolerogenic exosomes can potently inhibit allergy and hypersensitivity responses, usually acting nonspecifically, but can also proceed in an antigen-specific manner due to the coating of the exosome surface with antibodies. Deep analysis of processes mediated by exosomes should result in the development of early diagnostic biomarkers, as well as allergen-specific, preventive and therapeutic strategies. These will likely significantly diminish the risks of current allergen-specific parenteral desensitization procedures, and of the use of systemic immunosuppressive drugs. Since extracellular vesicles are physiological, they can be fashioned for the specific delivery of therapeutic molecular instructions through easily tolerated, noninvasive routes, such as oral ingestion, nasal administration, and perhaps even inhalation.

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Section: Role Of Bacterial Mev Of Dust In Airway Remodeling During Atmentioning

confidence: 99%

Functions of Exosomes and Microbial Extracellular Vesicles in Allergy and Contact and Delayed-Type Hypersensitivity

Nazimek

Bryniarski²,

Askenase³

2016

Int Arch Allergy Immunol

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“…Previous reports indicate that organic dust can induce airway inflammation related with Th1/Th17 cell responses or TLR2 signaling (23,24). Our previous findings showed that indoor dust collected from bed mattress induces neutrophilic pulmonary inflammation and that EVs in indoor dust also induce neutrophilic pulmonary inflammation, which is related with Th1 and Th17 cell responses (25). To our knowledge, this is the first report demonstrating that EVs derived from Gram-negative bacteria, especially E. coli, can induce neutrophilic inflammation and thereby emphysema mainly in an IL-17A-dependent manner.…”

Section: Discussionmentioning

confidence: 86%

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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“…Bacterial components in indoor dust, such as nanometre-sized extracellular vesicles, can evoke neutrophilic inflammation as well. In a mouse model of asthma, repeated intranasal application of indoor dust induced neutrophilic pulmonary inflammation accompanied by lung infiltration with both Th1 and Th17 cells [26].…”

Section: Animal Models For Non-eosinophilic Asthmamentioning

confidence: 99%

Non-eosinophilic Asthma Endotypes

Agache

2015

Curr Treat Options Allergy

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

Abstract: Indoor dust EV, especially derived from Gram-negative bacteria, is a possible causative agent of neutrophilic airway diseases.

Cited by 78 publications

References 34 publications

Functions of Exosomes and Microbial Extracellular Vesicles in Allergy and Contact and Delayed-Type Hypersensitivity

Functions of Exosomes and Microbial Extracellular Vesicles in Allergy and Contact and Delayed-Type Hypersensitivity

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

Non-eosinophilic Asthma Endotypes

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