<i><scp>S</scp>taphylococcus aureus</i>‐derived extracellular vesicles induce neutrophilic pulmonary inflammation via both <scp>T</scp>h1 and <scp>T</scp>h17 cell responses

Kim, M.-R.; Hong, Sung Wook; Choi, Eunjeong; Lee, Won Hee; Kim, Y.-S.; Jeon, Seong Gyu; Jang, Myoung Ho; Gho, Yong Song; Kim, Y.-K.

doi:10.1111/all.12001

Cited by 126 publications

(142 citation statements)

References 41 publications

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“…In addition, our previous work indicates that EVs in indoor dust are important in the development of neutrophilic inflammation in the lung (11). Previously, we also found that the Grampositive bacterium S. aureus produces EVs (9), which may be causally related to atopic dermatitis in the skin (28) and also neutrophilic inflammation in the lung (12). The present study showed that the repeated inhalation of E. coli EVs induced neutrophilic inflammation and thereby emphysema mainly via an IL-17A-dependent mechanism.…”

Section: Discussionsupporting

confidence: 72%

“…Our previous work has shown that E. coliderived EVs induce systemic inflammation mimicking sepsis after entering the bloodstream (10) and that EVs from indoor dust and also from Staphylococcus aureus can induce neutrophilic pulmonary inflammation (11,12). In the current study, we hypothesized that EVs from Gram-negative bacteria, especially E. coli, are an important cause of neutrophilic inflammation and thereby emphysema in the lung.…”

mentioning

confidence: 88%

“…Wild-type (WT), IFN-g-deficient, and TNF-a-deficient mice (12,13) (all C57BL/6 background) were purchased from The Jackson Laboratory (Bar Harbor, ME). IL-17A-deficient mice (C57BL/6 background) were gifted from Y.-C.…”

Section: Mice and Cell Culturesmentioning

confidence: 99%

“…IL-17A-deficient mice (C57BL/6 background) were gifted from Y.-C. Sung (Pohang University of Science and Technology [POSTECH], Pohang, Republic of Korea) (12). TLR2-deficient and TLR4-deficient mice (12) (both of C57BL/6 background) were purchased from Oriental BioService (Kyoto, Japan).…”

Section: Mice and Cell Culturesmentioning

confidence: 99%

“…To examine in vitro innate immune responses induced by E. coli-derived EVs in WT, TLR2-deficient, and TLR4-deficient mice, peritoneal macrophages were isolated as described previously (12). Briefly, thioglycollate-elicited peritoneal macrophages were seeded in 24-well plates, incubated with E. coli-derived EVs, TLR2 agonist (heat-killed Listeria monocytogenes, 10 7 cells/ml), or TLR4 agonist (LPS from E. coli K12), and the culture supernatants were collected 16 h after the application.…”

Section: The In Vitro Analysis Of Innate Immune Responsementioning

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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Section: Discussionsupporting

confidence: 72%

mentioning

confidence: 88%

Section: Mice and Cell Culturesmentioning

confidence: 99%

Section: Mice and Cell Culturesmentioning

confidence: 99%

Section: The In Vitro Analysis Of Innate Immune Responsementioning

confidence: 99%

See 3 more Smart Citations

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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Escherichia coli–derived and Staphylococcus aureus–derived extracellular vesicles induce MUC5AC expression via extracellular signal related kinase 1/2 and p38 mitogen‐activated protein kinase in human airway epithelial cells

Bae

Choi

Song

et al. 2016

Int Forum Allergy Rhinol

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In vitro characteristics of an airway barrier‐disrupting factor secreted by Staphylococcus aureus

Murphy

Ramezanpour

Drilling

et al. 2018

Int Forum Allergy Rhinol

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BackgroundStaphylococcus aureus is a major contributor to the pathophysiology of chronic rhinosinusitis (CRS). Previous research has shown that S. aureus–secreted products disrupt the airway barrier.MethodsS. aureus ATCC 13565 and 25923 strains were grown at exponential, postexponential, and stationary phases. Microbial conditioned media (CM) was collected from the cultures and ultrafiltered (UF). Liquid chromatography–electrospray ionization tandem mass spectrometry (LC‐ESI‐MS/MS) was performed on the UF‐CM. UF‐CM was subjected to heat and protease treatment, size fractionation, and ultracentrifugation (UC) separation. Human nasal epithelial cells grown at air‐liquid interface (HNEC‐ALI) cultures were exposed to purified alpha hemolysin (Hla), staphylococcal enterotoxin A (SEA), lipoteichoic acid (LTA), and UF‐CM. Barrier function outcomes were measured by transepithelial electrical resistance (TEER) and apparent permeability (Papp). UC fraction exposed cultures were subjected to immunofluorescence microscopy for tight junction (TJ) protein zonula occludens‐1 (ZO‐1).ResultsLC‐ESI‐MS/MS identified 107 proteins, with Hla being most abundant. Hla, SEA, and LTA did not alter the HNEC‐ALI barrier as measured by TEER or Papp. Barrier disruption caused by UF‐CM peaked in the postexponential phase, was sensitive to heat and protease treatment, >30‐kDa in size, and enriched in the UC fraction. HNEC‐ALI exposed to UF‐CM and UC demonstrated loss of ZO‐1 localization.ConclusionThese results suggest that the S. aureus factor responsible for TJ disruption in HNEC‐ALI cultures is either a protein‐macromolecule or a combination of secreted factors. The product is enriched in the UC fraction, suggesting it is associated with large structures such as membrane components or vesicles.

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

Abstract: Staphylococcus aureus EV can induce Th1 and Th17 neutrophilic pulmonary inflammation, mainly in a TLR2-dependent manner. Additionally, S. aureus EV enhance the development of airway hypersensitivity to inhaled allergens.

Cited by 126 publications

References 41 publications

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

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

Escherichia coli–derived and Staphylococcus aureus–derived extracellular vesicles induce MUC5AC expression via extracellular signal related kinase 1/2 and p38 mitogen‐activated protein kinase in human airway epithelial cells

In vitro characteristics of an airway barrier‐disrupting factor secreted by Staphylococcus aureus

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