Differential neutrophil activation in viral infections: Enhanced TLR-7/8-mediated CXCL8 release in asthma

Autor: Patrick C. Reading, Dominik Hartl, Brian G. Oliver, David Van Ly, Janette K. Burgess, Francesca Tang, Kirsten Spann, Katherine J. Baines
Přispěvatelé: Groningen Research Institute for Asthma and COPD (GRIAC), Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)
Jazyk: angličtina
Rok vydání: 2016
Předmět:
Lipopolysaccharides
Male
0301 basic medicine
Neutrophils
Respiratory System
formylmethionylleucylphenylalanine
Human rhinovirus
viral respiratory tract infection
Neutrophil Activation
chemistry.chemical_compound
Multiplicity of infection
Viral Respiratory Tract Infection
leukocyte elastase
leukocyte activation
neutrophils
resiquimod
Medicine
innate immunity
virus replication
clinical article
biology
beta 2 adrenergic receptor stimulating agent
adult
Toll-Like Receptors
lipopolysaccharide
article
neutrophil
N-Formylmethionine leucyl-phenylalanine
protein function
Orthomyxoviridae
Symptom Flare Up
forced expiratory volume
Respiratory Syncytial Viruses
3. Good health
polyinosinic polycytidylic acid
enzyme activity
respiratory virus
N-Formylmethionine Leucyl-Phenylalanine
rhinovirus
female
Matrix Metalloproteinase 9
cytokine release
priority journal
Virus Diseases
Neutrophil elastase
Respiratory virus
Female
medicine.symptom
enzyme release
Adult
Pulmonary and Respiratory Medicine
corticosteroid
Inflammation
interleukin 8
gelatinase B
reverse transcription polymerase chain reaction
03 medical and health sciences
cell isolation
male
respiratory viruses
Human respiratory syncytial virus
Humans
controlled study
Interleukin 8
human
degranulation
business.industry
human cell
Interleukin-8
short acting drug
asthma
supernatant
Asthma
toll like receptor 7
toll like receptor 8
enzyme linked immunosorbent assay
imiquimod
030104 developmental biology
chemistry
innate immune responses
Polyinosinic:polycytidylic acid
Immunology
disease exacerbation
biology.protein
Leukocyte Elastase
business
Influenza virus
Zdroj: Respirology, 21(1), 172-179. Wiley
ISSN: 1323-7799
Popis: © 2015 The Authors. Respirology published by Wiley Publishing Asia Pty Ltd on behalf of Asian Pacific Society of Respirology. Background and objective Respiratory viral infections are a major cause of asthma exacerbations. Neutrophils accumulate in the airways and the mechanisms that link neutrophilic inflammation, viral infections and exacerbations are unclear. This study aims to investigate anti-viral responses in neutrophils from patients with and without asthma and to investigate if neutrophils can be directly activated by respiratory viruses. Methods Neutrophils from peripheral blood from asthmatic and non-asthmatic individuals were isolated and stimulated with lipopolysaccharide (LPS) (1 μg/mL), f-met-leu-phe (fMLP) (100 nM), imiquimod (3 μg/mL), R848 (1.5 μg/mL), poly I:C (10 μg/mL), RV16 (multiplicity of infection (MOI)1), respiratory syncytial virus (RSV) (MOI1) or influenza virus (MOI1). Cell-free supernatants were collected after 1 h of neutrophil elastase (NE) and matrix metalloproteinase (MMP)-9 release, or after 24 h for CXCL8 release. Results LPS, fMLP, imiquimod and R848 stimulated the release of CXCL8, NE and MMP-9 whereas poly I:C selectively induced CXCL8 release only. R848-induced CXCL8 release was enhanced in neutrophils from asthmatics compared with non-asthmatic cells (P < 0.01). RSV triggered the release of CXCL8 and NE from neutrophils, whereas RV16 or influenza had no effect. Conclusion Neutrophils release CXCL8, NE and MMP-9 in response to viral surrogates with R848-induced CXCL8 release being specifically enhanced in asthmatic neutrophils. Toll-like receptor (TLR7/8) dysregulation may play a role in neutrophilic inflammation in viral-induced exacerbations. We aimed to investigate and compare neutrophil responses to bacterial compounds and viral mimetics as well as compare responses between people with and without asthma. We also investigated neutrophil responses to live respiratory viruses. Here we provide a novel comprehensive comparison showing differential and specific activation in innate immune cells. See Editorial, page 10
Databáze: OpenAIRE
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