Interleukin-17 mediates lung injury by promoting neutrophil accumulation during the development of contagious caprine pleuropneumonia

•CCPP is a highly contagious infectious disease of goats caused by Mccp infection.•Neutrophil infiltrates were present within the alveoli of CCPP goats.•IL-17 stimulated the production of neutrophil chemoattractants from lung epithelial cells.•These results should aid understanding of pathogenesis a...

Full description

Saved in:
Bibliographic Details
Published in:Veterinary microbiology 2020-04, Vol.243, p.108651-108651, Article 108651
Main Authors: Ma, Wen-Tao, Gu, Kui, Yang, Rui, Tang, Xi-Dian, Qi, Yu-Xu, Liu, Ming-Jie, Chen, De-Kun
Format: Article
Language:English
Subjects:
Chemotactic factors
Contagious caprine pleuropneumonia
Cytokine
Epithelial cells
Goats
IL-17
Infectious diseases
Inflammation
Interleukin 17
Leukocytes (neutrophilic)
Lungs
Morbidity
Neutrophil
Neutrophils
Pathogenesis
Pleuropneumonia
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:•CCPP is a highly contagious infectious disease of goats caused by Mccp infection.•Neutrophil infiltrates were present within the alveoli of CCPP goats.•IL-17 stimulated the production of neutrophil chemoattractants from lung epithelial cells.•These results should aid understanding of pathogenesis and control of goat CCPP. Contagious caprine pleuropneumonia (CCPP) is a highly contagious infectious disease of goats caused by Mycoplasma capricolum subspecies capripneumoniae (Mccp). CCPP outbreaks usually result in high morbidity and mortality of the affected goats, making this disease a major cause of economic losses to goat producers globally. However, the pathogenesis of CCPP remains unclear. Here, we show that IL-17-driven neutrophil accumulation is involved in the lung damage in CCPP goats. During CCPP development, intense inflammatory infiltrates could be observed in the injured lungs. Specifically, neutrophils were observed to be present within the alveoli. Increased IL-17 release drove the excessive influx of neutrophils into the lung, as IL-17 effectively stimulated the production of neutrophil chemoattractants from lung epithelial cells following Mccp infection. Our data highlight a critical role of IL-17-driven neutrophil accumulation in the pathogenesis of CCPP and suggest that IL-17 may potentially be a useful immunotherapeutic target for the treatment of CCPP.
ISSN:0378-1135
1873-2542
DOI:10.1016/j.vetmic.2020.108651