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IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.

Publication ,  Journal Article
Hu, S; He, W; Du, X; Yang, J; Wen, Q; Zhong, X-P; Ma, L
Published in: EBioMedicine
September 2017

To our knowledge, no studies have examined the role of IL-17 production by neutrophils in immune defense against Mycobacterium tuberculosis (MTB) infection and the pathogenesis of rheumatoid arthritis (RA) caused by MTB infection. Here, we determined that neutrophils express IL-17 in an autocrine IL-6- and IL-23-dependent manner during MTB infection. MTB H37Rv-induced IL-6 production was dependent on the NF-κB, p38, and JNK signaling pathways; however, IL-23 production was dependent on NF-κB and EKR in neutrophils. Furthermore, we found that Toll-like receptor 2 (TLR2) and TLR4 mediated the activation of the kinases NF-κB, p38, ERK, and JNK and the production of IL-6, IL-23, and IL-17 in neutrophils infected with MTB H37Rv. Autocrine IL-17 produced by neutrophils played a vital role in inhibiting MTB H37Rv growth by mediating reactive oxygen species production and the migration of neutrophils in the early stages of infection. However, IL-17 production by neutrophils contributed to collagen-induced arthritis development during MTB infection. Our findings identify a protective mechanism against mycobacteria and the pathogenic role of MTB in arthritis development.

Duke Scholars

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Published In

EBioMedicine

DOI

EISSN

2352-3964

Publication Date

September 2017

Volume

23

Start / End Page

88 / 99

Location

Netherlands

Related Subject Headings

  • Tuberculosis
  • Toll-Like Receptor 4
  • Toll-Like Receptor 2
  • Spleen
  • Neutrophils
  • NF-kappa B
  • Mycobacterium tuberculosis
  • Mice, Knockout
  • Mice
  • MAP Kinase Signaling System
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Hu, S., He, W., Du, X., Yang, J., Wen, Q., Zhong, X.-P., & Ma, L. (2017). IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection. EBioMedicine, 23, 88–99. https://doi.org/10.1016/j.ebiom.2017.08.001
Hu, Shengfeng, Wenting He, Xialin Du, Jiahui Yang, Qian Wen, Xiao-Ping Zhong, and Li Ma. “IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.EBioMedicine 23 (September 2017): 88–99. https://doi.org/10.1016/j.ebiom.2017.08.001.
Hu, Shengfeng, et al. “IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.EBioMedicine, vol. 23, Sept. 2017, pp. 88–99. Pubmed, doi:10.1016/j.ebiom.2017.08.001.

Published In

EBioMedicine

DOI

EISSN

2352-3964

Publication Date

September 2017

Volume

23

Start / End Page

88 / 99

Location

Netherlands

Related Subject Headings

  • Tuberculosis
  • Toll-Like Receptor 4
  • Toll-Like Receptor 2
  • Spleen
  • Neutrophils
  • NF-kappa B
  • Mycobacterium tuberculosis
  • Mice, Knockout
  • Mice
  • MAP Kinase Signaling System