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Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2.

Publication ,  Journal Article
Li, JL; Lim, CH; Tay, FW; Goh, CC; Devi, S; Malleret, B; Lee, B; Bakocevic, N; Chong, SZ; Evrard, M; Tanizaki, H; Lim, HY; Russell, B ...
Published in: J Invest Dermatol
February 2016

Deposition of immune complexes (ICs) in tissues triggers acute inflammatory pathology characterized by massive neutrophil influx leading to edema and hemorrhage, and is especially associated with vasculitis of the skin, but the mechanisms that regulate this type III hypersensitivity process remain poorly understood. Here, using a combination of multiphoton intravital microscopy and genomic approaches, we re-examined the cutaneous reverse passive Arthus reaction and observed that IC-activated neutrophils underwent transmigration, triggered further IC formation, and transported these ICs into the interstitium, whereas neutrophil depletion drastically reduced IC formation and ameliorated vascular leakage in vivo. Thereafter, we show that these neutrophils expressed high levels of CXCL2, which further amplified neutrophil recruitment and activation in an autocrine and/or paracrine manner. Notably, CXCL1 expression was restricted to tissue-resident cell types, but IC-activated neutrophils may also indirectly, via soluble factors, modulate macrophage CXCL1 expression. Consistent with their distinct cellular origins and localization, only neutralization of CXCL2 but not CXCL1 in the interstitium effectively reduced neutrophil recruitment. In summary, our study establishes that neutrophils are able to self-regulate their own recruitment and responses during IC-mediated inflammation through a CXCL2-driven feed forward loop.

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Published In

J Invest Dermatol

DOI

EISSN

1523-1747

Publication Date

February 2016

Volume

136

Issue

2

Start / End Page

416 / 424

Location

United States

Related Subject Headings

  • RNA, Messenger
  • Neutrophils
  • Neutrophil Infiltration
  • Mice, Inbred C57BL
  • Mice
  • Mast Cells
  • Male
  • Macrophages
  • Inflammation Mediators
  • Immune Complex Diseases
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Li, J. L., Lim, C. H., Tay, F. W., Goh, C. C., Devi, S., Malleret, B., … Ng, L. G. (2016). Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2. J Invest Dermatol, 136(2), 416–424. https://doi.org/10.1038/JID.2015.410
Li, Jackson LiangYao, Chun Hwee Lim, Fen Wei Tay, Chi Ching Goh, Sapna Devi, Benoit Malleret, Bernett Lee, et al. “Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2.J Invest Dermatol 136, no. 2 (February 2016): 416–24. https://doi.org/10.1038/JID.2015.410.
Li JL, Lim CH, Tay FW, Goh CC, Devi S, Malleret B, et al. Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2. J Invest Dermatol. 2016 Feb;136(2):416–24.
Li, Jackson LiangYao, et al. “Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2.J Invest Dermatol, vol. 136, no. 2, Feb. 2016, pp. 416–24. Pubmed, doi:10.1038/JID.2015.410.
Li JL, Lim CH, Tay FW, Goh CC, Devi S, Malleret B, Lee B, Bakocevic N, Chong SZ, Evrard M, Tanizaki H, Lim HY, Russell B, Renia L, Zolezzi F, Poidinger M, Angeli V, St John AL, Harris JE, Tey HL, Tan SM, Kabashima K, Weninger W, Larbi A, Ng LG. Neutrophils Self-Regulate Immune Complex-Mediated Cutaneous Inflammation through CXCL2. J Invest Dermatol. 2016 Feb;136(2):416–424.
Journal cover image

Published In

J Invest Dermatol

DOI

EISSN

1523-1747

Publication Date

February 2016

Volume

136

Issue

2

Start / End Page

416 / 424

Location

United States

Related Subject Headings

  • RNA, Messenger
  • Neutrophils
  • Neutrophil Infiltration
  • Mice, Inbred C57BL
  • Mice
  • Mast Cells
  • Male
  • Macrophages
  • Inflammation Mediators
  • Immune Complex Diseases