Microbe-dependent lymphatic migration of neutrophils modulates lymphocyte proliferation in lymph nodes

Nat Commun. 2015 May 14:6:7139. doi: 10.1038/ncomms8139.

Abstract

Neutrophil recruitment to the site of injury is an essential first step of an anti-bacterial response. However, little is known about the basis for and relevance of neutrophil migration from inflamed tissue into lymphoid organs. We established a photoconversion-based system to monitor the fate of neutrophils recruited to inflamed skin. While neutrophils are efficiently recruited to sites of both microbial and sterile lesions, subsequent re-localization to draining lymph nodes happens only when bacteria are present in the primary lesion. Skin egress of neutrophils occurs via lymphatic vessels and is dependent on CD11b and CXCR4 but not CCR7. Neutrophils are the predominant immune cell to migrate from inflamed skin into lymph nodes where they augment lymphocyte proliferation. Furthermore, inhibition of neutrophil migration from skin reduces T-cell proliferation in draining lymph nodes. Thus neutrophils mediate rapid cellular communication between the initial injury site and secondary lymphoid organs and modulate immune responsiveness.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Infections / blood
  • CD11b Antigen / biosynthesis
  • Cell Movement
  • Female
  • Immune System
  • Inflammation
  • Lymph Nodes / pathology*
  • Lymphatic Vessels
  • Lymphocyte Activation / immunology
  • Lymphocytes / cytology
  • Lymphocytes / microbiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neutrophil Infiltration*
  • Neutrophils / cytology
  • Neutrophils / microbiology*
  • Phenotype
  • Receptors, CCR7 / biosynthesis
  • Receptors, CXCR4 / biosynthesis
  • Skin / microbiology
  • Staphylococcus aureus / metabolism

Substances

  • CD11b Antigen
  • CXCR4 protein, mouse
  • Ccr7 protein, mouse
  • Receptors, CCR7
  • Receptors, CXCR4