title: Microbe-dependent lymphatic migration of neutrophils modulates lymphocyte proliferation in lymph nodes.
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.
authors.affiliation: 1] Immunology Division, The Garvan Institute of Medical Research, 384 Victoria street, Darlinghurst, New South Wales 2010, Australia [2] St Vincent's Clinical School, Faculty of Medicine, UNSW Australia, 390 Victoria street, Darlinghurst, New South Wales 2010, Australia.
authors.forename: Henry R
authors.initials: HR
authors.lastname: Hampton
authors.affiliation: Immunology Division, The Garvan Institute of Medical Research, 384 Victoria street, Darlinghurst, New South Wales 2010, Australia.
authors.forename: Jacqueline
authors.initials: J
authors.lastname: Bailey
authors.affiliation: Laboratory of Immunology Faculty of Pharmacy, Osaka-Ohtani University 3-11-1 Nishikiorikita,Tondabayashi-city, Osaka prefecture, 584-8540, Japan.
authors.forename: Michio
authors.initials: M
authors.lastname: Tomura
authors.affiliation: 1] Immunology Division, The Garvan Institute of Medical Research, 384 Victoria street, Darlinghurst, New South Wales 2010, Australia [2] St Vincent's Clinical School, Faculty of Medicine, UNSW Australia, 390 Victoria street, Darlinghurst, New South Wales 2010, Australia.
authors.forename: Robert
authors.initials: R
authors.lastname: Brink
authors.affiliation: 1] Immunology Division, The Garvan Institute of Medical Research, 384 Victoria street, Darlinghurst, New South Wales 2010, Australia [2] St Vincent's Clinical School, Faculty of Medicine, UNSW Australia, 390 Victoria street, Darlinghurst, New South Wales 2010, Australia.
authors.forename: Tatyana
authors.initials: T
authors.lastname: Chtanova
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000097:blood; D039481:CD11b Antigen / Q000096:biosynthesis; D002465:Cell Movement; D005260:Female; D007107:Immune System; D007249:Inflammation; D008198:Lymph Nodes / Q000473:pathology*; D042601:Lymphatic Vessels; D008213:Lymphocyte Activation / Q000276:immunology; D008214:Lymphocytes / Q000166:cytology / Q000382:microbiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D020556:Neutrophil Infiltration; D009504:Neutrophils / Q000166:cytology / Q000382:microbiology*; D010641:Phenotype; D054400:Receptors, CCR7 / Q000096:biosynthesis; D019718:Receptors, CXCR4 / Q000096:biosynthesis; D012867:Skin / Q000382:microbiology; D013211:Staphylococcus aureus / Q000378:metabolism
chemical_list: D039481:CD11b Antigen; C514936:CXCR4 protein, mouse; C515371:Ccr7 protein, mouse; D054400:Receptors, CCR7; D019718:Receptors, CXCR4