title: An essential role for TH2-type responses in limiting acute tissue damage during experimental helminth infection.
abstract: Helminths induce potent T helper 2 (TH2)-type immune responses that can mediate worm expulsion, but the role of this response in controlling the acute tissue damage caused by migrating multicellular parasites through vital tissues remains uncertain. We used a helminth infection model in which parasitic nematode larvae migrate transiently through the lung, resulting in hemorrhage and inflammation. We found that IL-17 initially contributed to inflammation and lung damage, whereas subsequent IL-4 receptor (IL-4R) signaling reduced elevations in IL-17 mRNA levels, enhanced the expression of insulin-like growth factor 1 (IGF-1) and IL-10 and stimulated the development of M2 macrophages, all of which contributed to the rapid resolution of tissue damage. These studies indicate an essential role for TH2-type immune responses in mediating acute wound healing during helminth infection.
authors.affiliation: Department of Medicine and Center for Immunity and Inflammation, New Jersey Medical School, University of Medicine & Dentistry of New Jersey, Newark, New Jersey, USA.
authors.forename: Fei
authors.initials: F
authors.lastname: Chen
authors.forename: Zhugong
authors.initials: Z
authors.lastname: Liu
authors.forename: Wenhui
authors.initials: W
authors.lastname: Wu
authors.forename: Cristina
authors.initials: C
authors.lastname: Rozo
authors.forename: Scott
authors.initials: S
authors.lastname: Bowdridge
authors.forename: Ariel
authors.initials: A
authors.lastname: Millman
authors.forename: Nico
authors.initials: N
authors.lastname: Van Rooijen
authors.forename: Joseph F
authors.initials: JF
authors.lastname: Urban
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Wynn
authors.forename: William C
authors.initials: WC
authors.lastname: Gause
mesh_terms: D000818:Animals; D005260:Female; D006374:Helminthiasis, Animal / Q000276:immunology*; D006470:Hemorrhage / Q000276:immunology / Q000469:parasitology; D007111:Immunity, Cellular; D007249:Inflammation / Q000276:immunology / Q000469:parasitology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D020381:Interleukin-17 / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D008168:Lung / Q000098:blood supply / Q000276:immunology / Q000469:parasitology; D008174:Lung Diseases, Parasitic / Q000276:immunology / Q000469:parasitology; D008264:Macrophages / Q000276:immunology / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D020556:Neutrophil Infiltration / Q000276:immunology; D009504:Neutrophils / Q000502:physiology; D009559:Nippostrongylus / Q000276:immunology; D017206:Strongylida Infections / Q000276:immunology; D018418:Th2 Cells / Q000502:physiology*
chemical_list: D020381:Interleukin-17; D015847:Interleukin-4; D007334:Insulin-Like Growth Factor I