title: Modulation of human peripheral blood eosinophil function by tumor necrosis factor-alpha.
abstract: Eosinophils are important effectors in helminthic parasitic infection. Tumor necrosis factor (TNF-alpha) has been implicated as a mediator in the host response to parasitic infection and enhances eosinophil-mediated helminthotoxicity. We have examined the direct effects of recombinant human (rh) TNF on eosinophil functions of degranulation and oxidative metabolism. This report describes the minimal effects of rhTNF-alpha on eosinophil superoxide anion generation and enzyme secretion, which do not satisfactorily explain the observed increases in helminthotoxicity. In contrast to other cell types, eosinophils are unique in their differential responses to interleukin-1 beta and TNF.
authors.affiliation: Department of Medicine, Tufts University School of Medicine, New England Medical Center Hospital, Boston, Mass.
authors.forename: E A
authors.initials: EA
authors.lastname: Whitcomb
authors.forename: J H
authors.initials: JH
authors.lastname: Wesolek
authors.forename: S H
authors.initials: SH
authors.lastname: Pincus
mesh_terms: D001192:Arylsulfatases / Q000378:metabolism; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D010587:Phagocytosis; D011994:Recombinant Proteins; D012636:Secretory Rate / Q000187:drug effects; D013481:Superoxides / Q000096:biosynthesis*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D001192:Arylsulfatases; D005966:Glucuronidase