Literature DB >> 6343237

Two inhibitors of neutrophil chemotaxis are produced by hyperimmunoglobulin E recurrent infection syndrome mononuclear cells exposed to heat-killed staphylococci.

H Donabedian, J I Gallin.   

Abstract

Mononuclear cells from normal volunteers and from patients with the hyperimmunoglobulin E recurrent infection syndrome (HIE) were cultured for 18 h with and without opsonized, heat-killed Staphylococcus aureus (OS). The supernatants from normal mononuclear cell cultures without OS revealed no inhibitory activity for neutrophil chemotaxis, whereas those from HIE patients revealed the previously reported 61,000-dalton factor. However, when normal cells were cultured with OS, they produced a proteinaceous, 56 degrees C-stable, 30,000- to 45,000-dalton factor which preferentially inhibited neutrophil versus monocyte chemotaxis. When HIE cells were exposed to OS, they produced the same 30,000- to 45,000-dalton factor as normal cells, as well as the 61,000-dalton factor that they produced spontaneously. Assay of 1,000-fold dilutions of supernatants from cultures of normal mononuclear cells with OS revealed a mean production of 7.8 +/- 5.4% inhibition of chemotaxis, whereas assay of 1,000-fold dilutions of supernatants from cultures of HIE mononuclear cells (spontaneously producing the 61,000-dalton factor) with OS revealed a 26.6 +/- 3.6% inhibition (P less than 0.02). The data indicate that in short-term culture both normal and HIE mononuclear cells produce an inhibitor of neutrophil chemotaxis when exposed to particulate heat-killed staphylococci but that HIE cells produce qualitatively and quantitatively more inhibitory activity.

Entities:  

Mesh:

Substances:

Year:  1983        PMID: 6343237      PMCID: PMC348154          DOI: 10.1128/iai.40.3.1030-1037.1983

Source DB:  PubMed          Journal:  Infect Immun        ISSN: 0019-9567            Impact factor:   3.441


  15 in total

1.  Protein measurement with the Folin phenol reagent.

Authors:  O H LOWRY; N J ROSEBROUGH; A L FARR; R J RANDALL
Journal:  J Biol Chem       Date:  1951-11       Impact factor: 5.157

2.  Neutrophil migration inhibition factor from T lymphocytes (NIF-T): a new lymphokine.

Authors:  R H Weisbart; D W Golde; L Spolter; P Eggena; H Rinderknecht
Journal:  Clin Immunol Immunopathol       Date:  1979-12

3.  Isolation of mononuclear cells and granulocytes from human blood. Isolation of monuclear cells by one centrifugation, and of granulocytes by combining centrifugation and sedimentation at 1 g.

Authors:  A Böyum
Journal:  Scand J Clin Lab Invest Suppl       Date:  1968

4.  Rapid identification of monocytes in a mixed mononuclear cell preparation.

Authors:  S B Tucker; R V Pierre; R E Jordon
Journal:  J Immunol Methods       Date:  1977       Impact factor: 2.303

5.  Neutrophil migration inhibition factor from T lymphocytes (NIF-T): selective removal of biologic activity by human peripheral blood neutrophils, myelocytic leukemia cells, and differentiated HL-60 cells.

Authors:  R H Weisbart; A J Lusis; G Chan; R Billing; R F Ashman; D W Golde
Journal:  J Immunol       Date:  1982-01       Impact factor: 5.422

6.  A 48-well micro chemotaxis assembly for rapid and accurate measurement of leukocyte migration.

Authors:  W Falk; R H Goodwin; E J Leonard
Journal:  J Immunol Methods       Date:  1980       Impact factor: 2.303

7.  Evidence that human leukocyte inhibitory factor (LIF) is an esterase.

Authors:  R E Rocklin; A S Rosenthal
Journal:  J Immunol       Date:  1977-07       Impact factor: 5.422

8.  Purification of a lymphoid cell line product with leukocyte inhibitory factor activity.

Authors:  D H Meshulam; H E Blair; B L Wong; S Charm; J Minowada; R E Rocklin
Journal:  Proc Natl Acad Sci U S A       Date:  1982-01       Impact factor: 11.205

9.  Mononuclear cells from patients with the hyperimmunoglobulin E-recurrent infection syndrome produce an inhibitor of leukocyte chemotaxis.

Authors:  H Donabedian; J I Gallin
Journal:  J Clin Invest       Date:  1982-05       Impact factor: 14.808

10.  The deactivation of rabbit neutrophils by chemotactic factor and the nature of the activatable esterase.

Authors:  P A Ward; E L Becker
Journal:  J Exp Med       Date:  1968-04-01       Impact factor: 14.307

View more
  4 in total

1.  No indication for a defect in toll-like receptor signaling in patients with hyper-IgE syndrome.

Authors:  E D Renner; I Pawlita; F Hoffmann; V Hornung; D Hartl; M Albert; A Jansson; S Endres; G Hartmann; B H Belohradsky; S Rothenfusser
Journal:  J Clin Immunol       Date:  2005-07       Impact factor: 8.317

2.  Abnormal humoral immune response to Staphylococcus aureus in patients with Staphylococcus aureus hyper IgE syndrome.

Authors:  L Matter; J A Wilhelm; F Roth; K Schopfer
Journal:  Clin Exp Immunol       Date:  1986-11       Impact factor: 4.330

3.  Immunoglobulins in the hyperimmunoglobulin E and recurrent infection (Job's) syndrome. Deficiency of anti-Staphylococcus aureus immunoglobulin A.

Authors:  S C Dreskin; P K Goldsmith; J I Gallin
Journal:  J Clin Invest       Date:  1985-01       Impact factor: 14.808

4.  Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced T(H)17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome.

Authors:  Ellen D Renner; Stacey Rylaarsdam; Stephanie Anover-Sombke; Anita L Rack; Janine Reichenbach; John C Carey; Qili Zhu; Annette F Jansson; Julia Barboza; Lena F Schimke; Mark F Leppert; Melissa M Getz; Reinhard A Seger; Harry R Hill; Bernd H Belohradsky; Troy R Torgerson; Hans D Ochs
Journal:  J Allergy Clin Immunol       Date:  2008-07       Impact factor: 10.793

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.