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Ca2+ response in neutrophils after exposure to bacterial N-formyl-methionyl-leucyl-phenylalanine: delayed response in

Ben Vainer1, Kasper Lamberth, Jens Brimnes

  • 1Department of Pathology, Rigshospitalet, Copenhagen, Denmark. vainer@rh.dk

European Journal of Gastroenterology & Hepatology
|March 1, 2003
PubMed
Abstract

Insights

Neutrophils from ulcerative colitis (UC) patients show a delayed calcium response to bacterial peptides like FMLP. This impaired calcium influx may be a key factor in UC neutrophil dysfunction.

Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Neutrophil migration into the colon is crucial in ulcerative colitis (UC) pathogenesis.
  • Bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulates calcium influx in neutrophils, essential for their function.
  • Impaired calcium-dependent ICAM-1/beta 2-integrin neutrophil migration is noted in UC patients.

Purpose of the Study:

  • To investigate calcium (Ca2+) influx in peripheral blood neutrophils from UC patients.
  • To assess the response to FMLP and binding of beta 2-integrins or ICAM-1.

Main Methods:

  • Spectrofluorometry was used to measure intracellular Ca2+ levels ([Ca2+]i).
  • Neutrophils were isolated from eight UC patients and eight healthy controls.
  • Cells were stimulated with FMLP, free ICAM-1, or antibodies targeting ICAM-1 and beta 2-integrins (CD11a, CD11b, CD11c, CD18).

Main Results:

  • FMLP exposure caused a significant delay in [Ca2+]i increase in UC neutrophils compared to controls (P < 0.01).
  • Antibody-mediated CD18 cross-linking induced a minor [Ca2+]i increase, with no difference between UC patients and controls.

Conclusions:

  • A delayed neutrophil response to bacterial peptides is a potential phenotype in UC patients.
  • The study discusses a possible link between FMLP-stimulated Ca2+ influx and CD11/CD18 upregulation in UC.

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