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Major Trauma Enhances Store-Operated Calcium Influx in Human Neutrophils

Hauser, Carl J. MD; Fekete, Zoltan MD, PhD; Livingston, David H. MD; Adams, John MD; Garced, Matthew BA; Deitch, Edwin A. MD

Journal of Trauma and Acute Care Surgery: April 2000 - Volume 48 - Issue 4 - p 592-598
Annual Meeting Articles

Purpose: Chemotaxins from inflammatory sites prime or activate neutrophils (PMN) by using cytosolic calcium ([Ca2+]i) fluxes as second messengers. [Ca2+]i can be mobilized rapidly by receptor-mediated entry or store-release, or more slowly by store-operated calcium influx (SOCI). We studied [Ca2+]i mobilization by chemotaxins and how trauma impacts the calcium entry mechanisms used by chemotaxins.

Methods: [Ca2+]i flux was studied by spectrofluorometry. The contributions of early and late [Ca2+]i currents to net calcium flux were compared after stimulation by more potent (fMLP, C5a, PAF) or less potent (IL-8, GRO-α, and LTB4) agonists. Store operated [Ca2+]i mobilization was reflected by the ratio of area under the [Ca2+]i efflux curve to peak [Ca2+]i (efflux curve). PMN from trauma patients (ISS > 25) and pair-matched volunteer (n = 7 pairs) were then primed and stimulated with thapsigargin to compare cell calcium stores and SOCI.

Results: Late [Ca2+]i mobilization made more important contributions to fMLP, PAF, and C5a signals than to IL-8, GRO-α, or LTB4 (p < 0.01 all comparisons). Calcium stores and store release were only marginally lower after injury (p = not significant), but trauma PMN showed far higher [Ca2+]i influx after thapsigargin (p = 0.007), and greater net SOCI (p = 0.034).

Conclusions: SOCI may play an important role in PMN activation, and trauma increases PMN SOCI. Prolonged elevations of [Ca2+]i due to enhanced SOCI may alter stimulus-response coupling to chemotaxins and contribute to PMN dysfunction after injury.

From the Department of Surgery, Division of Trauma, UMD-New Jersey Medical School, Newark, New Jersey.

Address for reprints: Carl J. Hauser MD, UMD/New Jersey Medical School, Department of Surgery, MSB G-524, 185 South Orange Avenue, Newark, NJ 07103; email:

Submitted for publication September 24, 1999.

Accepted for publication December 31, 1999.

Supported in part by grants from the Foundation of UMD/New Jersey Medical School, and from the AO/ASIF Research Foundation, Basel, Switzerland.

Presented at the 59th Annual Meeting of the American Association for the Surgery of Trauma, September 16–18, 1999, Boston, Massachusetts.

© 2000 Lippincott Williams & Wilkins, Inc.