Background: Neutrophils have an impressive array of microbicidal weapons, and in the presence
of a pathogen, progress from a quiescent state in the bloodstream to a completely activated state. Failure to
regulate this activation, for example, when the blood is flooded with cytokines after severe trauma, causes
inappropriate neutrophil activation that paradoxically, is associated with tissue and organ damage. Acidic
proteomic maps of quiescent human neutrophils were analyzed and compared to those of activated neutrophils
from severe trauma patients. The analysis revealed 114 spots whose measured volumes differed between
activated and quiescent neutrophils, with 27 upregulated and 87 downregulated in trauma conditions.
Among the identified proteins, grancalcin, S100-A9 and CACNB2 reinforce observed correlations between
motility and ion flux, ANXA3, SNAP, FGD1 and Zfyve19 are involved in vesicular transport and exocytosis, and GSTP1,
HSPA1 HSPA1L, MAOB, UCH-L5, and PPA1 presented evidence that activated neutrophils may have diminished protection
against oxidative damage and are prone to apoptosis. These are discussed, along with proteins involved in cytoskeleton
reorganization, reactive oxygen species production, and ion flux. Proteins such as Zfyve19, MAOB and albumin-
like protein were described for the first time in the neutrophil. In this work we achieved the identification of several
proteins potentially involved in inflammatory signaling after trauma, as well as proteins described for the first time in neutrophils.
Keywords: Neutrophils, trauma, proteome, systemic inflammatory response syndrome, inflammation, hemorrhagic shock, acute respiratory distress syndrome (ARDS), systemic inflammatory response syndrome (SIRS), Compensatory anti-inflammatory response syndrome (CARS), receptor-mediated agonists
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