Comparison of the Neutrophil Proteome in Trauma Patients and Normal Controls

Abstract

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.

Proteome Analysis of Human Neutrophil Granulocytes From Patients With Monogenic Disease Using Data-independent Acquisition

“…2 D ). This result is in sharp contrast to correlation coefficients obtained in other cells, which typically range from ∼0.4 to 0.8 (53, 54) and agrees with previous observations (13, 16, 55). Naive neutrophils have been shown previously to have reduced transcriptional activity (56).…”

“…We hypothesized that in-depth proteome-analysis may also provide additional cues for diagnosis of monogenic diseases, such as rare defects of neutrophil granulocytes. In the past, several laboratories have published data on the proteome of healthy neutrophil granulocytes (10–23), however all but one (10) quantified significantly fewer proteins compared with our study. We here systematically analyze proteome changes in neutrophils from patients with different monogenic diseases and demonstrate the usefulness of next-generation proteomics for guiding clinical genetic diagnostics.…”

“…Other laboratories have reported data on the proteome of human neutrophil granulocytes (10–23). Rieckmann et al studied the proteomes of leukocyte subpopulations and reported quantitation data for 6007 proteins in naive neutrophil granulocytes using a data-dependent acquisition method optimized for depth and using TrEMBL protein annotation.…”

Kinetic effects of TiO2 fine particles and nanoparticles aggregates on the nanomechanical properties of human neutrophils assessed by force spectroscopy

“…Neutrophils were isolated from human whole blood using a density gradient technique as described in a previous study [50]. Briefly, 12 mL of peripheral blood were drawn from three healthy individuals with sterile heparinized syringes and not pooled.…”

Evaluation of the effects of ischemic preconditioning on the hematological parameters of rats subjected to intestinal ischemia and reperfusion

“…Among the internal organs, the intestine is most sensitive to IRI 1 . Intestinal IRI can lead to damage in the intestinal mucosa and the release of various inflammatory mediators, potentially resulting in the development of systemic inflammatory response syndrome (SIRS) and further leading to multiple organ failure (MOF), especially acute lung injury (ALI) 4 - 7 . Ischemia-reperfusion causes local and systemic changes in hemodynamics, endothelial function, microcirculation, fluid equilibrium and metabolic homeostasis while also inducing the complement and inflammatory pathways 8 - 14 .…”