Abstract

BackgroundMajor trauma patients (TP) developing imbalanced immune response are at high risk for infectious post-injury complications including pneumonia. Neutrophils play a central role in the host defense against bacteria and thereby pathogenesis of infections. While there are numerous studies about neutrophil function after trauma, data about their biology in patients who suffer from pneumonia following trauma are sparse. Here, we studied the effect of serum isolated from patients who do and do not develop infection (inf.) on the biology of neutrophils from healthy volunteers.MethodsSera samples from eighteen TP with an injury severity score above 16 were obtained. Nine patients were grouped to no inf. group (TP without pneumonia), and nine to inf. group (TP with pneumonia). Samples were obtained at admission to emergency department (ED), a day prior pneumonia diagnosis (1 d prior inf) or at the day of diagnosis (1 d prior inf). Samples from the equal post-injury days in the corresponding no inf. group were used. Neutrophils from nine healthy volunteers were isolated. Effects for sera isolated from infected and non-infected patients on neutrophil biology were analyzed. Migratory capacity of neutrophils towards TP’s serum, their CD11b and CD62L membrane receptor expression and oxidative burst activity after stimulation with TP’s serum were determined and compared between groups.ResultsMigratory capacity of neutrophils was significantly increased after trauma and persisted during the study period. CD11b expression in all groups was significantly increased. CD62L expression decreased generally in samples from ED and recovered later to baseline. Stratifying no inf. and inf. groups showed significantly decreased migratory capacity, increased CD11b and significantly decreased CD62L expression in the no inf. group. These differences persisted during the complete observational period. ROS production was strongly reduced in the no inf. group compared to the inf. group at later experimental time points.ConclusionsThis data indicate that patients at risk for pneumonia development have differentially and early activated neutrophils following trauma compared to patients who are not at risk for post-injury complication. Studies about the differential biology of neutrophils and their immediately after trauma modified activity depending on the post-injury clinical course are warranted, and may deliver predictive or even therapeutic strategies to control inflammation.

Highlights

  • Major trauma patients (TP) developing imbalanced immune response are at high risk for infectious post-injury complications including pneumonia

  • A subgroup analysis after frequency-matching of patients according to the injury severity score (ISS) (± 6 points) and age showed that patients who developed pneumonia were statistically comparably injured with patients who did not develop clinical complications (ISS: 27.17 ± 3.65 vs. 24.43 ± 3.91, Table 1)

  • We have demonstrated that stimulating isolated neutrophils from healthy volunteers with sera samples from trauma patients increased the migratory rate of neutrophils immediately after trauma as well as in the later post-injury course

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Summary

Introduction

Major trauma patients (TP) developing imbalanced immune response are at high risk for infectious post-injury complications including pneumonia. In response to traumatic injury and the associated release of damage-associated molecular patterns (DAMPs), the body’s immunological and inflammatory processes at cellular and humoral levels become activated in order to neutralize non-infectious tissue insult, bacterial infections, and initiate tissue repair mechanisms [6, 7]. Neutrophils, critical inflammatory cells playing a key role in protection against bacterial infections, are believed to be central in the pathogenesis of infectious post-injury complications. Due to their numerous microbicidal defensive strategies including production of reactive oxygen species (ROS), neutrophils constitute the first line of defense against rapidly dividing bacteria, fungi and yeast [8]. As a marker of neutrophil activation after trauma elevated surface expression of CD11b that forms part of the heterodimeric integrin Mac-1 (macrophage associated antigen-1)

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