85 Host response in patients with ICU-acquired pneumonia Background Intensive Care Unit (ICU)-acquired pneumonia is one of the most frequently diagnosed infections in the ICU, with a – relative – attributable mortality of 13% [1, 2]. Important risk factors for ICU-acquired pneumonia include invasive procedures (particularly mechanical ventilation), the underlying medical condition, comorbidities, and severity of disease [3, 4]. In recent years much attention has been given to host response deviations in critically ill patients, including those with a sepsis admission diagnosis, that may render them vulnerable to secondary opportunistic infections [5–8]. In this context, the vast majority of research focused on critical illness-associated immune suppression as a key factor placing ICU patients at risk for infection [5–8]. Our group previously reported on host response aberrations in critically ill patients with sepsis prior to the development of ICU-acquired infections and found that these patients, rather than merely showing signs of immune suppression, demonstrated wide-ranging disturbances across multiple pathophysiological domains when compared with patients who did not develop an ICUacquired infection [9]. Additional studies have provided evidence for a sustained and complex dysregulation of the host response entailing both immune suppression and hyperinflammation in patients who remain on the ICU for prolonged periods of time, who oftentimes develop a chronic critical illness termed “persistent inflammation, immunosuppression and catabolism syndrome” or PICS [7]. We here tested the hypothesis that critically ill patients, irrespective of their primary reason for admission, exhibit broad anomalies in their host response both prior to and during ICU-acquired pneumonia, and that these are distinctive from patients who do not acquire pneumonia while on the ICU. For this, we measured 19 host response biomarkers providing insight into key pathophysiological pathways in plasma samples collected in a prospective observational study in patients admitted to 30 ICUs throughout Europe with various admission diagnoses (medical, trauma, surgical) and compared patients who developed pneumonia during their ICU stay (cases) with patients who did not develop pneumonia (controls). Our study aimed to obtain insight into: (1) host response protein differences between cases and controls prior to development of ICU-acquired pneumonia in the former group; (2) host response protein aberrations at the time of pneumonia diagnosis; (3) host response protein trajectories, i.e. the change in host response over time from prior to ICU-acquired pneumonia to the day of ICU-acquired pneumonia. Methods Patient population This study was conducted as part of the “Advanced understanding of Staphylococcus aureus and Pseudomonas aeruginosa Infections in EuRopE - Intensive Care Units” (ASPIRE-ICU) project, a study of adult ICU patients at 30 hospitals in 11 European countries that recruited participants between June 2015 and October 2018 [10]. Study methods have been reported elsewhere [11]. Briefly, patients with an expected length of ICU stay of 48 hours or more and who underwent mechanical ventilation at ICU admission (or were expected to undergo ventilation within 24 hours) were enrolled within 3 days after ICU admission in a 1:1 ratio of Staphylococcus (S.) aureus-colonized (identified by screening on admission) and noncolonized patients. The study protocol 5
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