Abstract
The severity of bloodstream infections (BSI) depends on pathogen, source, and host factors. Secretory leukocyte protease inhibitor (SLPI) counteracts tissue damage, balances inflammation, and is increased in pneumonia and sepsis. We aimed to evaluate whether SLPI production differs depending on etiology, disease severity, and sex in BSI and to correlate SLPI with markers of inflammation and immunosuppression. Of the adult patients with BSI, 109 were included and sampled repeatedly, from hospital admission through day 28. Controls (blood donors) were sampled twice. SLPI in plasma was measured with enzyme-linked immunosorbent assay (ELISA) technique. Streptococcus pneumoniae and Staphylococcus aureus etiology were associated with higher SLPI than Escherichia coli on days 1–2 and 3. On day 1–2, subjects with sepsis had higher SLPI concentrations than those with non-septic BSI. Pneumonia was associated with higher SLPI than a non-pulmonary source of infection. SLPI co-varied with inflammatory markers. SLPI concentrations did not differ with regard to sex in the full cohort, but men with pneumonia had higher SLPI than women on day 1–2. S. pneumoniae and S. aureus BSI were associated with higher SLPI, when compared to E. coli. Severity and pneumonia, as well as male sex in the pneumonia sub-cohort, were factors independently associated with higher SLPI.
Highlights
Electronic supplementary material The online version of this article contains supplementary material, which is available to authorized users.The clinical course of a bacterial infection is determined by the interaction of host factors, the infected organ, and the pathogen. [1]
This study reports independent associations between bacterial etiology, disease severity, lung focus, and plasma concentration of Secretory leukocyte protease inhibitor (SLPI) in community-onset bloodstream infection (BSI)
On days 1–2 and 3 after admission, subjects with S. pneumoniae and S. aureus etiology had higher plasma SLPI than E. coli
Summary
The clinical course of a bacterial infection is determined by the interaction of host factors, the infected organ, and the pathogen. Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection, but there are currently no criteria for measuring the dysregulated immune response, which can manifest as disproportionate pro-inflammation and/or a state of immunosuppression [2]. The causative microorganism is identified in 50–60%, and in 20–30% there is an associated bloodstream infection (BSI), defined as growth of one or more bacterial or fungal pathogens in one or more blood cultures [1, 5,6,7]. The reported incidence of BSI is in average 140–160/100,000/year in highincome countries, and the three most common etiologies are Escherichia coli, Staphylococcus aureus, and Streptococcus pneumoniae [8]
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