Cited by 37Antimicrobial Peptides and ActivitiesSepsis Diagnosis and TreatmentImmune Response and Inflammation

Inducibility of the endogenous antibiotic peptide β-defensin 2 is impaired in patients with severe sepsis

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Book, Malte, Chen, QiXing, Lehmann, Lutz E, Klaschik, Sven, Weber, Stefan, Schewe, Jens-Christian, Luepertz, Markus, Hoeft, Andreas +1 more·2007·Critical Care

Abstract

INTRODUCTION: The potent endogenous antimicrobial peptide human beta-defensin 2 (hBD2) is a crucial mediator of innate immunity. In addition to direct antimicrobial properties, different effects on immune cells have been described. In contrast to the well-documented epithelial beta-defensin actions in local infections, little is known about the leukocyte-released hBD2 in systemic infectious disorders. This study investigated the basic expression levels and the ex vivo inducibility of hBD2 mRNA in peripheral whole blood cells from patients with severe sepsis in comparison to non-septic critically ill patients and healthy individuals. METHODS: This investigation was a prospective case-control study performed at a surgical intensive care unit at a university hospital. A total of 34 individuals were tested: 16 patients with severe sepsis, 9 critically ill but non-septic patients, and 9 healthy individuals. Serial blood samples were drawn from septic patients, and singular samples were obtained from critically ill non-septic patients and healthy controls. hBD2 mRNA levels in peripheral white blood cells were quantified by real-time polymerase chain reaction in native peripheral blood cells and following ex vivo endotoxin stimulation. Defensin plasma levels were quantified by enzyme-linked immunosorbent assay. RESULTS: Endotoxin-inducible hBD2 mRNA expression was significantly decreased in patients with severe sepsis compared to healthy controls and non-septic critically ill patients (0.02 versus 0.95 versus 0.52, p < 0.05, arbitrary units). hBD2 plasma levels in septic patients were significantly higher compared to healthy controls and critically ill non-septic patients (541 versus 339 versus 295 pg/ml, p < 0.05). CONCLUSION: In contrast to healthy individuals and critically ill non-septic patients, ex vivo inducibility of hBD2 in peripheral blood cells from septic patients is reduced. Impaired hBD2 inducibility may contribute to the complex immunological dysfunction in patients with severe sepsis.

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  • In critical illness, bile salt production drops, IgA production is impaired, and the dense mucosal barrier of secreted antimicrobial peptides is lost.

    “bile salt production drops,17 IgA production is impaired,31 and the dense mucosal barrier of secreted antimicrobial peptides is lost.”

    From The microbiome and critical illness (2016) · cites this paper as [32]

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Authors
Book, M., Chen, Q., Lehmann, L. E., Klaschik, S., Weber, S., Schewe, J.-C., Luepertz, M., Hoeft, A., & Stuber, F.
Affiliations
University of Bonn (DE)
Corresponding author
Book, Malte
Venue
Critical Care
Published
2007-02-15
Volume
11
Issue
1
Pages
R19-R19
ISSN
1364-8535 (ISSN-L)
OpenAlex
W1556348464
Cited by
37
References
50
Citations by year
2026: 1 · 2025: 3 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 2 · 2013: 1 · 2012: 3
FWCI
2.78
Type
journal article
Language
en
Open access
Locations
  • Critical Care (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Deutsche Forschungsgemeinschaft (1929/1-1)
Topics
  • Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
human beta-defensin 2, severe sepsis, antimicrobial peptides, innate immunity, endotoxin stimulation, peripheral blood leukocytes, immunosuppression, critically ill patients
MeSH terms
Adult, Humans, Leukocytes, Prospective Studies, Reference Values, RNA, Messenger, Interleukin-6, Gene Expression, Case-Control Studies, Critical Illness, Sepsis, beta-Defensins

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