Phenotype and functions of natural killer cells in critically-ill septic patients

PLoS One. 2012;7(12):e50446. doi: 10.1371/journal.pone.0050446. Epub 2012 Dec 6.

Abstract

Rationale: Natural killer cells, as a major source of interferon-γ, contribute to the amplification of the inflammatory response as well as to mortality during severe sepsis in animal models.

Objective: We studied the phenotype and functions of circulating NK cells in critically-ill septic patients.

Methods: Blood samples were taken <48 hours after admission from 42 ICU patients with severe sepsis (n = 15) or septic shock (n = 14) (Sepsis group), non-septic SIRS (n = 13) (SIRS group), as well as 21 healthy controls. The immuno-phenotype and functions of NK cells were studied by flow cytometry.

Results: The absolute number of peripheral blood CD3-CD56(+) NK cells was similarly reduced in all groups of ICU patients, but with a normal percentage of NK cells. When NK cell cytotoxicity was evaluated with degranulation assays (CD107 expression), no difference was observed between Sepsis patients and healthy controls. Under antibody-dependent cell cytotoxicity (ADCC) conditions, SIRS patients exhibited increased CD107 surface expression on NK cells (62.9[61.3-70]%) compared to healthy controls (43.5[32.1-53.1]%) or Sepsis patients (49.2[37.3-62.9]%) (p = 0.002). Compared to healthy (10.2[6.3-13.1]%), reduced interferon-γ production by NK cells (K562 stimulation) was observed in Sepsis group (6.2[2.2-9.9]%, p<0.01), and especially in patients with septic shock. Conversely, SIRS patients exhibited increased interferon-γ production (42.9[30.1-54.7]%) compared to Sepsis patients (18.4[11.7-35.7]%, p<0.01) or healthy controls (26.8[19.3-44.9]%, p = 0.09) in ADCC condition.

Conclusions: Extensive monitoring of the NK-cell phenotype and function in critically-ill septic patients revealed early decreased NK-cell function with impaired interferon-γ production. These results may aid future NK-based immuno-interventions.

Trial registration: NTC00699868.

Trial registration: ClinicalTrials.gov NCT00699868.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Critical Illness
  • Cytokines / blood
  • Female
  • Humans
  • Killer Cells, Natural / cytology
  • Killer Cells, Natural / immunology*
  • Lymphocyte Count
  • Male
  • Middle Aged
  • Phenotype
  • Prospective Studies
  • Sepsis / blood
  • Sepsis / immunology*
  • Sepsis / mortality
  • Severity of Illness Index
  • Systemic Inflammatory Response Syndrome / blood
  • Systemic Inflammatory Response Syndrome / immunology*
  • Systemic Inflammatory Response Syndrome / mortality

Substances

  • Cytokines

Associated data

  • ClinicalTrials.gov/NCT00699868

Grants and funding

This work was supported by the Assistance Publique Hôpitaux de Marseille (Appel d’Offre Recherche Clinique) and by a grant from the Société de Réanimation de Langue Française (SRLF). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.