European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology
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Eur. J. Clin. Microbiol. Infect. Dis. · Mar 2014
Heterogeneity among septic shock patients in a set of immunoregulatory markers.
Immune activation is a regular feature of sepsis, but the incidence and nature of the ensuing inflammation-resolving and immunosuppressive component is less well understood. In this study, we compared immunoregulatory markers on blood leukocytes from patients with Gram-negative or Gram-positive sepsis or septic shock, and compared this to blood from patients with severe virosis or healthy controls. To this end, blood from 32 patients with sepsis, including ten cases with shock, and 12 patients with severe virosis were analysed by flow cytometry for the expression levels of monocyte HLA-DR, CD11c, CD14 and CD40, and for frequencies of CD163(+)-suppressive monocytes, HLA-DR(+) or CD40(+)-activated T cells and Tregs. ⋯ Signs of immunosuppression dominated in the septic shock and Gram-positive sepsis groups, whereas monocyte activation was common in Gram-negative sepsis patients without shock. However, the main finding was the large inter-individual variation of immune activation and immunosuppression, with no correlation to prognosis among the shock patients. The pronounced inter-individual variation in the analysed monocyte and lymphocyte markers forms a strong argument that, when immunomodulatory treatment is considered in a sepsis patient, it should be personalised and guided by a detailed immune status assessment.
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Eur. J. Clin. Microbiol. Infect. Dis. · Mar 2014
Trends in hospitalizations of patients with sepsis and factors associated with inpatient mortality in the Region of Madrid, 2003–2011.
The objectives of this investigation were to study the temporal trends in hospitalizations of patients with sepsis in the Region of Madrid (Spain) from 2003 to 2011 and analyze the factors associated with inpatient mortality. All sepsis hospitalizations from the minimum basic data set (MBDS) during 2003 to 2011 in the Region of Madrid were analyzed. Genderspecific crude and age-adjusted rates were calculated each year. ⋯ Death was most frequent among the elderly and in patients with more organ failures and comorbidities. In a populous region of Southern Europe, an upward trend in sepsis incidence was observed between 2003 and 2011, as well as a decreasing trend in mortality for sepsis inpatients. Mortality increased with age, comorbidities, and organ failures.
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Eur. J. Clin. Microbiol. Infect. Dis. · Mar 2014
Resolvin D1 improves survival in experimental sepsis through reducing bacterial load and preventing excessive activation of inflammatory response.
Sepsis is characterized as an uncontrolled inflammatory response. Spite et al. (Nature 461(7268):1287-1291, 2009) had demonstrated that resolvin D2, which is derived from docosahexaenoic acid (DHA), improves survival in cecal ligation and puncture (CLP)-initiated sepsis and enhances bacterial clearance without immune suppression. Resolvin D1, which is also derived from DHA and homologous with resolvin D2, is an endogenous anti-inflammatory and proresolving lipid molecule. ⋯ Compared with the vehicle control group, the survival rate and bacterial clearance of mice with sepsis induced by CLP were improved after resolvin D1 treatment, but the numbers of neutrophils in peritoneal lavage fluid, the inflammatory cytokines, the phosphorylation of the nuclear factor-κB (NF-κB) (P65) pathway, and the apoptosis rate of CD3(+) T lymphocytes of the thymus were suppressed. Resolvin D1 treatment improved survival in mice with sepsis induced by CLP, enhanced organism bacterial clearance, suppressed the increase of the numbers of neutrophils in peritoneal lavage fluid, reduced the release of inflammatory cytokines, and decreased the apoptosis rate of CD3(+) T lymphocytes of the thymus. These results suggest that resolvin D1 may attenuate the degree of inflammatory reaction in sepsis caused by CLP, without harming the host defense response.