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Highly Accessed Commentary

Immunological monitoring to prevent and treat sepsis

Raquel Almansa1, John Wain2, Eduardo Tamayo3, David Andaluz-Ojeda4, Ignacio Martin-Loeches5, Paula Ramirez6 and Jesús F Bermejo-Martin1*

Author Affiliations

1 Unidad de Investigación Biomédica del Clínico, Hospital Clínico Universitario de Valladolid, SACYL/IECSCYL, Avda Ramón y Cajal 3, 47005 Valladolid, Spain

2 Norwich Medical School, University of East Anglia. Norwich, NR4 7TJ, UK

3 Servicio de Anestesiología, Hospital Clínico Universitario de Valladolid, SACYL/IECSCYL, Avda Ramón y Cajal 3, 47005 Valladolid, Spain

4 Servicio de Medicina Intensiva, Hospital Clínico Universitario de Valladolid, SACYL/IECSCYL, Avda Ramón y Cajal 3, 47005 Valladolid, Spain

5 Centro de Críticos, Corporación Sanitaria y Universitaria Parc Taulí - Hospital de Sabadell, CIBER Enfermedades Infecciosas. Parc Taulí, 1. 08208 Sabadell, Spain

6 Servicio de Medicina Intensiva, Hospital Universitario y Politécnico la Fe, Bulevar del Sur, 46026 Valencia, Spain

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Critical Care 2013, 17:109  doi:10.1186/cc11922

Published: 25 January 2013

Abstract

The clinical, human and economic burden associated with sepsis is huge. Initiatives such as the Surviving Sepsis Campaign aim to effectively reduce risk of death from severe sepsis and septic shock. Nonetheless, although substantial benefits raised from the implementation of this campaign have been obtained, much work remains if we are to realise the full potential promised by this strategy. A deeper understanding of the processes leading to sepsis is necessary before we can design an effective suite of interventions. Dysregulation of the immune response to infection is acknowledged to contribute to the pathogenesis of the disease. Production of both proinflammatory and immunosuppressive cytokines is observed from the very first hours following diagnosis. In addition, hypogammaglobulinemia is often present in patients with septic shock. Moreover, levels of IgG, IgM and IgA at diagnosis correlate directly with survival. In turn, nonsurvivors have lower levels of C4 (a protein of the complement system) than the survivors. Natural killer cell counts and function also seem to have an important role in this disease. HLA-DR in the surface of monocytes and counts of CD4+CD25+ T-regulatory cells in blood could also be useful biomarkers for sepsis. At the genomic level, repression of networks corresponding to major histocompatibility complex antigen presentation is observed in septic shock. In consequence, cumulative evidence supports the potential role of immunological monitoring to guide measures to prevent or treat sepsis in a personalised and timely manner (early antibiotic administration, immunoglobulin replacement, immunomodulation). In conclusion, although diffuse and limited, current available information supports the development of large comprehensive studies aimed to urgently evaluate immunological monitoring as a tool to prevent sepsis, guide its treatment and, as a consequence, diminish the morbidity and mortality associated with this severe condition.