Humoral Factors From Musculoskeletal Polytrauma Patients Impair Antibacterial Responses Of Neutrophils In vitro

Polytrauma is associated with increased risk of sepsis, but the risk for implant infection is less clear. Neutrophil antibacterial responses are significantly reduced in polytrauma patients (n= 9, ISS≥15) for at least 5 days compared to healthy controls. Reduced neutrophil activity could influence implant infection in addition to sepsis.

[1]  R. O’Toole,et al.  2018 International Consensus Meeting on Musculoskeletal Infection: Research Priorities from the General Assembly Questions , 2019, Journal of orthopaedic research : official publication of the Orthopaedic Research Society.

[2]  H. Rohde,et al.  2018 international consensus meeting on musculoskeletal infection: Summary from the biofilm workgroup and consensus on biofilm related musculoskeletal infections , 2019, Journal of orthopaedic research : official publication of the Orthopaedic Research Society.

[3]  D. Messerer,et al.  Early Detection of Junctional Adhesion Molecule-1 (JAM-1) in the Circulation after Experimental and Clinical Polytrauma , 2015, Mediators of inflammation.

[4]  S. Heys,et al.  Older Patients Are Immunocompromised by Cytokine Depletion and Loss of Innate Immune Function After HIP Fracture Surgery , 2015, Geriatric orthopaedic surgery & rehabilitation.

[5]  D. Stubljar,et al.  Dynamics of inflammation biomarkers C-reactive protein, leukocytes, neutrophils, and CD64 on neutrophils before and after major surgical procedures to recognize potential postoperative infection , 2015, Scandinavian journal of clinical and laboratory investigation.

[6]  J. Lord,et al.  The systemic immune response to trauma: an overview of pathophysiology and treatment , 2014, The Lancet.

[7]  Heather N. Watson,et al.  Economic burden of periprosthetic joint infection in the United States. , 2012, The Journal of arthroplasty.

[8]  L. Filgueira,et al.  Serum after traumatic brain injury increases proliferation and supports expression of osteoblast markers in muscle cells. , 2010, The Journal of bone and joint surgery. American volume.

[9]  G. Paré,et al.  Class IA Phosphatidylinositide 3-Kinases, rather than p110γ, Regulate Formyl-Methionyl-Leucyl-Phenylalanine-Stimulated Chemotaxis and Superoxide Production in Differentiated Neutrophil-Like PLB-985 Cells1 , 2006, The Journal of Immunology.

[10]  N. Papadopoulos,et al.  Neutrophil functions in patients with fractures of the upper end of the femur , 1993, Calcified Tissue International.

[11]  Q. Myrvik,et al.  Antibiotic resistance of biomaterial-adherent coagulase-negative and coagulase-positive staphylococci. , 1990, Clinical orthopaedics and related research.

[12]  M. Lilly,et al.  Characterization of a new human diploid myeloid leukemia cell line (PLB-985) with granulocytic and monocytic differentiating capacity. , 1987, Blood.

[13]  J. Siegel,et al.  Trauma serum suppresses superoxide production by normal neutrophils. , 1986, Archives of surgery.

[14]  W. Zimmerli,et al.  Pathogenesis of foreign body infection. Evidence for a local granulocyte defect. , 1984, The Journal of clinical investigation.

[15]  P. Stewart Antimicrobial Tolerance in Biofilms , 2015, Microbiology spectrum.

[16]  D. Ambruso,et al.  Neutrophils from patients after burn injury express a deficiency of the oxidase components p47-phox and p67-phox. , 1996, Blood.