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  • 1
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    Online Resource
    Mass spectrometry‐based analysis on the impact of whole blood donation on the global plasma proteome
    Wiley ; 2023
    In:  Transfusion Vol. 63, No. 3 ( 2023-03), p. 564-573
    Details
    In: Transfusion, Wiley, Vol. 63, No. 3 ( 2023-03), p. 564-573
    Abstract: Biomonitoring may provide important insights into the impact of a whole blood donation for individual blood donors. Study Design and Methods Here, we used unbiased mass spectrometry (MS)‐based proteomics to assess longitudinal changes in the global plasma proteome, after a single blood donation for new and regular donors. Subsequently, we compared plasma proteomes of 76 male and female whole blood donors, that were grouped based on their ferritin and hemoglobin (Hb) levels. Results The longitudinal analysis showed limited changes in the plasma proteomes of new and regular donors after a whole blood donation during a 180‐day follow‐up period, apart from a significant short‐term decrease in fibronectin. No differences were observed in the plasma proteomes of donors with high versus low Hb and/or ferritin levels. Plasma proteins with the highest variation between and within donors included pregnancy zone protein, which was associated with sex, Alfa 1‐antitrypsin which was associated with the allelic variation, and Immunoglobulin D. Coexpression analysis revealed clustering of proteins that are associated with platelet, red cell, and neutrophil signatures as well as with the complement system and immune responses, including a prominent correlating cluster of immunoglobulin M (IgM), immunoglobulin J chain (JCHAIN), and CD5 antigen‐like (CD5L). Discussion Overall, our proteomic approach shows that whole blood donation has a limited impact on the plasma proteins measured. Our findings suggest that plasma profiling can be successfully employed to consistently detect proteins and protein complexes that reflect the functionality and integrity of platelets, red blood cells, and immune cells in blood donors and thus highlights its potential use for donor health monitoring.
    Type of Medium: Online Resource
    ISSN: 0041-1132 , 1537-2995
    URL: Issue
    URL: Article
    DOI: 10.1111/trf.v63.3
    DOI: 10.1111/trf.17254
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2018415-3
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  • 2
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    Online Resource
    Triggering receptor expressed on myeloid cells‐1 ( TREM ‐1) improves host defence in pneumococcal pneumonia
    Wiley ; 2014
    In:  The Journal of Pathology Vol. 233, No. 4 ( 2014-08), p. 357-367
    Details
    In: The Journal of Pathology, Wiley, Vol. 233, No. 4 ( 2014-08), p. 357-367
    Abstract: Streptococcus (S.) pneumoniae is a common Gram‐positive pathogen in community‐acquired pneumonia and sepsis. Triggering receptor expressed on myeloid cells‐1 ( TREM ‐1) is a receptor on phagocytes known to amplify inflammatory responses. Previous studies showed that TREM ‐1 inhibition protects against lethality during experimental Gram‐negative sepsis. We here aimed to investigate the role of TREM ‐1 in an experimental model of pneumococcal pneumonia, using TREM ‐1/3‐deficient ( Trem‐1/3 –/– ) and wild‐type (Wt) mice. Additionally ex vivo responsiveness of Trem‐1/3 –/– neutrophils and macrophages was examined. S. pneumoniae infection resulted in a rapid recruitment of TREM ‐1‐positive neutrophils into the bronchoalveolar space, while high constitutive TREM ‐1 expression on alveolar macrophages remained unchanged. TREM ‐1/3 deficiency led to increased lethality, accompanied by enhanced growth of S. pneumoniae at the primary site of infection and increased dissemination to distant organs. Within the first 3–6 h of infection, Trem‐1/3 –/– mice demonstrated a strongly impaired innate immune response in the airways, as reflected by reduced local release of cytokines and chemokines and a delayed influx of neutrophils. Trem‐1/3 –/– alveolar macrophages produced fewer cytokines upon exposure to S. pneumoniae in vitro and were less capable of phagocytosing this pathogen. TREM ‐1/3 deficiency did not influence neutrophil responsiveness to S. pneumoniae . These results identify TREM ‐1 as a key player in protective innate immunity during pneumococcal pneumonia, most likely by enhancing the early immune response of alveolar macrophages. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.2014.233.issue-4
    DOI: 10.1002/path.4361
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 1475280-3
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  • 3
    Online Resource
    Online Resource
    The impact of HIV infection on blood leukocyte responsiveness to bacterial stimulation in asymptomatic patients and patients with bloodstream infection
    Wiley ; 2016
    In:  Journal of the International AIDS Society Vol. 19, No. 1 ( 2016-01)
    Details
    In: Journal of the International AIDS Society, Wiley, Vol. 19, No. 1 ( 2016-01)
    Abstract: HIV‐induced changes in cytokine responses to bacteria may influence susceptibility to bacterial infections and the consequent inflammatory response. Methods We examined the impact of HIV on whole blood responsiveness to bacterial stimulation in asymptomatic subjects and patients with bacterial bloodstream infection (BSI). Whole blood was stimulated ex vivo with two bacterial Toll‐like receptor agonists (lipopolysaccharide and lipoteichoic acid) and two pathogens ( Streptococcus pneumoniae and non‐typhoidal Salmonella ), which are relevant in HIV‐positive patients. Production of interferon‐γ, tumour necrosis factor‐α, interleukin‐1β and interleukin‐6 was used as a read‐out. Results In asymptomatic subjects, HIV infection was associated with reduced interferon‐γ, release after stimulation and priming of the pro‐inflammatory cytokine response to non‐typhoidal Salmonella . In patients with BSI, we found no such priming effect, nor was there evidence for more profound sepsis‐induced immunosuppression in BSI patients with HIV co‐infection. Conclusions These results suggest a complex effect of HIV on leukocyte responses to bacteria. However, in patients with sepsis, leukocyte responses were equally blunted in patients with and without HIV infection.
    Type of Medium: Online Resource
    ISSN: 1758-2652 , 1758-2652
    URL: Article
    DOI: 10.7448/IAS.19.1.20759
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2467110-1
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  • 4
    Online Resource
    Online Resource
    Endoplasmic reticulum chaperone gp96 in macrophages is essential for protective immunity during Gram‐negative pneumonia
    Wiley ; 2016
    In:  The Journal of Pathology Vol. 238, No. 1 ( 2016-01), p. 74-84
    Details
    In: The Journal of Pathology, Wiley, Vol. 238, No. 1 ( 2016-01), p. 74-84
    Abstract: Klebsiella pneumoniae is among the most common Gram‐negative bacteria that cause pneumonia. Gp96 is an endoplasmic reticulum chaperone that is essential for the trafficking and function of Toll‐like receptors ( TLRs ) and integrins. To determine the role of gp96 in myeloid cells in host defence during Klebsiella pneumonia, mice homozygous for the conditional Hsp90b1 allele encoding gp96 were crossed with mice expressing Cre‐recombinase under control of the LysM promoter to generate LysMcre ‐ Hsp90b1 ‐flox mice. LysMcre ‐ Hsp90b1 ‐flox mice showed absence of gp96 protein in macrophages and partial depletion in monocytes and granulocytes. This was accompanied by almost complete absence of TLR2 and TLR4 on macrophages. Likewise, integrin subunits CD11b and CD18 were not detectable on macrophages, while being only slightly reduced on monocytes and granulocytes. Gp96‐deficient macrophages did not release pro‐inflammatory cytokines in response to Klebsiella and displayed reduced phagocytic capacity independent of CD18 . LysMcre ‐ Hsp90b1 ‐flox mice were highly vulnerable to lower airway infection induced by K. pneumoniae , as reflected by enhanced bacterial growth and a higher mortality rate. The early inflammatory response in Hsp90b1 ‐flox mice was characterized by strongly impaired recruitment of granulocytes into the lungs, accompanied by attenuated production of pro‐inflammatory cytokines, while the inflammatory response during late‐stage pneumonia was not dependent on the presence of gp96. Blocking CD18 did not reproduce the impaired host defence of LysMcre ‐ Hsp90b1 ‐flox mice during Klebsiella pneumonia. These data indicate that macrophage gp96 is essential for protective immunity during Gram‐negative pneumonia by regulating TLR expression. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.2016.238.issue-1
    DOI: 10.1002/path.4637
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 1475280-3
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  • 5
    Online Resource
    Online Resource
    Impact of HIV infection on the haemostatic response during sepsis and malaria
    Wiley ; 2016
    In:  British Journal of Haematology Vol. 173, No. 6 ( 2016-06), p. 918-926
    Details
    In: British Journal of Haematology, Wiley, Vol. 173, No. 6 ( 2016-06), p. 918-926
    Abstract: Patients positive for the human immunodeficiency virus ( HIV ) are more susceptible to sepsis and malaria, two conditions known to activate the coagulation system. As chronic HIV infection also influences haemostatic mechanisms, we determined the influence of HIV co‐infection on coagulation, anticoagulation and the endothelium during sepsis or malaria. We performed a prospective observational study in 325 subjects with or without HIV infection (103 with sepsis, 127 with malaria and 95 asymptomatic controls) in an HIV endemic area in Central Africa. We measured plasma biomarkers indicative of activation of distinct haemostatic mechanisms. Sepsis and malaria had similar effects with elevated markers of coagulation, reduced anticoagulation markers and activation of endothelium. In particular, asymptomatic HIV infection reduced the plasma levels of the anticoagulant co‐factor free protein S, and increased activation of the vascular endothelium, which were not normalized by combination antiretroviral therapy. HIV co‐infection during sepsis and malaria caused more profound changes in free protein S and von Willebrand factor in sepsis and malaria, and ADAMTS 13 in sepsis, while not influencing sepsis‐ or malaria‐induced coagulation activation. These results show for the first time that HIV infection augments selective haemostatic changes during sepsis and malaria, which may contribute to the enhanced morbidity of these conditions in HIV patients.
    Type of Medium: Online Resource
    ISSN: 0007-1048 , 1365-2141
    URL: Issue
    URL: Article
    DOI: 10.1111/bjh.2016.173.issue-6
    DOI: 10.1111/bjh.14006
    RVK:
    XA 34100
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 1475751-5
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