Plasma fibronectin as a marker of sepsis

Martín, Gracia Rubio; Prieto, J.; Cabo, Jorge Veiga de; Lus, Luisa Gomez; Barberán, José; Landa, Jose M.González; Fernández, Cristina

doi:10.1016/j.ijid.2003.10.005

Cited by 29 publications

(12 citation statements)

References 31 publications

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“…The importance of fibronectin in sepsis remains unclear, and very few results have been published so far. According to previous research, the concentration of plasma FN was significantly reduced in patients with sepsis compared to values measured in healthy volunteers [17], and pFN was indicated as an early sepsis marker. Additionally, lower plasma FN levels were observed in cases of fungal sepsis than in cases of bacterial sepsis [18].…”

Section: Introductionmentioning

confidence: 81%

Plasma and Cellular Forms of Fibronectin as Prognostic Markers in Sepsis

Lemańska-Perek

Krzyżanowska-Gołąb

Skalec

et al. 2020

Mediators of Inflammation

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Background. There is a pressing need for specific prognostic markers that could be used to monitor the severity of sepsis. The aims of our study were to investigate changes in the expression of different molecular forms of fibronectin in sepsis and to assess their relationship to the clinical severity and mortality of patients. Material and Methods. Forms of fibronectin: plasma (pFN), cellular (EDA-FN), FN-fibrin complexes, and fibronectin fragments were analyzed in 71 sepsis patients (survivors and nonsurvivors) and in the control by ELISA and immunoblotting. Results. The baseline pFN concentration of patients with sepsis was significantly lower than in the control (133.0 mg/L vs. 231.2 mg/L) (P<0.001), and in nonsurvivors, it was lower than in survivors (106.0 mg/L vs. 152.8 mg/L) (P=0.004). The baseline EDA-FN was significantly elevated in both sepsis groups (survivors: 6.7 mg/L; nonsurvivors: 9.4 mg/L) compared to the control (1.4 mg/L) (P<0.001). It should be noted that among patients with more severe sepsis, the EDA-FN level was higher in nonsurvivors than in survivors. Furthermore, molecular FN-fibrin complexes as well as FN fragments occurred much more frequently in nonsurvivors than in survivors. Conclusion. The study showed that in sepsis, changes in plasmatic and cellular form of fibronectin were associated with the severity of sepsis and may be useful predictors of outcome.

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Section: Introductionmentioning

confidence: 81%

Plasma and Cellular Forms of Fibronectin as Prognostic Markers in Sepsis

Lemańska-Perek

Krzyżanowska-Gołąb

Skalec

et al. 2020

Mediators of Inflammation

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“…FN has multiple functional domains that can bind to integrin, collagen, fibrin and heparin, and participate in cell adhesion, migration, proliferation and differentiation ( Hynes, 2012 ; Mao & Schwarzbauer, 2005 ; Pankov, 2002 ). More and more studies have demonstrated that FN plays an important role in assessement the severity of severe infection and sepsis ( Lemańska-Perek & Adamik, 2019 ; Ruiz Martin et al, 2004 ).…”

Section: Introductionmentioning

confidence: 99%

Construction of fibronectin conditional gene knock-out mice and the effect of fibronectin gene knockout on hematopoietic, biochemical and immune parameters in mice

Yuan

Yang

Wen

et al. 2020

PeerJ

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Fibronectin (FN) is a multi-functional glycoprotein that primarily acts as a cell adhesion molecule and tethers cells to the extra cellular matrix. In order to clarify the effect of FN deficiency on hematopoiesis, biochemical and immune parameters in mice. We constructed a tamoxifen-induced conditional (cre-loxp system) fibronectin knock-out (FnKO) mouse model on a C57BL/6 background, and monitored their behavior, fertility, histological, hematopoietic, biochemical and immunological indices. We found that the Fn KO mice had reduced fertility, high platelet counts, smaller bone marrow megakaryocytes and looser attachment between the hepatocyte and vascular endothelial junctions compared to the wild type (WT) mice. In contrast, the behavior, hematological counts, serum biochemical indices and vital organ histology were similar in both Fn KO and WT mice. This model will greatly help in elucidating the role of FN in immune-related diseases in future.

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“…A large release of TNF-α has been shown to be associated with harmful pathophysiological effects and increased mortality from septic shock [42]. In addition, the abnormally diminished concentration of plasma Fn has been used as a biomarker in evaluating sepsis [15]. The reduction in the plasma Fn concentration observed in patients with sepsis may arise from intravascular coagulation and cryofibrinogenemia, which is likely due to increased plasma Fn catabolism secondary to the intravascular formation of fibrin [15].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the abnormally diminished concentration of plasma Fn has been used as a biomarker in evaluating sepsis [15]. The reduction in the plasma Fn concentration observed in patients with sepsis may arise from intravascular coagulation and cryofibrinogenemia, which is likely due to increased plasma Fn catabolism secondary to the intravascular formation of fibrin [15]. However, the mechanisms underlying this reduction remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Once FAK is activated, downstream signaling pathways, such as those associated with MAPK-Erk kinases and Src-c-Jun NH2-terminal kinase (JNK)-c-Jun, which are key regulators controlling the expression of genes related to inflammation and cell adhesion, are also activated [12–14]. In addition, the expression level of plasma Fn is decreased and can be used as a biomarker for the evaluation of sepsis [15, 16]. It has been shown that the treatment of macrophages with lipopolysaccharide (LPS), the endotoxin of Gram-negative bacteria, leads to a decrease in Fn expression [16, 17].…”

Section: Introductionmentioning

confidence: 99%

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The expression of fibronectin is significantly suppressed in macrophages to exert a protective effect against Staphylococcus aureus infection

et al. 2017

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BackgroundFibronectin (Fn) plays a major role in the attachment of Staphylococcus aureus to host cells by bridging staphylococcal fibronectin-binding proteins (FnBPs) and cell-surface integrins. A previous study demonstrated that the phagocytosis of S. aureus by macrophages is enhanced in the presence of exogenous Fn. We recently found that FnBPs overexpression also enhances phagocytic activity. The effect of S. aureus infection on the expression of macrophage Fn was investigated.ResultThe level of Fn secreted by monocytes (THP-1), macrophages, human lung adenocarcinoma (A549) cells, and hepatocellular carcinoma (HepG2) cells in response to S. aureus infection was determined by Western blotting and it was significantly suppressed only in macrophages. The activation of signaling pathways associated with Fn regulation in macrophages and HepG2 cells was also investigated by Western blotting. Erk was activated in both macrophages and HepG2 cells, whereas Src-JNK-c-Jun signaling was only activated in macrophages. A significant decrease in macrophage viability was observed in response to S. aureus infection in the presence of exogenous Fn.ConclusionThe Src-JNK-c-Jun signaling pathway was activated in macrophages in response to S. aureus infection and resulted in the suppression of Fn expression. This suppression may play a protective role in macrophages against S. aureus infection. This study provides the first demonstration that Fn is suppressed in macrophages by S. aureus infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-017-1003-9) contains supplementary material, which is available to authorized users.

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Plasma fibronectin as a marker of sepsis

Cited by 29 publications

References 31 publications

Plasma and Cellular Forms of Fibronectin as Prognostic Markers in Sepsis

Plasma and Cellular Forms of Fibronectin as Prognostic Markers in Sepsis

Construction of fibronectin conditional gene knock-out mice and the effect of fibronectin gene knockout on hematopoietic, biochemical and immune parameters in mice

The expression of fibronectin is significantly suppressed in macrophages to exert a protective effect against Staphylococcus aureus infection

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