scholarly journals Role of procalcitonin and granulocyte colony stimulating factor in the early prediction of infected necrosis in severe acute pancreatitis

Gut ◽  
2000 ◽  
Vol 46 (2) ◽  
pp. 233-238 ◽  
Author(s):  
C A Muller
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Early Prediction ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Infected Necrosis ◽  
Stimulating Factor

scholarly journals Effects of Granulocyte Colony-Stimulating Factor on Opsonin Receptor Expression and Neutrophil Antibacterial Activity in a Mouse Model of Severe Acute Pancreatitis

2017 ◽  
Vol 71 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Tuo Hong-Fang ◽  
Peng Yan-Hui ◽  
Bao Lei ◽  
Zhang Wan-Xing
Keyword(s):  
Acute Pancreatitis ◽  
Mouse Model ◽  
Severe Acute Pancreatitis ◽  
Bacterial Translocation ◽  
Human Subjects ◽  
Receptor Expression ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Healthy Human ◽  
Stimulating Factor

The antimicrobial function of neutrophils, which is dependent on opsonin receptors, deteriorates in severe acute pancreatitis (SAP). Granulocyte colony-stimulating factor (G-CSF) putatively enhanced levels of the opsonin receptors CD11b and CD32/16 in healthy human subjects, and provided protection against infection in animal models of SAP. A statistically convincing study of the effect of G-CSF on CD32/16 expression in an SAP model is lacking. We used a mouse model of SAP to investigate the association between G-CSF administration and CD32/16 levels on neutrophils and bacterial translocation. G-CSF or saline was subcutaneously injected into SAP-induced mice. The pancreases were histologically examined, and leukocytes were stained to count neutrophils. The expression of CD11b and CD32/16 on neutrophils was measured by flow cytometry, and bacterial translocation was observed by bacterial culture.The numbers of CD11b and CD32/16-positive neutrophils were significantly elevated in the SAP mice treated with G-CSF, and the mean fluorescence intensities of these receptors on neutrophils were significantly elevated. Bacterial translocations to cavity organs were suppressed from 17% to 6% by G-CSF treatment. Our results indicated that the number of neutrophils significantly increased with increasing expression of CD11b and CD32/16 and their mean fluorescence intensities (MFIs). This inhibited bacterial translocation to other organs. These results are in accord with other studies in SAP dogs and SAP mice. Our findings suggest that G-CSF was effective in protecting against bacterial infection in SAP mice.

P–391 Role of subcutaneous granulocyte colony-stimulating factor infusion in thin endometrium

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
K Banerjee ◽  
B Singla
Keyword(s):  
Pregnancy Rate ◽  
Clinical Pregnancy ◽  
P Value ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Thin Endometrium ◽  
Group 2 ◽  
Stimulating Factor ◽  
Group 1

Abstract Study question To assess the role of subcutaneous granulocyte colony-stimulating factor (G-CSF) in thin endometrium cases. Summary answer G CSF has beneficial role to improve the endometrium thickness in thin endometrium. What is known already Endometrium is very important for embryo implantation and the endometrial thickness is the marker of receptivity of the endometrium. Study design, size, duration Study design - Retrospective analysis Size - 88 infertile females with thin endometrium (< 7 mm) in the age group of 23 to 40 years Duration - one year. Participants/materials, setting, methods In the group 1 of 44 females, subcutaneous infusion of G CSF (300 mcg/ml) was added along with other supplements and if lining was not more than 7 mm in 72 hours, then second infusion was given. In the group 2 of 44 females, only estradiol valerate and sildenafil were given.The efficacy of G CSF was evaluated by assessing the endometrium thickness before embryo transfer, pregnancy rates and clinical pregnancy rates. Main results and the role of chance There was no difference between the two groups regarding demographic variables, egg reserve, sperm parameters, number of embryos transferred and embryo quality. . The pregnancy rate was 60% (24 out of 40 cases) in the group 1 that was significantly higher than in-group 2 that was 31% (9 out of 29 cases) with p value < 0.0001. The clinical pregnancy rate was also significantly higher in-group 1 (55%) as compared to group 2 (24%) with p value < 0.0001. Limitations, reasons for caution Further larger cohort studies are required to explore the subcutaneous role of G CSF in thin endometrium. Wider implications of the findings: Granulocyte colony-stimulating factor has beneficial role to improve the endometrium thickness in thin endometrium. In most of previous studies, the intrauterine infusion of G CSF was given to improve the uterine lining. This is one of the few studies done that showed subcutaneous role of G CSF in thin endometrium. Trial registration number Not applicable

scholarly journals Interleukin-6 and the Granulocyte Colony-Stimulating Factor Receptor Are Major Independent Regulators of Granulopoiesis In Vivo But Are Not Required for Lineage Commitment or Terminal Differentiation

Blood ◽  
1997 ◽  
Vol 90 (7) ◽  
pp. 2583-2590 ◽  
Author(s):  
Fulu Liu ◽  
Jennifer Poursine-Laurent ◽  
Huai Yang Wu ◽  
Daniel C. Link
Keyword(s):  
Interleukin 6 ◽  
Terminal Differentiation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Normal Numbers ◽  
Stimulating Factor ◽  
Deficient Mice ◽  
Additional Loss

Multiple hematopoietic cytokines can stimulate granulopoiesis; however, their relative importance in vivo and mechanisms of action remain unclear. We recently reported that granulocyte colony-stimulating factor receptor (G-CSFR)-deficient mice have a severe quantitative defect in granulopoiesis despite which phenotypically normal neutrophils were still detected. These results confirmed a role for the G-CSFR as a major regulator of granulopoiesis in vivo, but also indicated that G-CSFR independent mechanisms of granulopoiesis must exist. To explore the role of interleukin-6 (IL-6) in granulopoiesis, we generated IL-6 × G-CSFR doubly deficient mice. The additional loss of IL-6 significantly worsened the neutropenia present in young adult G-CSFR–deficient mice; moreover, exogenous IL-6 stimulated granulopoiesis in vivo in the absence of G-CSFR signals. Near normal numbers of myeloid progenitors were detected in the bone marrow of IL-6 × G-CSFR–deficient mice and their ability to terminally differentiate into mature neutrophils was observed. These results indicate that IL-6 is an independent regulator of granulopoiesis in vivo and show that neither G-CSFR or IL-6 signals are required for the commitment of multipotential progenitors to the myeloid lineage or for their terminal differentiation.

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