Modulation of Innate Immunity by G-CSF and Inflammatory Response by LBPK95A Improves the Outcome of Sepsis in a Rat Model

المؤلفون المشاركون

Dahmen, Uta
Dirsch, Olaf
Fang, Haoshu
Hua, Chuanfeng
Weiss, Stefanie
Cheng, Wenhui
Rödel, Jürgen
Claus, Ralf A.
Liu, Anding

المصدر

Journal of Immunology Research

العدد

المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-12، 12ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2018-11-07

دولة النشر

مصر

عدد الصفحات

12

التخصصات الرئيسية

الأحياء

الملخص EN

Introduction.

Sepsis is the primary cause of death from infection.

We wanted to improve the outcome of sepsis by stimulating innate immunity in combination with modulating the severity of inflammatory responses in rats.

Method.

Sepsis was induced by the injection of feces suspension (control).

A 5-day course of G-CSF treatment was given before the septic insult (G-CSF).

The inflammatory response was decreased using various doses of the LPS-blocking peptide LBPK95A (5 mg/kg=100% Combi group, 0.5 mg/kg=10% Combi group, and 0.05 mg/kg=1% Combi group).

Survival rates were observed.

Bacterial clearance, neutrophil infiltration, tissue damage, and the induction of hepatic and systemic inflammatory responses were determined 2 h and 12 h after the septic insult.

Results.

High-dose LBPK95A (100% Combi) reduced the survival rate to 10%, whereas low-dose LBPK95A (10% and 1% Combi) increased the survival rates to 50% and 80%, respectively.

The survival rates inversely correlated with multiorgan damage as indicated by the serum levels of ALT and urea.

G-CSF treatment increased the white blood cell counts, hepatic neutrophil infiltration, and bacterial clearance in the liver, lung, and blood.

The blockade of the LPS-LBP interaction decreased neutrophil infiltration, led to increased white blood cell count, and decreased hepatic neutrophil infiltration, irrespective of dose.

However, bacterial clearance improved in the 1% and 10% Combi groups but worsened in the 100% Combi group.

G-CSF increased TNF-α and IL-6 levels.

Irrespective of dose, the blockade of the LPS-LBP interaction was associated with low systemic cytokine levels and delayed increases in hepatic TNF-α and IL-6 mRNA expression.

The delayed increase in cytokines was associated with the phosphorylation of STAT3 and AKT.

Conclusion.

Our results revealed that increasing innate immunity by G-CSF pretreatment and decreasing inflammatory responses using LBPK95A improved the survival rates in a rat sepsis model and could be a novel strategy to treat sepsis.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Fang, Haoshu& Hua, Chuanfeng& Weiss, Stefanie& Liu, Anding& Cheng, Wenhui& Claus, Ralf A.…[et al.]. 2018. Modulation of Innate Immunity by G-CSF and Inflammatory Response by LBPK95A Improves the Outcome of Sepsis in a Rat Model. Journal of Immunology Research،Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1192689

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Fang, Haoshu…[et al.]. Modulation of Innate Immunity by G-CSF and Inflammatory Response by LBPK95A Improves the Outcome of Sepsis in a Rat Model. Journal of Immunology Research No. 2018 (2018), pp.1-12.
https://search.emarefa.net/detail/BIM-1192689

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Fang, Haoshu& Hua, Chuanfeng& Weiss, Stefanie& Liu, Anding& Cheng, Wenhui& Claus, Ralf A.…[et al.]. Modulation of Innate Immunity by G-CSF and Inflammatory Response by LBPK95A Improves the Outcome of Sepsis in a Rat Model. Journal of Immunology Research. 2018. Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1192689

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1192689