RESUMEN
Sepsis is a systemic reaction syndrome caused by various infectious factors,and its core mechanism is immue disorder. Macrophages, known as the most important component of innate immunity, play an important role in the occurrence and development of sepsis. Macrophage polarization has been shown to be closely related to inflammation and immunity. In the occurrence and development of sepsis,the mechanisms are complex and unclearly. The release of inflammatory factors and the occurrence of inflammatory responses will be regulated by changes in macrophage polarization phenotype. Multiple signaling pathways such as Toll-like receptor 4/nuclear transcription factor-κB (TLR4/NF-κB), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), Janus kinase/signal transduction and transcription activator (JAK/STAT), adenosine-activated protein kinase-peroxisome proliferation-activated receptor γ (AMPK-PPARγ), Notch, C-Jun amino terminal kinase (JNK), nuclear factor E2-related factor 2 (Nrf2), etc. are involved in the regulation of macrophage polarization,and interact with each other.Regulation of macrophage polarization will be a new target for the prevention and treatment of the occurrence, development and prognosis of sepsis. This paper summarized the latest progress of macrophage polarization phenotype in the occurrence and development of sepsis, aiming to provide new ideas and methods for clinical prevention and treatment of sepsis.
RESUMEN
Objective Through studying change of serum level of IL-10 in patients of severe trauma with haemorrhagic shock,to investigate effect of severe trauma with haemorrhagic shock bypass on anti-infiammatory reaction in patients.Methods Menbers of experimental group are 43 patients of Severe trauma(ISS scope≥16).43 patients scheduled for attending with haemorrhagic shock are divided into simple severe trauma group(group B)and severe trauma with haemorrhagic shock(group C);and healthy control group(group A)is made up of randomly seleeted 20 healthy people of medical examination.Blood samples for cytokines and organ function were collected from the vetn of menbers of experimental group(B and C)with limosis at the following time:that day of injury,(T1),3th (T2),5th(T3),and 14th(T4)day after injury;blood samples of healthy control group(A)with limosis were collected at that day of examination;serum level of IL-10 was measured by radioimmunoassay.Results In experimental group(B and C),the serum peak level of IL-10 emerged on T3 and then stepped down;the serum peak level of them increased abviously compared with group A(P＜0.05 or P＜0.01).Furthermore,the serum level of them in C group was usually higher than that on the same time in group B.Conclusion It was longer and severer in time and degree that effects of severe trauma with haemorrhagic shock bypass on IL-10 of body compared with that of simple severe trauma.
RESUMEN
PURPOSE: The alpha-melanocyte-stimulating hormone (alpha-MSH) has been shown to interact with various cells of the immune and inflammatory system and down-regulate either the production or the action of the pro-inflammatory cytokines. In this study, we investigated the potential of alpha-MSH on preventing pancreatic islet cell from death and dysfunction by inflammatory cytokines released from peripheral blood mononuclear cells (PBMCs) in rat. METHODS: Rat pancreatic islets were co-cultured with PBMCs, stimulated by phorbol myrstic acid and ionomycin. alpha-MSH was treated to PBMCs for 2 hours before co-culture. Viability and apoptosis of islets were observed by MTT and FACS. Inflammatory cytokines and nitric oxide (NO) were measured. Insulin release from islet co-cultured with mononuclear cells was checked for the islet function. RESULTS: In comparison to control group, viability of islets with alpha-MSH treated mononuclear cells was increased and apoptosis was reduced significantly. Inflammatory cytokines such as TNF-alpha and IL-1beta were reduced in alpha-MSH-treated group. NO production in alpha-MSH-treated group was decreased. Insulin secretory function of islet was recovered in condition of alpha-MSH treatment. CONCLUSION: This study demonstrates that alpha-MSH protects cell death and preserves the secretory function of pancreatic islet cells from the pro-inflammatory reaction of mononuclear cells, and may have the potential to improve the graft survival in clinical islet transplantation.