OBJECTIVEto investigate the effect of somatostatin on inflammatory immune disorders and prognosis in patients with severe sepsis caused by abdominal diseases.

METHODSfifty-three patients with severe abdominal sepsis (age > 18 years, APACHE-II score > 15) from June 2005 to June 2009 were randomly divided into Somatostatin group (n = 23) and SSC Group (n = 30). Fifteen healthy volunteers of the same age range were chosen as Control group. The SSC group was treated with classical SSC therapy, and the Somatostatin Group was treated with the same regime plus 14-peptide somatostatin continuous infusion at the dose of 6 mg/24 h for 7 days. The serum levels of interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α) were determined by using ELISA. CD(4)(+), CD(8)(+) T cell subsets were determined by fluorescence activated cell sorter(FACS) and CD(4)(+)/CD(8)(+) was calculated. APACHE-II score was observed on admission (d1) and day 3, 7 and 14 after treatment. Morality rates in 28 days in two groups were recorded.

RESULTScompared with Control group, IL-10 and TNF-α levels were significantly elevated in patients with severe abdominal sepsis (P < 0.05), while CD(4)(+), CD(8)(+) T cell and CD(4)(+)/CD(8)(+) decreased significantly (P < 0.05). Compared with the Somatostatin group CD(4)(+), CD(8)(+) T cell and CD(4)(+)/CD(8)(+) on d7 and d14 in SSC Group were significantly increased (P < 0.05), while IL-10 and TNF-α decreased significantly(P < 0.05). APACHE-II scores on d3, d7, d14 of Somatostatin group were significantly lower than those of SSC group, and 28 d mortality rate also declined.

CONCLUSIONSin patients with severe abdominal sepsis, systemic inflammatory response and immune suppression exist simultaneously. Somatostatin has a dual immunomodulatory activity in these patients.

APACHE ; Case-Control Studies ; Female ; Humans ; Interleukin-10 ; blood ; Male ; Prognosis ; Prospective Studies ; Sepsis ; drug therapy ; etiology ; immunology ; Somatostatin ; therapeutic use ; T-Lymphocyte Subsets ; immunology ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVE: To determine the effect of activation of specific anti-tumor cytotoxic T lymphocytes (CTL) and the ability of cross-presentation in vitro by fusion of HLA-A2+ human dendritic cells (DCs) with HLA-A2- melanoma cells. METHODS: The HLA-A2+ human dendritic cells and HLA-A2- melanoma cells were fused by PEG and were cultivated in complete RPMI1640 media containing FCS (10%) and GM-CSF for 24-48 h, and then co-cultured fusion cells with Melan-A specific T cells. HLA-A2- melanoma cells were negative control,While T2 cells and DC+Pts were positive control. The activation of anti-tumor CTL elicited by the fusion cells was detected by intracellular cytokine staining. RESULTS: The immature DC could express CD80, CD83, CD86, HLA-DR, and HLA-ABC,but the mature DC induced by TNF-alpha, PGE-2, and CD40L further highly expressed above molecules. The rate of specific CTL cells primed by the fusion cells was 16.72%+/-4.26%, negative control was 0.21%+/-1.84%,and positive control was 28.60%+/-5.67%. The CTL from vaccine by fusing DC and LAR6 induced lysis of HLA-A2+ LAR1 cells. CONCLUSION The HLA-A2 restricted specific anti-tumor CTL can be induced in vitro by fusion of HLA-A2+ human dendritic cells with HLA-A2- melanoma cells.
Antigen Presentation ; immunology ; Antigens, Neoplasm ; immunology ; Cancer Vaccines ; immunology ; Cell Fusion ; Cell Line, Tumor ; Dendritic Cells ; cytology ; immunology ; HLA-A2 Antigen ; immunology ; Humans ; MART-1 Antigen ; immunology ; Melanoma ; immunology ; pathology ; T-Lymphocytes, Cytotoxic ; immunology

Aim To investigate the role of 1L-22 / IL- 22BP axis in hepatic ischeniia-reperfusion injury and its potential mechanism.Methods Short, medium, and long-term liver ischemia-reperfusion injury (IKI) and IRI + IL-22 mouse models were established, then the scrum IL-22 concentration, IL-22BP mRNA, IL- 22R a 1 mRNA and STAT3 pathway related protein expression in liver were detected to study the role and mechanism of IL-22 and IL-22 BP in liver IRI.Results Compared with short-term ischemia-reperfusion injury group, mice in middle and long-term ischemia- reperfusion injury groups showed more severe liver injury.The concentration of serum IL-22 significantly increased but the activation of STAT3 pathway was significantly inhibited in long-term ischernia-reperfusion group.The ratio of IL-22BP / IL-22R a 1 niRNA increased significantly with the prolongation of ischemia time.Liver injury was significantly alleviated and the activation of STAT3 pathway was markedly up-regulated after the administration of exogenous recombinant 1L-22 in mice with long-term ischemia-reperfusion injury.Conclusions IL-22 can protect liver from ischemia-reperfusion injur)'; however, IL-22BP / IL-22R a 1 mRNA ratio is a negative indicator of liver injury, and the mechanism may be related to the regulation of STAT3 pathway activation by IL-22 / il-22bp axis dur-ing liver IRI.