Biodegradation of crude oil by Chelatococcus daeguensis HB-4 and its potential for microbial enhanced oil recovery (MEOR) in heavy oil reservoirs.

Biodegradation of crude heavy oil was investigated with Chelatococcus daeguensis HB-4 that was isolated from the produced fluid of Baolige Oilfield in China. Batch growth characterization and crude oil degradation tests confirmed HB-4 to be facultative anaerobic and able to degrade heavy oil. The oil degradation was found to occur through degrading long hydrocarbons chains to shorter ones, resulting in oil viscosity reduction. By mixing crude oil with glucose, or using sole crude oil as carbon source, the content of light fractions (C8-C22) increased by 4.97% while heavy fractions (C23-C37) decreased by 7.98%. It was also found that bioemulsifiers were produced rather than commonly observed biosurfactants in the fermentation process, which was attributed to the extracellular degradation of hydrocarbons. Core flooding tests demonstrated 20.5% oil recovery by microbial enhancement, and 59.8% viscosity reduction, showing potential of strain HB-4 for application in the oil industry, especially in enhanced heavy oil recovery.

[Influence of excessive complement activation on pathological process of acute graft versus host disease in mice].

This study was aimed to explore the influence of excessive complement activation on the pathological process of acute graft-versus-host disease (aGVHD) in mice. A murine model with aGVHD was established by injecting cell mixture containing splenocytes and bone marrow cells at 2:1 ratio from donor C57BL/6(H-2K(b)) mice into recipient BALB/c (H-2K(d)) mice within 4-6 hours after 8 Gy (60)Co γ-ray total body irradiation. The mice received syngeneic bone marrow transplantation were used as control group. After transplantation, the mice were monitored daily for body weight and mortality. At day 14, all mice were sacrificed and each liver was freshly dissociated for histological analysis. The hepatic mRNA abundance for complement components C3a and C5a as well as receptors for these two anaphylatoxin were tested by real-time quantitative PCR method. And the levels of C3a and C5a production in liver were detected by ELISA. The deposition of complement C3 in liver was determined by immunofluorescence staining using frozen section. The results indicated that as compared with syngeneic bone-marrow transplantation control group, experimental animals underwent aGVHD characterized by weight loss, depilation, diarrhea and lassitude. Interestingly, the hepatic mRNA expression for complement anaphylatoxin family member C3a and C5a as well as their receptors C3aR and C5aR1 in mice with aGVHD were significantly up-regulated in comparison with control group (p < 0.05). Consistently, the content of C3a and C5a in liver increased markedly in mice with aGVHD (p < 0.01). For animals ongoing aGVHD, complement component C3 depositions were observed in hepatic portal areas, around which massive inflammatory cell infiltration was also observed. It is concluded that in aGVHD animals, excessive complement activation occurs, and the activated complement components participate in pathological process of the aGVHD.

CD3 mAb treatment ameliorated the severity of the cGVHD-induced lupus nephritis in mice by up-regulation of Foxp3+ regulatory T cells in the target tissue: kidney.

Teff/Treg imbalance orchestrated the onset and the progression of the lupus nephritis in a DBA/2→B6D2F1 murine model with cGVHD. In this paper, we first used 145-2C11 Ab to treat these human SLE-like diseased animals. The results showed that short-term low-dose anti-CD3 antibody treatment induced a significant remission of established proteinuria, production of autoantibodies, immune complex deposition and renal parenchyma lesions in lupus nephritic mice. Of note, we found a robust up-regulation of Foxp3 mRNA expression in the target tissue: kidney from mice with anti-CD3 antibody treatment compared to those with control IgG treatment. Likewise, an increased renal mRNA abundance for IL-10 was also observed in anti-CD3 antibody treated mice. In contrast, genes associated with inflammation and fibrosis as well as cytokines related to effector T cell responses were down-regulated by anti-CD3 mAb treatment. These findings suggested that short-term low-dose anti-CD3 antibody treatment might induced an IL-10-secreting Foxp3(+) regulatory T cells in this cGVHD target tissue: kidney, that suppressed the activation of effector T cells (Th1, Th2 and Th17), thus ameliorating the severity of the lupus nephritis in mice.