Antibody-catalyzed water-oxidation pathway

2008 ◽  
Vol 80 (8) ◽  
pp. 1849-1858 ◽  
Author(s):  
Paul Wentworth ◽  
Daniel P. Witter

The intrinsic ability of all antibodies to generate hydrogen peroxide (H2O2) from singlet dioxygen (1O2*) via the antibody-catalyzed water-oxidation pathway (ACWOP) has triggered a rethink of the potential role of antibodies both in immune defense, inflammation, and disease. It has been shown that photochemical activation of this pathway is highly bactericidal. More recently, cholesterol oxidation by-products that may arise from the ACWOP have been discovered in vivo and are receiving a great deal of attention as possible key players in atherosclerosis and diseases of protein misfolding, such as Alzheimer's disease and Parkinson's disease.

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Zhongbin Xia ◽  
Fanru Meng ◽  
Ying Liu ◽  
Yuxuan Fang ◽  
Xia Wu ◽  
...  

Background: Rheumatoid arthritis (RA) is a inflammatory disease that characterized with the destruction of synovial joint, which could induce disability. Inflammatory response mediated the RA. It has been reported that MiR-128-3p is significantly increased in RA, while the potential role was still unclear. Methods: T cells in peripheral blood mononuclear cell (PBMC) were isolated from the peripheral blood from people of RA and normal person were used. Real-time PCR was performed to detect the expression of MiR-128-3p, while the protein expression of tumor necrosis factor-α-induced protein 3 (TNFAIP3) was determined using Western blot. The levels of IL-6 and IL-17 were measured using enzyme-linked immunosorbent assay (ELISA). The expression of CD69 and CD25 was detected using flow cytometry. The RA mouse model was constructed for verification of the role of MiR-128-3p. Results: The expression of MiR-128-3p was significantly increased, while TNFAIP3 was decreased, the levels of IL-6 and IL-17 were also increased in the T cells of RA patients. Down-regulated MiR-128-3p significantly suppressed the expression of p-IkBα and CD69, and CD25in T cells. MiR-128-3p targets TNFAIP3 to regulate its expression. MiR-128-3p knockdown significantly suppressed the activity of nuclear factor κB (NF-κB) and T cells by up-regulating TNFAIP3, while cells co-transfected with si-TNFAIP3 abolished the effects of MiR-128-3p knockdown. The in vivo experiments verified the potential role of MiR-128-3p on RA. Conclusion: Down-regulated MiR-128-3p significantly suppressed the inflammation response of RA through suppressing the activity of NF-κB pathway, which was mediated by TNFAIP3.


2005 ◽  
Vol 3 (1) ◽  
pp. 45-58 ◽  
Author(s):  
Virender K. Sharma ◽  
Futaba Kazama ◽  
Hu Jiangyong ◽  
Ajay K. Ray

Iron(VI) and iron(V), known as ferrates, are powerful oxidants and their reactions with pollutants are typically fast with the formation of non-toxic by-products. Oxidations performed by Fe(VI) and Fe(V) show pH dependence; faster rates are observed at lower pH. Fe(VI) shows excellent disinfectant properties and can inactivate a wide variety of microorganisms at low Fe(VI) doses. Fe(VI) also possesses efficient coagulation properties and enhanced coagulation can also be achieved using Fe(VI) as a preoxidant. The reactivity of Fe(V) with pollutants is approximately 3–5 orders of magnitude faster than that of Fe(VI). Fe(V) can thus be used to oxidize pollutants and inactivate microorganisms that have resistance to Fe(VI). The final product of Fe(VI) and Fe(V) reduction is Fe(III), a non-toxic compound. Moreover, treatments by Fe(VI) do not give any mutagenic/carcinogenic by-products, which make ferrates environmentally friendly ions. This paper reviews the potential role of iron(VI) and iron(V) as oxidants and disinfectants in water and wastewater treatment processes. Examples are given to demonstrate the multifunctional properties of ferrates to purify water and wastewater


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Judit Gil-Zamorano ◽  
João Tomé-Carneiro ◽  
María-Carmen Lopez de las Hazas ◽  
Lorena del Pozo-Acebo ◽  
M. Carmen Crespo ◽  
...  

Abstract The role of miRNAs in intestinal lipid metabolism is poorly described. The small intestine is constantly exposed to high amounts of dietary lipids, and it is under conditions of stress that the functions of miRNAs become especially pronounced. Approaches consisting in either a chronic exposure to cholesterol and triglyceride rich diets (for several days or weeks) or an acute lipid challenge were employed in the search for intestinal miRNAs with a potential role in lipid metabolism regulation. According to our results, changes in miRNA expression in response to fat ingestion are dependent on factors such as time upon exposure, gender and small intestine section. Classic and recent intestinal in vitro models (i.e. differentiated Caco-2 cells and murine organoids) partially mirror miRNA modulation in response to lipid challenges in vivo. Moreover, intestinal miRNAs might play a role in triglyceride absorption and produce changes in lipid accumulation in intestinal tissues as seen in a generated intestinal Dicer1-deletion murine model. Overall, despite some variability between the different experimental cohorts and in vitro models, results show that some miRNAs analysed here are modulated in response to dietary lipids, hence likely to participate in the regulation of lipid metabolism, and call for further research.


2010 ◽  
Vol 10 (9) ◽  
pp. S74-S75
Author(s):  
Mary Beth M. Grabowsky ◽  
Nicholas A. Pallotta ◽  
Matthew W. Connelly ◽  
Brett Van Etten ◽  
Rebecca A. MacDonald ◽  
...  

1988 ◽  
Vol 2 (2) ◽  
pp. 346-353 ◽  
Author(s):  
C. Chen ◽  
M.E. Wilson

Eikenella corrodens is a facultatively anaerobic Gram-negative bacterium which is among the predominant cultivable microflora of periodontal lesions characterized by loss of attachment level. In the present study, we examined the potential role of complement-mediated killing in host defense against this periodontopathic organism. Seven clinical isolates obtained from human subgingival plaque and one reference strain of E. corrodens were characterized with respect to (a) susceptibility to the bactericidal properties of pooled human serum and (b) the role of the classical and/or alternative pathway(s) of complement in effecting killing of sensitive strains. Six strains, including the reference strain, were found to be variably serum-sensitive, exhibiting 1-12.5% survival after two hr of incubation in the presence of 20% pooled human serum. The remaining two isolates were serum-resistant. Both serum-resistant and serum-sensitive strains consumed complement via the classical pathway in normal but not in hypogammaglobulinemic serum, thus ruling out an antibody-independent mechanism of classical pathway activation. Four of six serum-sensitive strains exhibited little or no loss of viability following incubation with serum depleted of the classical pathway component Clq. One strain which was resistant to killing by normal human serum was, nevertheless, highly susceptible to complement-mediated killing in the presence of rabbit immune serum. Two additional serum-sensitive strains were killed, albeit to a lesser extent, in Clq-depleted serum, indicative of a role of the alternative pathway in killing of some serum-sensitive strains. These results indicate a potential role for complement-mediated killing in host defense against Gram-negative periodontal bacteria such as E. corrodens. However, the ultimate contribution of this immune defense mechanism may be defined, at least in part, by the presence of a humoral response to key bacterial membrane constituents.


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