The primary chemical mechanism of the beneficial medical/biological action of negative air ions necessary for life was studied. Air ion deficiency is the cause of many illnesses and treatment with air ion inhalation is effective in many cases. However, its application is limited by the absence of knowledge of the primary mechanism of its action. The superoxide anion O 2 was detected in the flow of negative air ions generated by an electroeffluvial air ionizer. Earlier, the appearance of hydrogen peroxide in solutions treated with air ions was shown. The presence of these reactive oxygen species in ultralow and low concentrations (10 12-10 6 M) suggested that the primary mechanism for the beneficial medical/biological action of negative air ions is moderate activation of free radical peroxidative oxidation within a physiological range that is lower than in tissues under pathology. It was shown in patients that treatment with inhalation of negative air ions did not induce pathological changes in superoxide dismutase activity and, under simultaneous administration of a food antioxidant, led to its mild increase. The latter, along with some previous results, supports the proposed mechanism. In addition, taking the proposed mechanism into consideration, air ion doses for treatment can be selected on an individual basis and should depend on the redox state of the patient. This should achieve better results for medical treatment with ionized air.

The effect of prolonged consumption of a vitamin-antioxidant mixture (VAM) on the frequency of spontaneous and in vitro gamma-radiation-induced micronuclei (MN) in peripheral blood lymphocytes in donors of various ages was investigated. Three groups of donors were recruited: (i) 56-83 years old (35 subjects), (ii) 23-30 years old (13 subjects), and (iii) 63-82 years old (12 subjects). Blood was sampled every 4 months for one year in all donors of the three groups. After the first sampling of blood, the donors of groups (i) and (ii) took VAM containing the vitamins A, C, E, as well as beta-carotene, folic acid, and rutin daily for 4 months. After the second blood sampling, the intake of VAM was terminated. The third blood sample was taken 4 months after termination of VAM intake. A part of the blood was exposed to gamma-radiation and the frequency of spontaneous and induced MN in lymphocytes was assayed. The analyses showed that the frequency of spontaneous and in vitro gamma-ray-induced MN in aged donors was significantly higher than that in young donors. No seasonal variations in MN frequency were observed in human lymphocytes during one year. Aged donors showed a statistically significant decrease in spontaneous MN in lymphocytes after a 4 month period of consumption of VAM. The intake of VAM by both aged and young donors promoted a decrease in MN induced lymphocytes in vitro by gamma-radiation. The results of our observations enable the suggestion that consumption of VAM favours a decrease in the chromosome damage produced by endogenous and exogenous factors in human lymphocytes.

Systemic inflammation plays a crucial role in formation of various pathological conditions, including sepsis, burns, and traumas. The main effector cells participating in progression of systemic inflammation response and sepsis are monocytes, which regulate both innate and acquired immunity via phagocytosis, synthesis of cytokines and chemokines, antigen presentation, and lymphocyte activation. Thus, the monocytes are considered as a link between innate and acquired immunity. The monocyte subpopulations taken into consideration in the study essentially determine the progression of systemic inflammation and could serve as targets for therapeutic intervention. The complexity of the analysis of pathophysiology of systemic inflammation lies in its high variability conditioned by individual peculiarities of the patients and inflammation progression specifications. To overcome these limitation, model of experimental endotoxemia (EE) is used. The results of EE, in turn, cannot be directly extrapolated on patients with the systemic inflammatory response. This review is dedicated to discussing the role of monocyte subpopulations in progression of systemic inflammation/sepsis and EE.

PurposeHouse dust mites Dermatophagoides pteronyssinus are the main source of major inhalatory allergens inducing inflammatory response. Mite extract contain both allergenic proteins and lipopolysaccharides (LPS). The main allergenic protein, Der p 2, is a functional homolog of sMD-2, a protein providing blood cell response on LPS. Der p 2 may restore the response to LPS in absence of MD-2, but its interaction with LPS in whole blood is unknown. We studied the effect of Der p 2 on LPS-mediated activation of human whole blood cells.MethodsInteraction of Der p 2 and LPS was studied on eight healthy donors. The whole blood was incubated with extract of house dust mite Dermatophagoides pteronyssinus (DP-e), recombinant antigenic protein Der p 2 variant 5 (rDep 2), Escherichia coli lipopolysaccharide and their combination. Supernatants were collected for ELISA analysis of protein content. Activation degree was determined by change in concentration of TNF-α, IL-8, IL-1Ra cytokines and sMD-2 protein.Resultsextract of mite Dermatophagoides pteronyssinus (DP-e) possessed weak inherent activity and did not cause significant increase of cytokine production. Simultaneous activation of blood cells by LPS and DP-e led to considerable increase of pro-inflammatory cytokine production. We have shown the intrinsic inducing activity of Der p 2 allergen on sMD-2 protein and TNF-α cytokine expression.ConclusionsDer p 2 allergen enhances the response of human whole blood cells to external LPS by inducing additional expression of LPS-transporting protein sMD-2. The obtained data show an important role of LPS contamination of allegrens in the progress of allergic inflammatory response.