. (1971). Brit. J. industr. Med., 28, 179-185. Effects of chrysotile and acid-treated chrysotile on macrophage cultures. The addition of chrysotile asbestos to monolayer cultures of peritoneal and alveolar macrophages produces an increase in membrane permeability, as measured by eosin uptake and lactic dehydrogenase activity of the supernatant fluid. The lactate synthesis is increased, however. It is suggested that the permeability of the cell membrane is increased while dust particles are being phagocytosed, which may take several hours when the particles are fibrous, but that this does not imply cell damage.Treatment of chrysotile with acid, which leaves a silica surface, results in a product that reduces lactate synthesis, implying cytotoxicity. This change is counteracted by poly(2-vinylpyridine 1-oxide). The polymer does not affect the properties of the native chrysotile.Quartz particles that have been inhaled are phagocytosed by macrophages in the lung. The particles exert a cytotoxic effect and pulmonary fibrosis follows the death of macrophages. Macrophage cultures have been used to study the cytotoxicity of quartz and the ability of certain organic polymers to counteract its toxicity. Three tests that may be used are (1) the viability test, in which the uptake of acid dyes by macrophages is determined, (2) the estimation of lactic dehydrogenase (LDH) activity in the culture fluid, and (3) measurement of the rate of lactate synthesis by the cells.If a substance exerts a toxic effect on a cell, the cell membrane becomes more permeable so that acid dyes will pass into the cell and enzymes are released (Beck, 1968); decreased metabolism is shown by a decrease in the rate of lactate synthesis. An inert dust (e.g., corundum) affects viability and LDH values only slightly and it increases the rate of lactate synthesis because the work done in phagocytosing the particles increases the metabolic rate (Beck, 1968). Beck, Bruch, and Brockhaus (1963) showed that poly(2-vinyl-pyridine 1-oxide) (PVNO) reduced or even abolished the cytotoxic action of quartz particles on macrophage cultures.The published results on the effects of asbestos on cell cultures are confusing. Beck, Sack, and Bruch (1967b) found no cytochemical, optical or electron microscopical evidence of cell damage when chrysotile and other types of asbestos were incubated with mouse fibroblasts. Sack (1967), who used monolayer cultures of mouse fibroblasts (cell-line L), and peritoneal macrophages from the guinea-pig, and Beck (1970), who used alveolar macrophages from the guinea-pig, were unable to show any certain cytotoxic effects when asbestos was added although some differences were observed. Pernis, Vigliani, Marchisio, and Zanardi (1966) found no damage to mouse fibroblasts (cell-line L), KB-cells, and peritoneal macrophages of guinea-pigs, and no effect on the metabolic activity of the cells as judged by lactate production.However, Parazzi, Pemis, Secchi, and Vigliani (1968) found that, three methods (loss of fluorochromasia, LDH activity, and...
Poly-2-vinylpyridine 1 -oxide of molecular weight greater than 50,000 inhibits fibrogenesis normally associated w i t h the presence of quartz in the lungs of animals and the cytotoxic actions of silica in cultures of phagocytic cells. Poly-4-vinylpyridine 1 -oxide has little effect. Since the pathogenic effects of silica may be due to monosilicic acid produced in the cells, a study has been made of the interaction of monosilicic acid and each of these polymers. The interaction of each polymer and monosilicic acid is evidenced by a shift in the ultraviolet absorption peaks and a change in the viscosity of polymer solutions. The complex formed by the 2-isomer is stable up to 60'. as is shown by the viscosity-temperature curve, but that formed by the 4-isomer decomposes when warmed. From its ultraviolet absorption, poly-2-vinylpyridine 1 -oxide is thought to be a compact structure with stacked pyridine rings and closely packed oxygen atoms along one side of the polymer chain. This allows bonding of the silicic acid b y three hydroxy-groups. Silicic acid probably forms loose interchain cross-links w i t h poly-4-vinylpyridine oxide.
Objective Controversy exists regarding an association between Helicobacter pylori infection and asthma in children. We examined the hypotheses of inverse associations of H. pylori seroprevalence and pepsinogen (PG) levels, as markers of gastric inflammation, with asthma in children. Methods A hospital‐based case‐control study was conducted among children aged 4.8 to 17.3 years in Israel. Confirmed asthma cases (n = 75) were recruited through a pulmonary clinic, and controls (n = 160) without asthma were enrolled. Using enzyme‐linked immunosorbent assays we measured the presence of H. pylori immunoglobulin G (IgG) antibodies, IgG antibodies to cytotoxin‐associated gene A antigen (CagA) (virulent factor), serum PG levels and exposure to other enteric pathogens (Shigella flexneri). Multivariable logistic regression models were applied. Results H. pylori IgG seropositivity was 25% and 40% among cases and controls, respectively (P = .03). H. pylori CagA IgG seropositivity was associated with reduced risk of asthma (adjusted odds ratio [OR], 0.33 [95% CI, 0.11‐0.95] but not for the CagA negative serology (adjusted OR, 0.70 [95% CI, 0.32‐1.54]). Children who were H. pylori seropositive with a PGI:PGII of ≤6.78 (severe gastric inflammation) had a lower likelihood of asthma (adjusted OR, 0.31 [95% CI, 0.10‐0.89]) than did seronegative children. Exposure to Shigella flexneri did not differ between cases and controls, nor according to H. pylori seropositivity. Among the asthmatic children, pulmonary function did not differ according to H. pylori seropositivity. Conclusions H. pylori infection and its related gastric inflammation may have a protective role in the risk of pediatric asthma and further research into a potential causal pathway is required.
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