Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At 37 degrees C, valproic acid was weakly bound by a PFCE through an interaction with the emulsifiers that was independent of both buffer and PFCE concentration. The binding by PFCE was dependent on valproic acid concentration in 0.1 M buffer, but not in 0.2 M buffer. The addition of PFCE to 4% HSA increased the percent free valproic acid due to both HSA dilution and displacement of HSA bound drug. This displacement was apparently due to an interaction with the PFC liquids and/or intact PFCE droplets, and with the oleic acid component of the PFCE.
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PMID:Perfluorochemical emulsion effect on human albumin binding of valproic acid. 178 38

Cells forming antibodies to HSA were determined by the haemolytic plaque technique in the spleens of chickens in which tolerance to HSA was induced on the day of hatching. After immunization with HSA 2 weeks after hatching, no anti-HSA PFC or their very low numbers were observed in chickens rendered tolerant by the dose of 100 mg HSA. In a considerable proportion of the chickens, in which tolerance was induced by 1 mg or 0.1 mg of HSA, PFC were detected, though in statistically significantly lower numbers than in control birds. In tolerant chickens receiving 100 mg of HSA after hatching, the number of PFC after immunization at 4 weeks of age was statistically significantly and at 6 weeks non-significantly lower than in the controls. After immunization with BSA at 4 weeks of age, chickens injected with 100 mg HSA after hatching had the number of anti-HSA plaque-forming cells higher than the controls, but the difference was not statistically significant.
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PMID:Antibody-producing cells in chickens tolerant to human serum albumin. 638 82

The suppressive effects of four agents on several types of in vitro immune response and on in vitro responses to T and B mitogens were studied comparatively in spleen cells from C57B1/6 mice, previously injected with each of these agents. It was found that the in vitro PFC response to sheep erythrocytes was the most constantly and extensively inhibited: from 56% after treatment with Con A to 85% after treatment with HSA; LPS and C. parvum also provoked a strong inhibition (74-78%). Inhibition of MLC was constant but less effective, ranging from 36% (LPS) to 57% (C. parvum); HSA and Con A depressed it by about 50%. The CML reaction was substantially inhibited by C. parvum (50%), moderately by Con A and LPS (respectively, 23 and 28%) and slightly by HSA (15%). The inhibition of mitogenic response to PHA and LPS varied widely with the agent used: the PHA response was strongly inhibited by Con A (84%) to a lesser extent by C. parvum (54%) and even less by LPS (27%), whereas HSA did not affect it. LPS reactivity was well inhibited by C. parvum (57%), moderately by Con A (25%), slightly by HSA and not at all by LPS. Most of these agents produced a slight but significant prolongation of skin graft survival time. In vitro experiments using mixtures of spleen cells from treated and normal animals showed that these inhibitory effects were mediated by suppressive cells that developed as a result of the treatment used. The degree of inhibition observed in the mixed cultures satisfactorily paralleled the direct inhibition observed in cells from treated animals. The more consistently suppressive agents seemed to be C. parvum and Con A, the effects of the other two (HSA and LPS) on the cellular responses studied were less regular.
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PMID:Non-specific inhibitory processes of immunological and mitogenic cellular responses. 644 6

Intrapulmonary instillation of proteins into rabbit lungs with BCG-induced granulomatous inflammation results in greater transport of these molecules into the blood, and the primary route is probably the pulmonary lymphatics. In addition, rabbits with inflamed lungs develop a more potent systemic immune response when exposed to soluble antigens as an aerosol. The current study was done to further study the mechanisms of this phenomenon using the Jerne plaque technique. Intrapulmonary immunization with soluble antigens (solubilized SRBCs and HSA) resulted in a greater PFC response to both antigens when the lungs exhibited BCG-induced granulomatous inflammation. A previous study demonstrated that more antigen administered intratracheally was found in the HLNs when the lungs displayed granulomatous inflammation. However, in the present study, we did not observe an enhanced PFC response in HLN cells when antigens were introduced into inflamed lungs. When rabbits with BCG-inflamed lungs were immunized i.v., they did not develop an enhanced PFC response in the spleen. Immunization into the respiratory tract of normal rabbits with large doses (300 micrograms) of soluble antigens also resulted in a substantial PFC response in the spleen that was quantitatively greater than that induced by the same i.v. dose. These data indicate that (1) administration of antigens into inflamed lung results in an enhanced systemic immune response, (2) although larger quantities of soluble antigens administered by the pulmonary route accumulate in the HLN when lungs are inflamed, cells from this tissue do not exhibit an enhanced PFC response, and (3) large doses of soluble antigens instilled into normal lungs induce a greater systemic immune response that the same doses administered i.v. This study further demonstrates the importance of pulmonary inflammation and the immune response to inhaled antigens and provides insight as to how individuals with chronic inflammatory lung disease can react in an augmented fashion to environmental antigens.
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PMID:Enhancement of systemic immune response by immunization into chronically inflamed lungs. 704 59