Biomedical subjects
Publications and source records attributed to W J Hopkins.
Urinary glycosaminoglycan (GAG) levels were measured by the Whiteman assay in five monkeys following induction of an E. coli urinary tract infection. Urinary GAG levels rose as the infection developed and returned to baseline levels as the infection resolved. Elevated urinary GAG levels may be a marker for the tissue injury incurred by such infections and may offer insight into their pathophysiology.
Cynomolgus monkeys received either vaginal immunization with formalin-killed E. coli or vaginal instillation of excipient without the bacteria. At 2, 7, 14 and 21 days after induction of a urinary tract infection with live E. coli, immunized monkeys showed enhanced clearance of bacteriuria compared to non-immunized controls. Immunized monkeys also showed increased levels of urinary anti-E. coli IgA and IgG after the immunizing and infecting procedures. Induction of heightened local immunity by vaginal immunization may lessen host susceptibility to urinary tract infections.
Cynomolgus monkeys were infected intravesically with two different strains of uropathogenic Escherichia coli. A quantitative enzyme-linked immunosorbent assay method was used to monitor secretory and serum immune responses to the induced cystitis. Anti-E. coli secretory immunoglobulin A (sIgA) and IgG urinary antibodies were generated as a result of the cystitis. Urinary sIgA levels against the E. coli strains tested were highest at 25 to 31 days after cystitis induction, and urinary IgG levels were highest at 31 to 45 days after induction. Anti-E. coli IgM was not detected in the urine. The antibody response in serum was characterized by IgM, IgG, and IgA immunoglobulin production. IgM levels in serum rose at 14 days after cystitis induction and were sustained for another 1 to 2 weeks. Increases in serum IgG levels began at 7 to 21 days of infection and persisted in some cases for up to 70 days. Serum IgA to the infecting E. coli was produced within 1 week after cystitis induction and remained at elevated levels throughout the course of the cystitis. These results demonstrate the capacity of primates to spontaneously resolve a cystitis and to mount both local and systemic immune responses against the infecting bacteria.
Twenty-eight Escherichia coli strains isolated from the urine of patients with urinary tract infections were assayed for fimbrial type, in vitro capacity to agglutinate guinea pig red blood cells, and in vivo adherence to rat bladder uroepithelium. A direct correlation was found between hemagglutinating capacity and in vivo adherence. Strains with both Type 1 and P fimbriae showed the greatest adherence in vivo. Of the 28 strains, seven did not manifest either Type 1 or P fimbriae but agglutinated red blood cells and did adhere in vivo. In studies on bacterial adherence and urinary tract infections, both in vivo and in vitro studies may contribute to understanding the relevance of bacterial adhesins in initiating urinary tract infections.
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Antibody responses of normal and congenitally athymic (nu/nu) mice were measured to the phosphorylcholine determinant of a pneumococcal C-polysaccharide. The plaque-forming cell responses of athymic mice were approximately tenfold higher than for intact controls. This enhancement was equivalent to that obtained by treatment of controls with antithymocyte serum. In both cases, the enhanced responses presumably result from a lack of suppressor T cells. Reconstitution of athymic mice with normal thymocytes restored both suppressor and helper T cell functions. Whereas suppressor activity did not appear until 6 days after transplantation of T cells, helper activity was fully restored within 24 h and had diminished by 6 days.
Treatment of BALB/c mice with heterologous anti-thymocyte serum (ATS) increases their response to the C-polysaccharide of a rough strain of Pneumococcus, R36A, but suppresses their response to a vaccine of the whole organism. Phosphorylcholine is the major antigenic determinant for both the C-polysaccharide and vaccine. ATS also suppresses the response to phosphorylcholine when it is coupled to various protein carriers. In so far as was examined, ATS had no effect on adherent cells or the capability of adherent cells and antigen to stimulate an antibody response in non-adherent cells. The contrasting effects of the antiserum can best be accounted for by assuming that it acts on at least two different populations of thymic-derived cells.
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