H A Verbrugh
University of Minnesota
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Featured researches published by H A Verbrugh.
Journal of Medical Microbiology | 1981
Willemien C. van Dijk; H A Verbrugh; Marijke E. van der Tol; Roel Peters; J. Verhoef
The opsonic and protective capacities of rabbit antisera against Escherichia coli O, K and core-glycolipid cell-wall antigens were compared with specific antibody titres as measured by agglutination and enzyme-linked immunosorbent assay. Anti-O antisera were opsonic and protective against two noncapsulate strains. Only anti-K antisera were opsonic and protective against a K-antigen-containing strain. In a mouse model anti-core-glycolipid antiserum was not protective against challenge even by a strain bearing only core glycolipid.
Antimicrobial Agents and Chemotherapy | 1982
G R Elliott; Phillip K. Peterson; H A Verbrugh; M R Freiberg; J R Hoidal; P G Quie
After an initial 2-h incubation with phagocytic cells, the growth of surviving intracellular Staphylococcus aureus was examined in the presence of subinhibitory concentrations of penicillin, cephalothin, and clindamycin. One-tenth of the minimal inhibitory concentrations of these antibiotics markedly reduced bacterial growth in normal polymorphonuclear leukocytes. In contrast, when human alveolar macrophages were studied, no inhibition of growth was seen. Subinhibitory concentrations of these antibiotics and polymorphonuclear leukocytes acted synergistically to reduce intracellular survival of S. aureus. This synergy did not appear to be dependent upon the microbicidal potential of the leukocyte respiratory burst, since no differences were found when polymorphonuclear leukocytes obtained from patients with chronic granulomatous disease were compared with those from normal donors. Images
European Journal of Clinical Microbiology & Infectious Diseases | 1982
Yvette Debets-Ossenkopp; Elaine L. Mills; W. C. van Dijk; H A Verbrugh; J. Verhoef
Many viral infections predispose to bacterial superinfection, and it has been suggested that the increased susceptibility to bacterial infections is at least in part due to the effect of virus on the phagocytic cell function. Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2]) treated leukocytes with3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 107 EID50 units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.
The Journal of Infectious Diseases | 1981
H A Verbrugh; Roel Peters; Maja Rozenberg-Arska; Phillip K. Peterson; J. Verhoef
Journal of Immunology | 1982
H A Verbrugh; Phillip K. Peterson; B Y Nguyen; S P Sisson; Y Kim
Journal of Immunology | 1980
H A Verbrugh; W C van Dijk; Roel Peters; M E van Erne; M R Daha; Phillip K. Peterson; J. Verhoef
Infection and Immunity | 1979
W C Van Dijk; H A Verbrugh; M. E. Van Der Tol; Roel Peters; J. Verhoef
Journal of Clinical Microbiology | 1984
H A Verbrugh; William F. Keane; W.E. Conroy; Phillip K. Peterson
Infection and Immunity | 1982
B. Y. T. Nguyen; Phillip K. Peterson; H A Verbrugh; Paul G. Quie; John R. Hoidal
Immunology | 1979
H A Verbrugh; W C Van Dijk; Roel Peters; M. E. Van Der Tol; J. Verhoef