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W Hawthorne

Publications and source records attributed to W Hawthorne.

7 recordsLinked to original sources
PubMed2000

CD8+ T cells are capable of rejecting pancreatic islet xenografts.

BACKGROUND: In this study, the capacity of CD8+ T cells to act as a potential effector mechanism in pancreatic xenograft rejection was examined. METHODS: The fate of pancreatic islet xenografts was studied in mice deficient in MHC class II molecules and CD4+ T cells. Fetal pig pancreas (FPP) or Wistar rat islets (RI) were transplanted into nondiabetic or streptozotocin-induced diabetic I-A knock-out (CII K/O) mice. RESULTS: CII K/O mice were capable of rejecting both RI and FPP grafts. RI graft survival was not prolonged compared with wild type C57BL/6 controls. However, FPP grafts did survive longer in CII K/O recipients than in C57BL/J6 mice. Both RI and FPP graft rejection were CD8+ T-cell phenomena in CII K/O mice, as anti-CD8 monoclonal antibody prolonged graft survival, there were increased CD8+ T cells in the grafts and spleens of CII K/O recipients, and cell-mediated cytotoxicity was a CD8+ T-cell phenomenon associated with activation of the perforin/granzyme B system. By contrast, RI and FPP graft rejection was a CD4+ T cell-dependent phenomenon in wild type C57BL/6 mice with graft survival prolonged by anti-CD4 monoclonal antibody. There were increased numbers of CD4+ T cells, and cell-mediated cytotoxicity was a CD4+ T-cell phenomenon associated with activation of the Fas/FasL lytic pathway. CONCLUSIONS: The results demonstrate that, in the absence of CD4+ T cells, CD8+ T cells were capable of rejecting both rat and pig pancreatic islet xenografts.

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PubMed2000

Does in situ replacement of a staphylococcal infected vascular graft with a rifampicin impregnated gelatin sealed Dacron graft reduce the incidence of subsequent infection?

BACKGROUND: The aim of this study was to treat methicillin-resistant Staphylococcus aureus (MRSA) or S. epidermidis prosthetic vascular graft infections by in situ replacement with a rifampicin bonded Gelsoft graft. METHODS: Interposition grafts were placed in the carotid artery of 56 sheep and the graft surface directly inoculated with 10(8) colony forming units of MRSA or S. epidermidis. At three weeks, grafts were harvested and sheep allocated to three groups. In the MRSA group, sheep received grafts soaked in 1.2 mg/ml (12), 10 mg/ml (10) and no rifampicin (7). For S. epidermidis, sheep received grafts soaked in 1.2 mg/ml (10), 10 mg/ml (9) and no rifampicin (8). There were two deaths, in the MRSA study group. Remaining sheep were euthanased and grafts harvested three weeks following regrafting. Swabs were taken to assess bacterial growth in the perigraft tissues, and external and internal graft surfaces. A 3-5 mm segment of graft was incubated in broth medium. RESULTS: For MRSA, no statistical difference between the groups was reached for any of the measured parameters. For S. epidermidis, a significant reduction was reached for total infected specimens in the 10 mg/ml group compared to both control (p<0.001) and 1.2 mg/ml (p<0.005) groups. Graft re-infection was also less likely to occur with S. epidermidis than MRSA. CONCLUSIONS: Replacement of S. epidermidis infected vascular grafts with 10 mg/ml rifampicin soaked Gelsoft graft is effective in reducing subsequent S. epidermidis infection. This conclusion cannot be extended to MRSA infected vascular grafts.

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PubMed1999

Does in situ replacement of a staphylococcal infected vascular graft with a rifampicin impregnated gelatin sealed Dacron graft reduce the incidence of subsequent infection?

BACKGROUND: The aim of this study was to treat methicillin-resistant Staphylococcus aureus (MRSA) or S. epidermidis prosthetic vascular graft infections by in situ replacement with a rifampicin bonded Gelsoft graft. METHODS: Interposition grafts were placed in the internal carotid artery of 56 merino sheep and the graft surface directly inoculated with 10(8) colony forming units (CFU) of MRSA (29) or S. epidermidis (27). At three weeks, grafts were harvested and sheep allocated to three groups. In the MRSA infected group, sheep received grafts soaked in 1.2 mg/ml (12), 10 mg/ml (10) and no (7) rifampicin. For S. epidermidis, sheep received grafts soaked in 1.2 mg/ml (10), 10 mg/ml (9) and no (8) rifampicin. There were two deaths, in the MRSA study group, one each from the rifampicin treated groups. The remaining sheep were euthanased and grafts harvested three weeks following regrafting. Grafts at harvests were assessed for perigraft abscess formation, anastomotic disruption and graft thrombosis. Swabs were taken to assess bacterial growth in the perigraft tissues, and external and internal graft surfaces. A 3-5 mm segment of graft was incubated in a broth medium. For S. epidermidis the remainder of the graft was ground and then incubated in a broth medium. RESULTS: For MRSA, no statistical difference between the groups was reached for any of the measured parameters. For S. epidermidis, a significant reduction was reached for total infected specimens in the 10 mg/ml group compared to both control (p<0.001) and 1.2 mg/ml (p<0.005) groups. Graft reinfection was also less likely to occur with S. epidermidis than MRSA. CONCLUSIONS: In conclusion, replacement of S. epidermidis infected vascular grafts with 10 mg/ml rifampicin soaked Gelsoft graft is effective in reducing subsequent S. epidermidis infection. This conclusion cannot be extended to MRSA infected vascular grafts.

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