Antibiotic Therapy Determines Subcutaneous Escherichia coli Abscess Formation After CD 18 Inhibition in Rabbits
| Autor: | S. R. Sharar, John M. Harlan, G. A. Talbott, James C. Paulson, Robert K. Winn |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
medicine.drug_class
Antibiotics CD18 Penicillins medicine.disease_cause Microbiology Cell Movement Ampicillin Animals Medicine Abscess Escherichia coli Escherichia coli Infections General Nursing Antibacterial agent business.industry Ceftriaxone Rehabilitation Antibodies Monoclonal hemic and immune systems medicine.disease Cephalosporins P-Selectin medicine.anatomical_structure CD18 Antigens General Health Professions Immunology Leukocytes Mononuclear Emergency Medicine Surgery Rabbits Burns business medicine.drug Subcutaneous tissue |
| Zdroj: | Journal of Burn Care & Rehabilitation. 19:284-291 |
| ISSN: | 0273-8481 |
| DOI: | 10.1097/00004630-199807000-00003 |
| Popis: | Monoclonal antibodies (MAbs) that interrupt polymorphonuclear neutrophil (PMN)-endothelial cell adhesion can ameliorate PMN-mediated injury, including burn-induced inflammatory injury, but can also impair PMN-mediated defense against bacterial infection. We report the effects of combined anti-adhesion and antibiotic therapy on local infectious sequelae after subcutaneous Escherichia coli inoculation in rabbits treated with anti-CD18 (60.3) or anti-P-selectin (PB1.3) MAb. Ampicillin or ceftriaxone were administered for 72 hours. PMN emigration was assessed at 24 hours and local infectious sequelae at 7 days. In ampicillin/60.3-treated rabbits, E. coli inoculation resulted in impaired PMN emigration and increased infectious complications, with abscesses forming at a 10,000-fold lower inoculation concentration compared with other MAb-antibiotic treatment groups. We conclude that (1) CD18, but not P-selectin blockade interferes with PMN emigration and host defense to subcutaneous E. coli, and (2) appropriate antibiotic therapy can prevent the local infectious events caused by CD18 inhibition. |
| Databáze: | OpenAIRE |
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