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Analysis of local and systemic inflammatory responses induced by polymicrobial peritonitis in mice.
BACKGROUND: Abdominal sepsis induces a local production of proinflammatory mediators that may trigger both septic shock and organ-system dysfunction. AIMS: The present study analyzed exudation, cell migration, and CD11a and CD18 subset cells of both local and systemic responses induced by fecal peri...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
2001
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781716/ https://www.ncbi.nlm.nih.gov/pubmed/11759107 |
Sumario: | BACKGROUND: Abdominal sepsis induces a local production of proinflammatory mediators that may trigger both septic shock and organ-system dysfunction. AIMS: The present study analyzed exudation, cell migration, and CD11a and CD18 subset cells of both local and systemic responses induced by fecal peritonitis in mice. METHODS: Animals were anesthetized and, after performing a midline incision in the abdomen, the cecum was ligated and punctured twice with a needle. Sham-operated animals were included. Some groups were previously treated with Evans blue dye (intravenously) to further evaluate the amount of tissue and abdominal cavity leakages. RESULTS: Fecal peritonitis triggered a local inflammatory reaction with an increased number of leukocytes and exudation between 6 and 48 h (p < 0.01). Although CD11a/CD18-positive cells in the abdomen peaked after 24h, a significant decrease of them was detected after 48 h (p < 0.05). At the studied period of time (6-48 h), different degrees of exudation in several organs occurred, whereas a significant late recruitment (24 h) of CD11a/CD18 cells into the lungs was observed. CONCLUSIONS: In this model, cell migration and exudation at the site of injury occurred in parallel. However, in the lungs, the recruitment of leukocytes that express CD11a/CD18 adhesion molecules constitutes a non-dependent event in relation to fluid leakage accumulation at this site. |
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