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Inflammatory peritoneal cell profile in distinct models of peritoneal injury

Objective

To evaluate the dynamics of the acute peritoneal inflammatory response, based on characteristics of peritoneal cell populations, in the setting of peritoneal primary and secondary injuries resulting from sepsis.

Design

Experimental study using distinct models of sepsis to evaluate peritoneal inflammation.

Setting

Research laboratory at Federal University of Santa Catarina.

Subjects

Female Swiss mice.

Interventions

Animals were infected through intravenous (iv) or intraperitoneal (ip) injections of Escherichia coli in the following concentrations LD0, LD50 and LD100, while control animals received no intervention prior to sacrifice. Samples of peritoneal exudate were obtained at 4, 8, 12 and 24 h intervals after inoculation and submitted to flow cytometry analysis.

Measurements and main results

We found an early and intense growth in peritoneal cell population following ip injury. Granulocytes are the predominant cells in this process and correlate with mortality. LD100 group shows a reduction in this population at 12 and 24 h. There is an absolute and relative reduction in the macrophage cell population at 4, 8, 12 and 24 h. Following iv injury, peritoneal residents cell pattern does not suffer major modification, except for the 24 h LD0 group, in which granulocytes and lymphocytes increase and macrophages decrease.

Conclusions

This model suggests that, following E coli peritoneal challenge in mice, when a marked and maintained grow in the gralulocyte population occurs, it is associated with survival. Also, a reduction on the migration of this population, or its destruction, indicates uncontrolled systemic inflammation and death. Macrophage migration would be linked to the initiation of the specific immune response, and its population is not correlated with survival outcome.

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Andrade, J., Cavalcanti de Lima Filho, J., Spinelli, L. et al. Inflammatory peritoneal cell profile in distinct models of peritoneal injury. Crit Care 5 (Suppl 3), P26 (2001). https://doi.org/10.1186/cc1359

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  • DOI: https://doi.org/10.1186/cc1359

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