Search PubMed⌕ Search

Biomedical subjects

B Bournonville

Publications and source records attributed to B Bournonville.

7 recordsLinked to original sources
PubMed1998

Surgical trauma does not decrease resistance to infection.

OBJECTIVE: To investigate the effect on survival of two operations done at various intervals before the induction of monobacterial or multibacterial peritonitis in rats. DESIGN: Laboratory study. SETTING: Teaching hospital, Belgium. MATERIAL: Inbred male white wistar R/A rats. INTERVENTIONS: Posterolateral laparotomy, hindleg amputation, or control (anaesthetic only) (n=90 animals in each group), followed by induction of Escherichia coli or Staphylococcus aureus peritonitis at 1, 7 or 14 days. Further groups of rats were similarly operated on (50 in each group), but peritonitis was induced by caecal ligation and puncture. MAIN OUTCOME MEASURE: Survival 7 days after induction of peritonitis. RESULTS: Of the rats in which E. coli was used to induce peritonitis 27/28 (96%), 29/29 (100%), and 21/30 (70%) had survived 7 days after induction of peritonitis in the group that underwent posterolateral laparotomy, compared with 18/30 (60%), 20/28 (71%), and 18/28 (64%) in the control group; p 0.001, 0.002, and 0.78, respectively. The figures for hindleg amputation were 21/27 (78%), 23/27 (85%), and 17/30 (57%). The corresponding figures for S. aureus peritonitis were for posterolateral laparotomy 28/30 (93%), 20/30 (67%), and 24/29 (83%) compared with controls 21/30 (70%), 9/30 (30%), and 20/29 (69%); p 0.04, 0.009, and 0.75, respectively. The figures for hindleg amputation were 21/30 (70%), 12/30 (40%), and 23/30 (77%). Similar results were obtained with peritonitis induced by caecal ligation and puncture. CONCLUSIONS: Although surgical trauma may depress various aspects of the immune response in rats, it does not decrease their resistance to intraperitoneal microbial infections. The previous opening of the peritoneal cavity seemed to improve survival in our model.

Animals↗
PubMed1998

Absence of direct relationship between intraperitoneal cellular influx and resistance to experimental peritonitis.

Intraperitoneal inflammation is an essential defence mechanism against microbial invasion of the abdominal cavity. We have recently demonstrated that a single contact with heat killed E. Coli or Staphylococcus aureus increased the intraabdominal leukocyte influx in rats later challenged by these microorganisms. The aim of the present study was to investigate some of the mechanisms of this phenomenon and to determine its effect on rats survival in an experimental model of peritonitis. The intraabdominal influx of leukocytes following intraperitoneal injection of E. coli, Pseudomonas aeruginosa or Staphylococcus was stimulated by previous intraperitoneal injection of heat killed microbes. The phenomenon was not specific, pretreatment with E. Coli enhanced the intraperitoneal inflammatory reaction against Pseudomonas and vice versa. On the contrary, pretreating the rats with heat killed microorganisms specifically improved their survival after induction of peritonitis with live bacteria, there was no cross-protection. Heat killed staphylococcus aureus which stimulated a subsequent inflammatory reaction against heat killed E. Coli had no effect on the mortality rates of E. Coli peritonitis. In conclusion, there is no direct relationship between resistance to peritonitis and the amount of leukocytes migrating into the abdominal cavity.

Animals↗
PubMed1996

Role of CD18-dependent and CD18-independent mechanisms in the increased leukocyte adhesiveness and in the variations of circulating white blood cell populations induced by anti-CD3 monoclonal antibodies.

Anti-CD3 antibodies induce a quick and profound depletion of peripheral blood mononuclear cells (PBMCs) that is not well understood. We studied the effect of OKT3, a mouse monoclonal antibody against the human CD3 complex, on the in vitro adhesion of human PBMCs to monolayers of fresh and fixed human umbilical vein endothelial cells (HUVECs). OKT3 induced an increased adhesiveness of PBMCs. This phenomenon was blocked with anti-CD18 antibodies, indicating the participation of beta 2 integrins. As this increased adhesiveness could explain the lymphopenia by adhesion of PBMCs to endothelial cells and their sequestration in some peripheral vascular beds, we studied the effect of anti-CD18 antibodies in vivo on mice injected with 145/2C11, a hamster monoclonal antibody against murine CD3. Mice treated with 145/2C11 presented with a transient granulocytopenia and a sustained reduction in PBMCs. A monoclonal anti-CD18 antibody prevented the granulocytopenia but had no effect on the drop in PBMCs. Consequently, the in vivo depletion of PBMCs after administration of an anti-CD3 monoclonal antibody involves CD18-independent mechanisms, while the transient drop in polymorphonuclear cells appears to be CD18-dependent.

Adult↗
PubMed1996

Direct activation of human peritoneal mesothelial cells by heat-killed microorganisms.

OBJECTIVE: The aim of the study was to determine if human peritoneal mesothelial cells (HPMCs) can be activated directly by bacterial products contained in preparations of heat-killed Escherichia coli and staphylococci. SUMMARY BACKGROUND DATA: It has been shown recently that cytokine-activated HPMCs produce the inflammatory mediators, interleukin-1, interleukin-6, interleukin-8, and macrophage chemotactic protein-1. Studies concerning the effects of bacterial products on HPMCs are scarce and have not yielded conclusive results. METHODS: Growth-arrested HPMC monolayers were prepared from cell suspensions obtained by enzymatic disaggregation of small pieces of omentum. They were incubated for 24 hours with heat-killed E. coli (ATCC 25922), heat-killed staphylococci (ATCC 25933), or E. coli lipopolysaccharide, and the release of various cytokines in the culture media was measured by radioimmunoassays or enzyme-linked immunosorbent assays. Results were expressed as mean +/- standard error of the mean in picograms per milliliter of supernatant and analyzed with the Wilcoxon test; p values of less than 0.05 were considered significant. RESULTS: Baseline production of interleukin-6, interleukin-8, the chemokine "regulated upon activation, normal T cell expressed and secreted" (RANTES), and macrophage chemotactic protein-1 varied widely from one omental preparation to the other. E. coli increased the release of these mediators: from 1206 +/- 316 pg/mL to 8480 +/- 2189 pg/mL for interleukin-6, from 285 +/- 58 pg/mL to 3164 +/- 1053 pg/mL for interleukin-8, from 7 +/- 5 pg/mL to 684 +/- 264 pg/mL for RANTES, and from 2212 +/- 346 pg/mL to 7726 +/- 1473 pg/mL for macrophage chemotactic protein-1. Heat-killed staphylococci did not alter significantly the production of RANTES or macrophage chemotactic protein-1 but increased the production of the two other cytokines from 1325 +/- 389 pg/mL to 2206 +/- 523 pg/mL for interleukin-6 and from 318 +/- 70 pg/mL to 819 +/- 265 pg/mL for interleukin-8. CONCLUSIONS: The authors' results show that HPMCs are able to react to a direct stimulation with heat-killed microbes. They suggest that HPMCs, as well as resident macrophages, participate actively in the initiation and possibly in the modulation of intraperitonen inflammatory reactions.

Chemokine CCL2↗
PubMed1993

Modulation of inflammatory reactions by previous contact with Escherichia coli in rats.

OBJECTIVE: To find out if contact with Escherichia coli had any effect on a subsequent inflammatory reaction induced by the same micro-organism. DESIGN: Controlled laboratory study. SETTING: University laboratory. MATERIAL: Male white Wistar rats divided into groups of 6 to 10. INTERVENTIONS: Pretreatment with sponges soaked in 1 x 10(9) heat killed E. coli inserted either subcutaneously into the back or intraperitoneally into the right hypochondrium, and 14 days later repeat challenge. Controls received sponges soaked either in saline with penicillin and streptomycin or with carrageenan lambda. Pretreatment with live or heat killed E. coli or E. coli endotoxin injected intradermally or intraperitoneally (controls were given saline). MAIN OUTCOME MEASURES: Number of white cells present in the inflammatory infiltrate and the peritoneal cavity, and titres of anti-E. coli antibody. RESULTS: Pretreatment of Wistar rats with heat-killed or live E. coli (ATCC 25922) was followed by increase in the cellular infiltrates at the site of subsequent challenge with the same micro-organism. The effect was not related to the synthesis of anti-E. coli antibodies. CONCLUSION: Surgical patients have commonly been in previous contact with E. coli; this might affect their inflammatory reactions if they came into contact with the organism after operation. Further studies are needed to clarify the precise mechanisms and clinical relevance of these findings.

Animals↗
PubMedDate not supplied

Modulation of inflammatory reactions by surgical trauma: lack of relationship with corticosteroid secretion.

The effect of surgery on inflammation was studied in male Wistar R/A rats using the carrageenin-induced edema model. Swelling of the paw was measured in standardized arbitrary units 2, 4, and 6 hr after a subcutaneous injection of carrageenin iota in the subplantar region of the right hind limb. It was significantly depressed in rats submitted to laparotomy (5.0 +/- 0.4, 8.0 +/- 1.0, 13.7 +/- 1.9) when compared with controls simply anesthetized with ether (6.2 +/- 0.5, 15.5 +/- 1.2, 23.7 +/- 0.6) (p less than 0.001 at 4 and 6 hr). This inhibition lasted for at least 24 hr and was also observed after amputation, although in these experiments, the difference between operated animals and controls was not significant. Alterations of the inflammatory cellular infiltrate were studied using polyurethane sponges soaked with carrageenin lambda implanted subcutaneously in control animals and rats undergoing laparotomy or amputation. The total number of cells recovered from these sponges 5 hr after implantation was smaller in operated rats (2.9 +/- 0.4 x 10(6) cells after laparotomy, 3.1 +/- 1.0 x 10(6) cells after amputation) when compared with controls (11.1 +/- 1.9 x 10(6) cells and 10.3 +/- 1.3 x 10(6) cells) (p less than 0.001 for laparotomy and p less than 0.005 for amputation). The inhibitory effect of operative trauma was not abolished by bilateral adrenalectomy performed 12 days before laparotomy. In rats, surgical trauma induces a depression of remote inflammatory reactions. This phenomenon is not related to increased corticosterone levels.

Adrenal Glands↗