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.


BACKGROUND
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.
Kinnaert
P
P
Laboratoire Pluridisciplinaire de Recherches Expérimentales Biomédicales, Université Libre de Bruxelles, Belgium.
De Wilde
J P
JP
Bournonville
B
B
Husson
C
C
Salmon
I
I
D018932:Chemokine CCL2 / Q000096:biosynthesis*; D018946:Chemokine CCL5 / Q000096:biosynthesis*; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology; D004926:Escherichia coli; D006358:Hot Temperature; D006801:Humans; D016898:Interferon-alpha / Q000494:pharmacology; D015850:Interleukin-6 / Q000096:biosynthesis*; D016209:Interleukin-8 / Q000096:biosynthesis*; D010537:Peritoneum / Q000166:cytology* / Q000276:immunology; D013211:Staphylococcus aureus
D018932:Chemokine CCL2; D018946:Chemokine CCL5; D016898:Interferon-alpha; D015850:Interleukin-6; D016209:Interleukin-8