Novel Potentiation of Interleukin 1[small alpha] Production in Endotoxin-Stimulated IC-21 Cells by Ambient Pressure Augmentation

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Abstract

Background

We hypothesized that increased ambient pressure would increase the production of interleukin 1[small alpha] by endotoxin-stimulated macrophages, based on the clinical observation that patients with "pus under pressure" demonstrate systemic toxic effects (a priori hypothesis).

Design and Setting

In vitro experiment in the laboratory.

Interventions

A murine macrophage line, IC-21 cells, was seeded into 6-well plates, 25x104 cells per well. Cells were incubated under atmospheric (ATM) or increased (ATM+60 mm Hg) ambient pressure (AP) in the presence or absence of endotoxin (lipopolysaccharide [LPS]). The IC-21 production of interleukin 1[small alpha] was determined at 2, 4, 8, and 12 hours. Four groups were examined: group 1: AP ATM, no LPS; group 2: AP ATM+60 mm Hg, no LPS; group 3: AP ATM and LPS, 500 ng/mL; and group 4: AP ATM+60 mm Hg and LPS, 500 ng/mL.

Main Outcome Measures

The IC-21 production of interleukin 1[small alpha].

Results

Interleukin 1[small alpha] production at 2, 4, 8, and 12 hours (mean [ +/- SD] picograms per 106 cells) was as follows: group 1: 3.0 (+/- 5.9), 8.1 (+/- 10.3), 50.5 (+/- 51.1), and 6.1 (+/- 4.1), respectively; group 2: 228.7 (+/- 110.2), 141.0 (+/- 141.8), 112.5 (+/- 98.5), and 118.2 (+/- 79.8), respectively; group 3: 37.2 (+/- 13.3), 191.5 (+/- 86.5), 627.3 (+/- 184.3), and 600.7 (+/- 67.1), respectively; and group 4: 601.2 (+/- 49.9), 1050.9 (+/- 190.6), 2684.2 (+/- 562.2), and 3144.7 (+/- 388.4), respectively. The production of IL-1[small alpha] by group 3 was significantly greater (P<.04, unpaired Student t test) at 4, 8, and 12 hours than that by groups 1 or 2. Likewise, the production of IL-1[small alpha] by group 4 was significantly greater (P<.001, unpaired Student t test) at all time points than that by groups 1, 2, or 3.

Conclusions

Our data support the hypothesis that pressure may be a novel potentiator of the macrophage proinflammatory cytokine response to endotoxin. This provides a possible explanation for the phenomenon of systemic illness seen with "pus under pressure."

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