We compared the effect of 20 mm Hg increased pressure (approximating normal interstitial tissue pressure) with that of ambient pressure (resembling pressure in inflamed tissues) on tumor necrosis factor (TNF)-α and interleukin (IL)-1β production by undifferentiated (monocytic) and PMA (phorbol 12-, myristate 13-acetate)-differentiated (macrophage-like) THP-1 cells with or without lipopolysaccharide (LPS) (10 ng/mL).
Pressure stimulated spontaneous macrophage TNF-α secretion (30.5 ± 6.3 vs. 49.1 ± 2.8 pg/mL, P <.02), but not monocyte TNF-α secretion. Pressure did not stimulate IL-1β release. As expected, LPS increased basal cytokine release. After LPS stimulation, pressure still tended to stimulate macrophage TNF-α, but inhibited monocyte TNF-α secretion (P <.05). In contrast, pressure inhibited IL-1β release by both LPS-treated monocytes (986 ± 134 vs. 595 ± 226 pg/mL, P <.02) and macrophages (3,112 ± 229 vs. 979 ± 61 pg/mL, P <.01).
Extracellular pressure may regulate TNF-α and IL-1β secretion differentially by monocytes and macrophages.