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IL-1 activates the Na+/H+ antiport in a murine T cell

Civitelli, R ; Teitelbaum, SL ; Hruska, KA ; Lacey, DL

The Journal of immunology (1950), 1989-12, Vol.143 (12), p.4000-4008 [Periódico revisado por pares]

United States: Am Assoc Immnol

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Título:
IL-1 activates the Na+/H+ antiport in a murine T cell
Autor: Civitelli, R ; Teitelbaum, SL ; Hruska, KA ; Lacey, DL
Assuntos: Amiloride - pharmacology ; Animals ; Carrier Proteins - drug effects ; Carrier Proteins - metabolism ; Cell Line ; Cytosol - metabolism ; Fluorescent Dyes ; Hydrogen-Ion Concentration ; Indoles ; Interleukin-1 - metabolism ; Interleukin-1 - pharmacology ; Lymphocyte Activation - drug effects ; Mice ; Receptors, Immunologic - drug effects ; Receptors, Interleukin-1 ; Recombinant Proteins - pharmacology ; Sodium-Hydrogen Exchangers ; T-Lymphocytes - enzymology ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; Tetradecanoylphorbol Acetate - pharmacology
É parte de: The Journal of immunology (1950), 1989-12, Vol.143 (12), p.4000-4008
Descrição: One of the early events following growth factor exposure is elevation of intracellular pH, a process mediated by the Na+/H+ antiport. We studied the effects of human rIL-1 alpha (HrIL-1 alpha) on intracellular pH (pHi) and calcium ([Ca2+]i) in a murine T cell line (MD10 cells), which proliferates in response to IL-1 alone. By using the intracellularly trapped fluorescent dyes (2(1),7(1)-bis-2-carboxyethyl)-5(and -6) carboxyfluorescein) and indo-1, we monitored immediate to early changes of pHi and [Ca2+]i in response to HrIL-1 alpha. Exposure to HrIL-1 alpha (120 pM) leads to an early, sustained intracellular alkalinization (delta pH = + 0.09 +/- 0.03) that plateaus within 20 min. Lower concentrations of the monokine (12 pM, 1.2 pM) have a positive but not statistically significant effect on pHi. These effects parallel the degree of MD10 IL-1R saturation predicted by the KD (49 pM) as assessed by 125I-HrIL-1 alpha binding by MD10 cells (Bmax = approximately 1300). Both the MD10 IL-1 receptor KD and the HrIL-1 alpha concentration required to induce early measurable alkaline pH shifts, however, exceed by three orders of magnitude the HrIL-1 alpha ED50 (50 fM) required for MD10 proliferation. The IL-1-induced rise in pHi is both sodium dependent and amiloride sensitive, indicative of activation of the Na+/H+ antiport. Additionally, PMA (100 nM) and IL-2 (2 nM) alkalinize MD10 cells, with the rise in pHi as a result of PMA exceeding the maximal IL-1 effect (delta pH = + 0.13 +/- 0.04). Furthermore, although PMA alkalinizes cells previously exposed to HrIL-1 alpha, the monokine does not alter the pHi of PMA-treated MD10 cells. Importantly, intracellular alkalinization induced by either HrIL-1 alpha or PMA is inhibited by staurosporine (1 mu iM). Finally, HrIL-1 alpha does not change MD10 [Ca2+]i, in either an acute or sustained fashion. These results indicate that IL-1 activates the Na+/H+ antiport in T cells by a mechanism that is unrelated to changes in [Ca2+]i but may involve protein kinase C activation.
Editor: United States: Am Assoc Immnol
Idioma: Inglês

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IL-1 activates the Na+/H+ antiport in a murine T cell

Civitelli, R ; Teitelbaum, SL ; Hruska, KA ; Lacey, DL

United States: Am Assoc Immnol

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