Surfactant protein A regulates cytokine production in the monocytic cell line THP-1

Sergey G. Kremlev, Todd M. Umstead, David Phelps

Research output: Contribution to journalArticle

86 Citations (Scopus)

Abstract

Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-α within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1β increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-α and IL-1β increased in response to SP-A, peaking within 2 h. The increases in TNF-α mRNA and protein induced by SP-A were inhibited by surfactant lipids. For IL-Iβ and IL-8, the lipids either had no inhibitory influence or inhibited less than for TNF-α. This suggests that the ability of macrophages to participate in inflammatory reactions is enhanced by SP-A alone or by mixtures of lipids and SP-A containing more SP-A than in normal surfactant, as occurs in many conditions leading to inflammation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume272
Issue number5 16-5
StatePublished - May 1 1997

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Pulmonary Surfactant-Associated Protein A
Cytokines
Cell Line
Tumor Necrosis Factor-alpha
Interleukin-1
Surface-Active Agents
Lipids
Interleukin-8
Messenger RNA
Interleukin-6
Enzyme-Linked Immunosorbent Assay
Macrophages

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

Cite this

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abstract = "Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-α within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1β increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-α and IL-1β increased in response to SP-A, peaking within 2 h. The increases in TNF-α mRNA and protein induced by SP-A were inhibited by surfactant lipids. For IL-Iβ and IL-8, the lipids either had no inhibitory influence or inhibited less than for TNF-α. This suggests that the ability of macrophages to participate in inflammatory reactions is enhanced by SP-A alone or by mixtures of lipids and SP-A containing more SP-A than in normal surfactant, as occurs in many conditions leading to inflammation.",
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Surfactant protein A regulates cytokine production in the monocytic cell line THP-1. / Kremlev, Sergey G.; Umstead, Todd M.; Phelps, David.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 272, No. 5 16-5, 01.05.1997.

Research output: Contribution to journalArticle

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AB - Surfactant lipids inhibit cytokine production by immune cells, and surfactant protein A (SP-A) stimulates it. By enzyme-linked immunosorbent assay and mRNA blotting, we studied proinflammatory cytokine production by the monocytic cell line THP-1. SP-A caused increases in tumor necrosis factor (TNF)-α within 1 h, peaking at 4 h and then declining. Interleukin (IL)-1β increased and stayed elevated for 24 h. SP-A stimulated IL-8 also, peaking at 4 h, rapidly declining, and peaking again at 24 h. SP-A-dependent changes were detected for IL-6, but at higher SP-A doses. mRNA levels for TNF-α and IL-1β increased in response to SP-A, peaking within 2 h. The increases in TNF-α mRNA and protein induced by SP-A were inhibited by surfactant lipids. For IL-Iβ and IL-8, the lipids either had no inhibitory influence or inhibited less than for TNF-α. This suggests that the ability of macrophages to participate in inflammatory reactions is enhanced by SP-A alone or by mixtures of lipids and SP-A containing more SP-A than in normal surfactant, as occurs in many conditions leading to inflammation.

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