DOI: 10.1152/ajplung.00427.2002. Surfactant protein A inhibits alveolar macrophage cytokine production by CD14-independent pathway

Surfactant protein A inhibits alveolar macrophage cytokine production by CD14-independent pathway

10.1152/ajplung.00427.2002

Crossref journal-article

American Physiological Society

American Journal of Physiology-Lung Cellular and Molecular Physiology (24)

Abstract

The lung collectin surfactant protein A (SP-A) has both anti-inflammatory and prophagocytic activities. We and others previously showed that SP-A inhibits the macrophage production of tumor necrosis factor (TNF)-α stimulated by the gram-negative bacterial component LPS. We propose that SP-A decreases the production of proinflammatory cytokines by alveolar macrophages via a CD14-independent mechanism. SP-A inhibited LPS-simulated TNF-α production in rat and mouse macrophages in the presence and absence of serum (72% and 42% inhibition, respectively). In addition, SP-A inhibited LPS-induced mRNA levels for TNF-α, IL-1α, and IL-1β as well as NF-κB DNA binding activity. SP-A also diminished ultrapure LPS-stimulated TNF-α produced by wild-type and CD14-null mouse alveolar macrophages by 58% and 88%, respectively. Additionally, SP-A inhibited TNF-α stimulated by PMA in both wild-type and TLR4-mutant macrophages. These data suggest that SP-A inhibits inflammatory cytokine production in a CD14-independent manner and also by mechanisms independent of the LPS signaling pathway.

Bibliography

Alcorn, J. F., & Wright, J. R. (2004). Surfactant protein A inhibits alveolar macrophage cytokine production by CD14-independent pathway. American Journal of Physiology-Lung Cellular and Molecular Physiology, 286(1), L129âL136.

Authors 2

John F. Alcorn (first)
Jo Rae Wright (additional)

References 46 Referenced 47

Dates

Type	When
Created	21 years, 6 months ago (Jan. 30, 2004, 7:55 p.m.)
Deposited	2 years, 3 months ago (April 27, 2023, 4:21 p.m.)
Indexed	4 months, 3 weeks ago (March 30, 2025, 6:23 p.m.)
Issued	21 years, 7 months ago (Jan. 1, 2004)
Published	21 years, 7 months ago (Jan. 1, 2004)
Published Print	21 years, 7 months ago (Jan. 1, 2004)

Funders 0

None

BibTeX

@article{Alcorn_2004, title={Surfactant protein A inhibits alveolar macrophage cytokine production by CD14-independent pathway}, volume={286}, ISSN={1522-1504}, url={http://dx.doi.org/10.1152/ajplung.00427.2002}, DOI={10.1152/ajplung.00427.2002}, number={1}, journal={American Journal of Physiology-Lung Cellular and Molecular Physiology}, publisher={American Physiological Society}, author={Alcorn, John F. and Wright, Jo Rae}, year={2004}, month=jan, pages={L129–L136} }

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  "abstract": "<jats:p>The lung collectin surfactant protein A (SP-A) has both anti-inflammatory and prophagocytic activities. We and others previously showed that SP-A inhibits the macrophage production of tumor necrosis factor (TNF)-\u03b1 stimulated by the gram-negative bacterial component LPS. We propose that SP-A decreases the production of proinflammatory cytokines by alveolar macrophages via a CD14-independent mechanism. SP-A inhibited LPS-simulated TNF-\u03b1 production in rat and mouse macrophages in the presence and absence of serum (72% and 42% inhibition, respectively). In addition, SP-A inhibited LPS-induced mRNA levels for TNF-\u03b1, IL-1\u03b1, and IL-1\u03b2 as well as NF-\u03baB DNA binding activity. SP-A also diminished ultrapure LPS-stimulated TNF-\u03b1 produced by wild-type and CD14-null mouse alveolar macrophages by 58% and 88%, respectively. Additionally, SP-A inhibited TNF-\u03b1 stimulated by PMA in both wild-type and TLR4-mutant macrophages. These data suggest that SP-A inhibits inflammatory cytokine production in a CD14-independent manner and also by mechanisms independent of the LPS signaling pathway.</jats:p>",
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