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Infection and Immunity, December 2000, p. 6611-6617, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interaction of Surfactant Protein A with Lipopolysaccharide and Regulation of Inflammatory Cytokines in the THP-1 Monocytic Cell Line

Mingchen Song and David S. Phelps*

Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033

Received 12 July 2000/Returned for modification 11 August 2000/Accepted 6 September 2000

Pulmonary surfactant protein A (SP-A) is involved in innate immunity in the lung. In this study we investigated the interaction of SP-A with different serotypes of lipopolysaccharide (LPS) on the regulation of inflammatory cytokines in vitro. In the human monocytic cell line, THP-1, combining SP-A with lipid A or rough LPS further enhanced lipid A- or rough LPS-stimulated tumor necrosis factor alpha (TNF-alpha ) mRNA levels, while SP-A-elicited increases in TNF-alpha mRNA levels were partially neutralized. In contrast, the combination of smooth LPS and SP-A resulted in additive effects on TNF-alpha mRNA levels. We also demonstrated that there was cross-tolerance between SP-A and LPS in THP-1 cells. Pretreatment of THP-1 cells with LPS modestly inhibited the response of these cells to subsequent challenge with SP-A, with regard to the production of TNF-alpha , whereas there was no or little effect on the production of interleukin-1beta (IL-1beta ) and IL-8. Conversely, pretreatment of THP-1 cells with SP-A markedly increased the response to subsequent challenge with LPS with regard to the production of IL-1beta and IL-8, although the production of TNF-alpha was modestly decreased. However, a synergistic stimulatory effect was observed when the two agents were added simultaneously to the cells. NF-kappa B formation was downregulated in SP-A- but not in LPS-induced tolerant cells. These results suggested that SP-A exhibits different interactions with distinct serotypes of LPS. In addition, SP-A is different from LPS with regard to the induction of cross-tolerance, and these actions may be mediated, at least in part, through different mechanisms.

* Corresponding author. Mailing address: Department of Pediatrics, Rm. C7814, The Pennsylvania State University College of Medicine, P.O. Box 850, Hershey, PA 17033. Phone: (717) 531-5925. Fax: (717) 531-8985. E-mail: dsp4{at}psu.edu.

Infection and Immunity, December 2000, p. 6611-6617, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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