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Journal of Endotoxin Research
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Immunostimulatory activity of aminoalkyl glucosaminide 4-phosphates (AGPs): induction of protective innate immune responses by RC-524 and RC-529

Jory R. Baldridge

Corixa Corporation, Hamilton, Montana, USA

Christopher W. Cluff

Corixa Corporation, Hamilton, Montana, USA

Jay T. Evans

Corixa Corporation, Hamilton, Montana, USA

Michael J. Lacy

Corixa Corporation, Hamilton, Montana, USA

Jeffrey R. Stephens

Department of Chemistry, Seattle University, Seattle, Washington, USA

Valerie G. Brookshire

Corixa Corporation, Hamilton, Montana, USA

Rong Wang

Corixa Corporation, Hamilton, Montana, USA

Jon R. Ward

Corixa Corporation, Hamilton, Montana, USA

Yvonne M. Yorgensen

Corixa Corporation, Hamilton, Montana, USA

David H. Persing

Corixa Corporation, Seattle, Washington, USA

David A. Johnson

Corixa Corporation, Hamilton, Montana, USA, dajohn{at}corixa.com

Earlier we showed that the structural requirements for adjuvanticity among the aminoalkyl glucosaminide 4-phosphate (AGP) class of synthetic immunostimulants may be less strict than those for other endotoxic activities, including the induction of nitric oxide synthase in murine macrophages and cytokine production in human whole blood. The known role of nitric oxide and pro-inflammatory cytokines in the activation of host defenses against infection prompted us to examine the ability of certain AGPs to enhance non-specific resistance in mice to Listeria monocytogenes and influenza infections as well as to stimulate the production of pro-inflammatory cytokines in mouse splenocytes, human PBMCs, and human U937 histiocytic lymphoma cells. Intranasal administration of RC-524 or RC-529 to mice 2 days prior to a lethal influenza challenge provided significant protection in each case. Similarly, the intravenous administration of these AGPs induced resistance to L. monocytogenes infection as measured by survival or reduction of bacteria in the spleen. Activation of the innate immune response by AGPs appears to involve activation of Toll-like receptor 4 (TLR4) because RC-524 failed to elicit a protective effect in C3H/HeJ mice which have a defect in TLR4 signaling or induce significant cytokine levels in C3H/HeJ splenocytes. Both AGPs also stimulated pro-inflammatory cytokine release in human cell cultures in a dose-dependent manner.

Journal of Endotoxin Research, Vol. 8, No. 6, 453-458 (2002)
DOI: 10.1177/09680519020080061501
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