TABLE 2.1.

AOAH inactivates LPS

Animal host	Assay	LPS used	Reduction in activity after AOAH treatment	References
A. Evidence that AOAH-treated LPS has decreased bioactivity in vivo
Rabbit	Dermal Shwartzman reaction	Salmonella typhimurium	~100-fold	Munford and Hall (1986)
Rabbit	CSF leukocytosis	Haemophilus influenzae type b		Syrogiannopoulos et al. (1988)
Mouse	Hepatomegaly	Escherichia coli	>10-fold	Shao et al. (2007)
Mouse	Polyclonal antibody production	E. coli, Neisseria meningitidis	~100-fold	Lu et al. (2005)

Cell source	Cell type	Assay	Reduction in activity after AOAH treatment	References
B. Evidence that AOAH-treated LPS has decreased bioactivity in vitro
Human	Umbilical vein endothelial cells	Leukocyte adhesion	~90%	Pohlman et al. (1987)
Human	Umbilical vein endothelial cells	Production of prostanoids, plasminogen activator inhibitor-1	~90%	Riedo et al. (1990)
Human	Neutrophils	Adherence, superoxide production, secondary granule protein release, CD11b expression	>95%	Dal Nogare and Yarbrough (1990)
Human	Monocyte (THP- 1 cell)	IL-1 production, NF-κB activation	>95%	Kitchens et al. (1992)
Mouse	Splenocytes	Proliferation	10–500-fold	Erwin et al. (1991), Lu et al. (2005), Munford and Hall (1986)
Mouse	Macrophages, dendritic cells	Cytokine production	50-fold or greater	Lu et al. (2003, 2005)

Cell source	Cell type	Assay	Inhibition by equimolar concentration of dLPS (%) in vitro	References
C. Evidence that AOAH-treated LPS can inhibit LPS-induced cell responses
Human	Endothelial cells	Neutrophil adhesion	~30%	Kovach et al. (1990), Pohlman et al. (1987)
Human	Endothelial cells	Prostanoid, plasminogen activator inhibitor-1 production	~60%	Riedo et al. (1990)
Human	Monocytes (THP-1 cell line)	NF-κB activation	66%	Kitchens and Munford (1995), Kitchens et al. (1992)
Mouse	Splenocytes	Proliferation, antibody production	20–40%	Erwin et al. (1991), Lu et al