High dose of lipopolysaccharide pre-treatment prevents OVA-induced anaphylactic decreases in rectal temperature in the immunized mice.
It remains unclear whether lipopolysaccharide (LPS) pre-treatment, which prevents Th2-type responses via Toll-like receptor 4 (TLR4), inhibits anaphylaxis. To determine the dose-dependent effects of LPS pre-treatment on anaphylactic decreases in rectal temperature caused by ovalbumin (OVA) re-exposure in immunized mice, C3H/HeN mice were divided into vehicle/OVA (0 mg/kg LPS), L-LPS/OVA (0.5 mg/kg LPS), M-LPS/OVA (1.0 mg/kg LPS) and H-LPS/OVA (3.0 mg/kg LPS) groups. After receiving these treatments, the mice were systemically immunized with OVA. Negative control mice were not immunized with OVA (N-OVA). After measuring the serum levels of OVA-specific IgE and IgG1 antibodies, the mice were examined for changes in their rectal temperature and plasma histamine concentration after OVA re-exposure. The allergen-specific IgE and IgG1 concentrations in sera from L-LPS/OVA, M-LPS/OVA and H-LPS/OVA mice were significantly lower than those in sera from vehicle/OVA mice despite OVA immunization. However, the antibody levels in all OVA-immunized mice, with the exception of the IgG1 levels in H-LPS/OVA mice, were significantly higher than those in N-OVA mice. Interestingly, H-LPS/OVA mice were the only group that did not exhibit a decrease in rectal temperature, since the rectal temperatures in vehicle/OVA, L-LPS/OVA and M-LPS/OVA mice were significantly decreased by OVA re-exposure. Furthermore, the decrease in rectal temperature after OVA re-exposure in L-LPS/OVA mice, which did not exhibit an increase in the plasma histamine concentration, was significantly prevented by treatment with a platelet-activating factor (PAF) receptor antagonist alone. Taken together, the present results indicate that high-dose LPS pre-treatment may prevent anaphylaxis in OVA-immunized mice, and that this mechanism may depend on inhibition of the IgG-PAF pathway rather than the IgE-histamine pathway.
Shiva
Daisuke
D
Division in Health Science, Kawasaki University of Medical Welfare, Kurashiki, Okayama, Japan. dshiva@aoni.waseda.jp
Matsumoto
Takashi
T
Kremenik
Michael J
MJ
Kato
Yasuko
Y
Yano
Hiromi
H
D000485:Allergens / Q000276:immunology; D000707:Anaphylaxis / Q000139:chemically induced / Q000276:immunology* / Q000517:prevention & control*; D000818:Animals; D000917:Antibody Formation / Q000276:immunology; D001831:Body Temperature / Q000187:drug effects*; D006632:Histamine / Q000097:blood; D007114:Immunization; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000276:immunology; D007074:Immunoglobulin G / Q000096:biosynthesis / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D051379:Mice; D010047:Ovalbumin / Q000494:pharmacology*; D010972:Platelet Activating Factor / Q000494:pharmacology; D012007:Rectum / Q000187:drug effects* / Q000276:immunology*
D000485:Allergens; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D007073:Immunoglobulin E; D006632:Histamine; D010047:Ovalbumin