Several investigators have hypothesized that endotoxin may act as an adjuvant, enhancing the development of an IgE response to natural rubber latex proteins following respiratory exposure. These studies were conducted to evaluate the role of endotoxin in the development of latex sensitization following two other relevant routes of exposure, topical and subcutaneous (sc). Groups of female BALB/c mice were exposed to 0, 5, 10 or 25 microg of lipopolysaccharide (LPS) alone or in conjunction with 25microg of non-ammoniated latex (NAL). For topical studies mice were dosed 5 days a week to the shaven, derm-abraded, dorsal thorax. For sc studies animals were exposed once weekly by injection between the scapulae. Total IgE levels were monitored weekly and at the termination of the study; splenocyte proliferation assays were preformed and cytokine levels were quantified on in vitro splenocyte cultures. Following topical administration, animals simultaneously exposed to NAL and LPS (a11 doses) showed approximate 50% decreases in total IgE production as compared to animals exposed to N AL alone. Animals exposed sc to NAL and LPS demonstrated more dramatic decreases in IgE levels with values reaching less than 10% of the levels in mice exposed to NAL alone. A similar decrease in in vitro splenocyte proliferation was seen. A minimal effect on proliferation was seen following in vitro stimulation with NAL in splenocytes from animals topically sensitized to NAL in the presence of LPS. However, in animals sc sensitized to NAL in the presence of LPS an approximate 50% reductions in proliferation occurred. An increase in IL-2 levels were seen in splenocyte culture supernatants from these animals, which may hinder the class switch to IgE. Data from these studies suggest that the route of exposure to endotoxin may play a role in modulation of the IgE response to latex allergens.
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