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Exposure to dust may involve co-exposure to agents which are allergens, together with those which are pro-inflammatory. To study the effects of such a co-exposure, the humoral and inflammatory responses were studied in guinea pigs inhaling the T-cell-dependent antigen ovalbumin (OVA) and the inflammatory agents (1 --> 3)-beta-D-glucan and lipopolysaccharide (LPS). The effects were evaluated as inflammatory cells in the lung and serum antibodies to OVA. LPS caused a stimulation of the OVA-induced antibody production which was abolished by simultaneous exposure to (1 --> 3)-beta-D-glucan. An increase of eosinophils after OVA exposure was decreased by co-exposure to (1 --> 3)-beta-D-glucan. The results demonstrate a complex interaction between adaptive and innate immune mechanisms in the lung, determined by exposure to common contaminants in airborne dust.
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Rylander et al. (1998) studied this question.
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