Lipopolysaccharide (LPS or endotoxin) administered prenatally to mice led to the development of lower anti-OVA IgE and IgG1 levels, eosinophilia in BAL fluid, and reduced phorbol 12-myristate 13-acetate (PMA), inomycin, and OVA-induced T helper (Th) 2 cytokine production in the offspring [7,8]. The gene discussed is IGHE; the disease is Increased total eosinophil count.