Hypersensitivity to bacteria in eczema.

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Abstract
The sera of persons with generalized eczema (Whitfield-type) or with disseminated nummular eczema were examined for complement-activating antibacterial antibodies to determine if some eczematous changes result from an antibody-mediated cytotoxic reaction. Bacteria dying in the stratum corneum release soluble antigens, some of which diffuse into the stratum Malpighii and become firmly absorbed to the epidermal cells. Antibacterial antibody and complement diffusing into the epidermis react with the antigens acquired by the cells and may induce vacuolation or lysis. Phenol-extracted and freeze-press-extracted antigens (both containing teichoic acids) from Staphylococcus aureus and a Micrococcus (Baird-Parker types SI and MI, respectively) are adsorbed by monolayers of human skin, embryo or amnion. Cells acquiring the antigen(s) are severely damaged when treated with sera containing the appropriate antibacterial antibodies and complement. IgM [immunoglobulin M] complement-fixing antibody appears to be much more cytotoxic in this test than IgG. The cytotoxic activity of a serum is specific for the acquired bacterial antigen and appears to depend on a sufficient concentration of the effective antibody and not on the presence of antibodies with special properties. Explants of full thickness skin treated with bacterial antigen extracts were unharmed by the antibodies that were cytotoxic for monolayers of skin cells treated with the same antigens. The in vitro cytotoxic test should represent a potential in vivo cytotoxic phenomenon, because skin cell monolayers from 2 patients adsorbed bacterial antigen prepared from cultures obtained from the same patients and were damaged by autologous serum containing anti-staphylococcal antibody and complement. It seems probable that this may be an aggravating but not necessarily an initiating factor in many cases of eczema.