Hypersensitivity to bacteria in eczema

SUMMARY The sera of persons with generalized eczema (Whitfield‐type) or with disseminated nummular eczema were examined for complement‐activating antibacterial antibodies to test the hypothesis that some eczematous change results 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 adsorbed 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 aeids) from Staphy‐lococcus aureus and a micrococcus (Baird‐Parker types Si and Ml respectively) are adsorbed by mono‐layers of human skin, embryo or amnion. Cells acquiring the antigen(s) are severely damagedwhen treated with sera containing the appropriate antibacterial antibodies and complement. IgM comple‐ment 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 thatwere 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 two 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.