BriefDefinitive Report PASSIVE ACQUIRED MUCOSAL IMMUNITY TO GROUP A STREPTOCOCCI BY SECRETORY IMMUNOGLOBULIN A BY

M protein is a major surface component of group A streptococci, and more than 80 distinct serological types exist . Antigenic variability resides in the NH2-terminal distal portion ofthe fibrillarM protein molecule, whereas the COOH-terminal half is highly conserved among different M serotypes (1, 2) . With few exceptions, only serum IgGdirected to the antigenically variable portion ofM protein initiates opsonization and phagocytosis of streptococci by polymorphonuclear leukocytes (3) . The presence of type-specific antibodies in serum correlates with protection against group A streptococcal pharyngitis in humans (4, 5), which involves inflammation of the nasopharyngeal mucosa and underlying tissue. Alternatively, this organism can colonize the pharyngeal mucosa leading to a carrier state without clinical signs . The carrier state can persist after the development of type-specific serum antibodies (5, 6), suggesting that opsonic IgG is protective only after streptococcal infection (i .e ., pharyngitis) is established. While humans are considered to be the primary reservoir for group A streptococci, natural infection has been reported to occur in mice with the M50 serotype (7, 8) . Streptococci administered intranasally to mice can cause death by colonizing and subsequently invading the mucosal barrier and disseminating to systemic sites . Immunological protection against lethal streptococcal infection by the intranasal route might occur at either a mucosal or nonmucosal (underlying tissue, systemic) site . Secretory IgA (sIgA) can protect mucosal surfaces from colonization by pathogenic bacteria, and the effector functions of sIgA differ from those of serum-derived Igs. We investigated the role of anti-M protein-specific sIgA in protecting against streptococcal infection at the mucosa . Using a mouse model, live streptococci were mixed with affinity-purified antibodies and were administered intranasally. The data indicate that passively acquired anti-M protein sIgA given by the intranasal route protected mice against streptococcal infection, whereas opsonic serum Ig administered intranasally was without effect . The results suggest that sIgA can protect at the mucosa, and may preclude the need for opsonic IgG in preventing streptococcal infection.