ABSTRACT
INTRODUCTION The spleen is the largest lymphoid organ in the body, at a crossroads between arterial blood supply and venous return. It acts as a mechanical filter for particulate antigens and microorganisms. As a part of the immune system, the spleen is involved in production of immune mediators like opsonins. A decrease in the level of factors responsible for opsonization, such as properdin and tuftsin, occurs in splenectomized patients (1,2). Complement levels are generally normal after splenectomy, but defective activation of alternate pathway has been reported. In addition, neutrophil and natural killer cell function and cytokine production are impaired (3). The ability of the spleen to remove encapsulated bacteria is especially significant, because these organisms evade antibody and complement binding (4). The antibody response to capsular polysaccharide (in encapsulated bacteria) in normal adults consists of IgM and IgG2. In patients with asplenia, IgM production is impaired, recognition of carbohydrate antigens and removal of opsonized particles containing encapsulated organisms are defective. There is no compensatory mechanism within the immune system to overcome these defects in patients with asplenia or suboptimal splenic function. Consequently asplenic and hyposplenic patients are susceptible to fulminant infections, e.g., overwhelming postsplenectomy infections (OPSIs) (4,5).
