The Gram-negative pleomorphic bacterium Haemophilus
influenza type b (Hib) is the most common cause of
bacterial meningitis in children below the age of 2. Virtually all infants between 3 and 18 month of age lack anticapsular
antibodies. This is typical for the response to a T-cell-independent
antigen. 3-5% of this group harbour Hib in the nasopharynx, but the incidence of disease is 1000-fold less. This implicates other factors in host susceptibility in addition to the absence of such
antibodies. Under physiological conditions the purified
complement subcomponent C1q interacts with
polyribosylribitolphosphate (PRP), the capsular
polysaccharide of Hib. The complex formation of C1q, the most basic
serum protein, with this polyanion was demonstrated by several methods:
agarose gel electrophoresis followed by immunoprecipitation in the gel and Coomassie staining; western blot analysis of C1q-PRP complexes; complex formation in electrophoretic separation of PRP; retardation of electrophoretic mobility of PRP was checked by blotting of this
polysaccharide. These results were confirmed by time- and dose-dependent alteration of antigenetic properties detected by C1q-Sandwich-ELISA after coincubation with PRP. Preincubation of serum treated Hib with C1q significantly enhanced the O2-metabolism of polymorphonuclear leucocytes in chemiluminescence assay. Infants of the susceptible age group develop
antibodies to several Hib outer
membrane proteins (OMP) and
lipooligosaccharides (LOS) in response to
infection. The complement activation by
immune complexes might be inhibited by the formation of C1q-PRP complexes. Our results do not support the thesis that C1q can be activated by the interaction with PRP as shown before for other
polyanions. Differing C1q to PRP ratios could be a possible explanation for different host susceptibilities.