Protection against Escherichia coli K1 infection in newborn rats by antibody to K1 capsular polysaccharide antigen

Abstract

The protective value of antibody to the K1 capsular polysaccharide antigen of Escherichia coli was investigated in a newborn rat model of E. coli K1 infection. Pregnant rats were immunized intravenously with E. coli, and the agglutinating titer to meningococcal group B polysaccharide, which is identical to K1 polysaccharide, was measured in the serum of rats and their offspring. Convalescent serum from rat mothers showed an increased antibody titer in animals injected twice but not once with E. coli K1. Although no agglutinating antibody was detected in the serum of rat pups, animals suckled by mothers having a meningococcal group B agglutinating titer of 1:8 or greater had reduced infection and mortality rates after intraperitoneal injection with E. coli K1 compared with animals suckled by mothers having a low titer of agglutinating antibody (P less than 0.05). In addition, greater protection could be conferred on rat sucklings by oral supplementation with a horse serum rich in antibody to meningococcal group B polysaccharide, suggesting that antibody was abosorbed from the gastrointestinal tract and by itself could be protective. These studies demonstrated that antibody to the capsular polysaccharide of E. coli K1 altered the severity of E. coli K1 infection. Final clearance of bacteria from the blood appeared to await the maturation of other host defense systems in the newborn rat.

Preconceptual Priming Overrides Susceptibility to Escherichia coli Systemic Infection during Pregnancy

“…These results showing protection against E. coli invasive infection transferred by serum is consistent with the ability of E. coli -specific antibodies to mediate protection against invasive E. coli infection in other infection contexts, including other rodent infection models ( 65 – 71 ). To further evaluate the priming and accumulation of protective antibodies after primary E. coli infection, levels of E. coli -specific antibodies in the sera of E. coli -primed mice were compared with those of naive control mice.…”

Current status of meningococcal group B vaccine candidates: capsular or noncapsular?

“…The N. meningitidis B capsule is made up of a 200-residue homopolymer of NeuNAc in a(2-8) linkage (polyox2-8NeuNAc) (88,125,162). This structure is both chemically and immunologically indistinguishable from that encountered in the capsule of E. coli Kl (105), an important cause of meningitis in newborns (30,112,169,183). It is also present in Pasteurella haemolytica serotype A2, an important veterinary pathogen (4), as well as in Moraxella nonliquefaciens, a normally nonpathogenic commensal recovered in about 17% of human nasal specimens (32,46).…”

“…in humans, both children and adults (236), without harmful effects. Animals hyperimmune to N. meningitidis B do not show anomalous symptoms in spite of achieving high levels of polya2-8NeuNAc-specific antibody (9,30). The absence of detectable autoimmune disease in a patient having a monoclonal gammopathy with extremely high levels of IgM specific for polyox2-8NeuNAc, and which cross-reacted with denatured DNA and polynucleotides (73,102,103), is another argument in favor of anticapsular vaccine developmental efforts.…”

The elusive determinants of bacterial interference with non-specific host defences

“…typhimurium; acid polysaccharides of encapsulated staphylococci; a glycolipoprotein from the surface slime of Ps. a e r u g i n o s a ; the capsular polysaccharide of H. influenzae type b; and capsular material of B a ct ero id esfra g ilis (Smith 1976, 19775 Denson & Mandell 1980Bartell & Krikszens 1980;Bortolussi & Ferrieri 1980;Wilton 1981;Quie et al 1981;Hunter et al 1982;Easmon 1983;Penn 1983;Stendahl 1983). As yet the capsular materials of the following organisms have only been associated with resistance to attachment and ingestion in vitro, although more investigation would show them strongly implicated and probably relevant to infection in vivo: meningococci, type B streptococci, Klebsiella pneumoniae, Pasteurella multocida and Campylobacter fetus (Densen & Mandell 1980;Robbins et al 1980;Wilton 1981;Quie et al 1981;Easmon 1983;Penn 1983).…”