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Intravenous immunisation of rabbits with 10⁹Lactobacillus fermentum cells elicited a response, specific for lipoteichoic acid (LTA), detectable as IgM plaque-forming cells (PFC) in the spleen by day 2 and as thiol-sensitive 19s antibodies in sera by day 3. Direct PFC responses peaked at day 6, with no indirect PFC demonstrable at that time. Specific IgG PFC appeared after 14 days. A second intravenous injection 5 weeks later induced a 10-fold higher IgM PFC response to LTA which reached a maximum on day 4. An enhanced specific IgG PFC response was also observed. Serum analysis showed further evidence of the anamnestic IgM response to LTA. The results are discussed in terms of the T-dependence of the LTA immunogen.

Humoral immune responses to lipoteichoic acid (LTA) as a surface antigen of Lactobacillus jermentum were assessed in rabbits and mice. Intravenous injection of rabbits with whole bacteria was effective, over a wide range of doses (10⁴ to 10¹⁰ cells), in eliciting antibodies to LTA. In mice, significant levels of anti-LTA antibodies were induced only following intraperitoneal injection of 10⁸ to 10⁹L. fermentum cells. Rabbit antibodies to LTA were predominantly of the IgM class and were specific for the polyglycerol phosphate and carbohydrate moieties of the LTA. In contrast, both IgM and IgG anti-LTA antibodies were produced in the mouse, and antibody specificity was restricted to the polyglycerol phosphate sequence.

Regimens of intravenous injections of saline-washed Lactobacillus fermentum elicited hypersensitivity reactions in rabbits. Pathological investigation revealed evidence consistent with induction of aggregate anaphylaxis, characterised by acute cor pulmonale. Additional evidence of similar tissue injury was observed in livers of rabbits which had received several intravenous injections of L. fermentum. Deposition of immune complexes in kidney glomeruli was demonstrated in only 1 out of 11 animals. Skin testing experiments revealed that lipoteichoic acid was involved in type I and type III antibody-mediated hypersensitive states. The involvement of bacterial cell surface components and extracellular products in such reactions implies a potential role in host tissue injury.

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