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* Novartis Horsham Research Center, Novartis Pharmaceutical Ltd., Horsham, United Kingdom;
SR Pharma, Center Point, London, United Kingdom; and
Department of Medical Microbiology, Windeyer Institute of Medical Sciences, Royal Free and University College Medical School, London, United Kingdom
This report examines the effect of heat-killed Mycobacterium
vaccae in a mouse model of allergic pulmonary inflammation. The
s.c. administration of M. vaccae 3 wk before the
immunization significantly reduced Ag-induced airway hyperreactivity
and the increase in the numbers of eosinophils observed in the
bronchoalveolar lavage fluid, blood, and bone marrow, even though no
detectable changes in either cytokine (IL-4, IL-13, IL-5, and IFN-
)
or total IgE levels were observed. Furthermore, transfer of splenocytes
from OVA-immunized and M. vaccae-treated mice into
recipient, OVA-immunized mice significantly reduced the
allergen-induced eosinophilia by an IFN--independent mechanism,
clearly indicating that the mechanism by which M. vaccae
induces its inhibitory effect is not due to a redirection from a
predominantly Th2 to a Th1-dominated immune response. The protective
effect of M. vaccae on the allergen-induced eosinophilia
lasted for at least 12 wk after its administration, and the treatment
was also effective in presensitized mice. Moreover, the allergen
specificity of the inhibitory effect could be demonstrated using a
double-immunization protocol, where M. vaccae treatment
before OVA immunization had no effect on the eosinophilic inflammation
induced by later immunization and challenge with cockroach extract Ag.
Taken together, these results clearly demonstrate that M.
vaccae is effective in blocking allergic inflammation by a
mechanism independent of IFN-, induces long term and Ag-specific
protection, and therefore has both prophylactic and therapeutic
potential for the treatment of allergic
diseases.
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