ISSN:
1432-1831
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The capacity of anti-IgM treated, B-cell-depleted mice to control infection by Listeria monocytogenes was evaluated. Suppression was achieved with a hyperimmune rabbit anti-mouse-IgM antiserum (IRS), with affinity-purified IRS (IRP), or with an affinity-purified, monoclonal, rat anti-mouse-IgM antibody (LO-MM-9). B-cell depletion in specifically treated mice was judged to be complete by the following criteria: absence of significant response to a B-cell mitogen lipopolysaccharide, absence of B-cells with detectable IgM or kappa light chain on their surface, absence of detectable IgM, and presence of free anti-IgM antibodies in serum. BALB/c mice, conventionally treated from birth with IRS, had an increased capacity to clear L. monocytogenes from the blood during the first 5 min after intravenous infection. Furthermore, control of infection seemed to be enhanced during the first 24 h but was found to be impaired when assessed 3 and 4 days after initiation of infection. These effects were, however, not IRS specific, because control mice treated with normal rabbit serum behaved comparably. Mortality caused by 2 × 103 L. monocytogenes injected intraperitoneally into BALB/c mice susceptible to L. monocytogenes was increased more in NRSthan in IRS-treated mice when both were compared with untreated control mice. Therefore, chronic injection of IRS or NRS seemed to disturb anti-L. monocytogenes immunity, rendering an evaluation of the role of antibodies impossible. Chronic treatment of mice, born from and raised by mothers similarly treated with monoclonal, rat anti-mouse IgM (LO-MM-9), showed that initial blood clearance (at 5 min), early (1–24 h) and late (3–5 day) bactericidal anti-Listeria activity in spleens and livers and also susceptibility as monitored by mortality were comparable to those observed in untreated BALB/c. These results demonstrate formally that antibodies, whether naturally pre-existant or specifically induced, do not play a role in either non-immunological early or subsequent T-cell-dependent control of primary Listeria monocytogenes infection in mice.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00232892
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