Immunoglobulin Class-Specific Antibody Response in Serum, Spleen, Lungs, and Bronchoalveolar Washings After Primary and Secondary Sendai Virus Infection of Germfree Mice

Abstract

Immunoglobulin class-specific antibodies were measured by a solid-phase radioimmunoassay in serum, bronchoalveolar washings (BAW), lung cell lysates, and spleen cell lysates in germfree mice after intranasal (i.n.) and intraperitoneal (i.p.) primary and secondary 10 5 , 10 4 , and 10 3 mean tissue culture infective doses (TCID 50 ) of live parainfluenza 1 (Sendai) virus. The earliest antibody detected in lungs after i.n. virus challenge was immunoglobulin G (IgG), followed by IgM and, lastly, IgA. The local IgA response after both primary and secondary i.n. virus challenge was lowest after the severest infection. It is suggested that the delayed appearance of IgA antibody and the lower response after severe lung damage may be related to a temporary local secretory component-producing cell deficiency. The lungs were a major source of serum IgG antibody after both primary and secondary i.n. virus challenge. Only IgG and IgM antibodies were detectable in lung cell lysates after the i.n. 10 3 TCID 50 secondary response. A secondary response was detected in IgG, IgA, and IgM after secondary i.n. challenge with the other two doses. The lung response to all of primary and secondary i.p. doses of virus was exclusively IgG and IgM. Calculation of radioimmunoassay antibody per microgram of IgG, IgA, and IgM in serum and BAW after both i.n. and i.p. virus challenges showed that, when BAW antibody was present, the ratio in BAW was always higher than that in serum. This finding in the i.n. mice, together with the presence of IgA antibody-containing cells in the lungs, strongly indicates local manufacture and secretion of IgA antibodies in these animals and suggests that the same conclusion could apply to local IgG and IgM antibodies after both i.n. and i.p. challenges.

Protection of mice from wild-type Sendai virus infection by a trypsin-resistant mutant, TR-2

“…4). It was reported that in Sendai virus-infected mice, the number of IgA-secreting plasma cells in bronchial submucosa increased for a period of more than 50 days (4), IgA antibody was detectable in bronchoalveolar washings for at least 5 weeks, and reinfection stimulated its production for a longer period (7).…”

Solid-phase micro-radioimmunoassay to measure immunoglobulin class-specific antibody to Mycoplasma pulmonis

“…It was found that for each immunoglobulin class assay, the linear part of the curves B/Bo against reciprocal of dilution, for sera obtained at various times after infection, were not always parallel. Because of these differences it was not possible to calculate the titers of test sera by applying the B/Bo value obtained at each dilution of a test serum directly to the standard curve as described by Charlton and Blandford (7). To overcome problems associated with the slope of the curves, the method described in Results was therefore used to calculate units of antibody in test sera.…”

Analysis of the primary T-cell response to Sendai virus infection in C57BL/6 mice: CD4+ T-cell recognition is directed predominantly to the hemagglutinin-neuraminidase glycoprotein

“…In studying the pathogenesis of acute Sendai virus infection in the mouse, Blandford and Heath (4) showed a temporal relationship between the presence of immune complexes on the surface of desquamated respiratory epithelial cells and the detection of viral antigens in both alveolar macrophages and bronchial lymph nodes. Presence of viral antigen in alveolar macrophages is likely due to Fc receptor-mediated uptake, since these cells are not readily infected with Sendai virus in vivo (10,34). Macrophages comprise 40 to 60% of unseparated BAL (21) and may function to nonselectively present processed viral antigens captured by immune complex uptake (53).…”