Responses of mice immunized with influenza virus by serosol and parenteral routes

Immunoglobulin-containing cells were revealed by immunofluorescence in lung sections from mice infected with influenza virus by the aerosol route. The numbers of immunoglobulin A (IgA)and IgM-containing cells were increasing by day 3 of the infection, whereas IgG-containing cells appeared a few days later. The responding B-cell populations appeared in two principal locations: along major airways and in consolidated lesions within lung parenchyma. IgA-containing cells were the most numerous isotype, occurring predominantly in the lamina propria of the airways. IgG-containing cells were the least frequently encountered class along airways and appeared most often within consolidated lung lesions in clustered groupings. Cells staining for mu chain appeared along the airways and in lung lesions. The population of IgM-containing cells declined approximately 30 days after infection. Cells producing alpha and gamma chains were still numerous on day 46. Assays for virus-reactive antibodies in lung secretions were positive on day 8 of the infection. The IgM titers were the first to decline, but virus-binding antibodies for all classes were still present on day 33. The implications of immune responses in viral pneumonitis were considered.

mentioning

confidence: 99%

Dynamics of B-lymphocytes in the lungs of mice exposed to aerosolized influenza virus

Owens¹,

Osebold²,

Zee³

1981

“…Using the technique of bronchopulmonary lavage, Waldman et al (21) demonstrated immunoglobulin G (IgG) and IgA in bronchoalveolar fluids from human volunteers immunized with inactivated influenza virus vaccine by the aerosol route. Recently, Scott and Sydiskis (19) reported immunoglobulin levels in mice immunized with influenza virus. In the present study the severity of influenza infection was related to quantitative changes in the serum albumin and immunoglobulin contents of respiratory secretions.…”

mentioning

confidence: 99%

Antibody responses and interferon titers in the respiratory tracts of mice after aerosolized exposure to influenza virus

Zee¹,

Osebold²,

Dotson³

1979

We studied the temporal appearance of immunoglobulins (immunoglobulins G1, G2, M, and A) and interferon in lung savage fluids of mice after aerosol exposure to influenza virus in six animal groups in which mortality rates ranged from 0 to 24%. Immunoglobulin levels in the lung lavage fluids were markedly higher in mouse groups with higher mortality rates (16, 20, and 24%) than in those with low mortality rates 40, 2.5, and 7.5%). Analysis of serum albumin in the respiratory secretions as an index of edema indicated that increased immunoglobulin G levels during the early phase of infection were due to increased vascular permeability. The detection of virus-neutralizing antibodies and antibodies reactive with influenza virus antigens in the lavage fluids at 6 to 8 days postinfection suggested local immunoglobulin synthesis as a result of antigenic stimulation. Both systemic and local antibody productions contributed to immunoglobulin levels in the respiratory secretions after aerosolized influenza virus infection. Peak levels of interferon in the lavage fluids were reached before detection of significant levels of virus-neutralizing antibody in the serum or the lung lavage.

“…The appearance of IgG before IgM has also been demonstrated in normal mice following Sendai virus infection (unpublished data). A similarly delayed appearance of IgA antibody followed nonlethal influenza A infection in normal mice (18). In contrast, some reports on infections in humans indicate that local IgA antibodies may appear exclusively (21).…”

Section: Discussionmentioning

confidence: 87%

“…Virus inoculation of the respiratory tract results in production of local secretory immunoglobulin A (IgA), IgG (2, 21), and, sometimes, trace amounts of IgM (7,18) antibody in bronchoalveolar washings (BAW). Studies of the immunoglobulin class of lung cells after respiratory virus infection in rodents have shown an initial IgG accumulation with few IgM-containing cells and a somewhat later IgA accumulation (6).…”

mentioning

confidence: 99%

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

Charlton

Blandford

1977

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.