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M Frühwirth

Publications and source records attributed to M Frühwirth.

24 records · Page 2Linked to original sources
PubMed1994

Immune response in the lungs following oral immunization with bacterial lysates of respiratory pathogens.

We have investigated the local immune response of the BALB/c mouse respiratory tract after oral immunization with a bacterial lysate of seven common respiratory pathogens. After two immunization on five consecutive days, we examined the immunoglobulin (immunoglobulin G [IgG], IgM, and IgA) secretion rates of cells isolated from the lungs and compared them with those of spleen cells of orally immunized and nonimmunized animals by using a new test system based on time-resolved fluorescence. The procedure followed the principle of the classical ELISPOT test with nitrocellulose-bottomed microtiter plates, but europium (Eu3+)-linked streptavidin rather than enzyme-conjugated streptavidin was used, with the advantage of quantifying secreted immunoglobulins instead of detecting single antibody-secreting cells. Lymphocytes isolated from the lungs of treated animals revealed significant increases in total and antigen-specific IgA synthesis compared with the rates of the controls, whereas IgG and IgM production rates showed no remarkable differences. In addition, the sera of treated mice revealed higher antigen-specific IgA titers but not increased IgM and IgG levels. We conclude that priming the gut-associated lymphoid tissue with bacterial antigens of pneumotropic microorganisms can elicit an enhanced IgA response in a distant mucosal effector site, such as the respiratory tract, according to the concept of a common mucosa-associated immune system.

Adjuvants, Immunologic↗
PubMed1994

[Enhanced antibody production by lung lymphocytes after oral immunization with Bordetella pertussis surface antigens].

The purpose of our study was to evaluate the effect of oral vaccination with Bordetella pertussis surface antigens on the immune response at the site of antigen application. We orally immunized female BALB/c mice on five consecutive days and repeated this procedure after a free interval of 10 days. Lymphocytes of the lung (LL), Peyer's patches (PPL) and lamina propria of the gut (LPL) were isolated and the immunoglobulin secretion rate was measured with time-resolved immunofluorescence. Oral immunization was found to enhance the IgA secretion rate by 69.9% in LL compared to unimmunized animals. The IgG synthesis in LL was increased by 28.1% and the IgM synthesis by 14.1%. In addition, an improvement of 47.8% was observed for the IgG secretion in LPL and PPL. Thus, our results demonstrate a strong local immune response after oral immunization with Bordetella pertussis.

Administration, Oral↗
PubMed1991

Cardiac myosin-induced myocarditis as a model of postinfectious autoimmunity.

Immunization with purified cardiac myosin induces autoimmune myocarditis in A strain mice. Because this disease parallels Coxsackievirus B3 (CB3)-induced myocarditis in many respects, we are now using the immunization model as a virus-free system to study certain forms of immunologically-mediated heart disease. In the present article we will describe several characteristics of the humoral and cellular autoimmune response acting in myosin-induced myocarditis. Furthermore, we discuss hypotheses which might explain how myosin-reactive T cells recognize and attack the heart tissue.

Animals↗
PubMed1991

Cellular infiltrate, major histocompatibility antigen expression and immunopathogenic mechanisms in cardiac myosin-induced myocarditis.

Immunization with cardiac myosin induces severe myocarditis in genetically predisposed mice. The disease closely parallels that seen after infection with Coxsackievirus B3 and is characterized by a diffuse interstitial cellular infiltrate. To analyze the immunopathologic events in the heart tissue of cardiac myosin-immunized A/J and A.SW mice, the phenotype of inflammatory cells and the expression of class I and class II major histocompatibility (MHC) antigens (Ag) was examined at different time points using the immunoperoxidase method. On day 14 after the initial immunization, very few inflammatory cells were seen, whereas on day 21 the lesions were severe and extended over the whole ventricular wall. At both time points tested, the inflammatory infiltrate was composed of Mac-1+ cells, representing 70 to 80% of the infiltrate, and Thy-1.2+ cells, representing 20 to 25%. These Thy-1.2+ cells consisted of CD4+ cells and to a lesser extent of CD8+ cells. Essentially, no B cells were found on day 14, and on day 21 their frequency was only 1 to 2%. Furthermore, massive Ig deposits were observed along the infiltrated myofibers. Both on day 14 and 21, MHC class II Ag expression was associated with cells of the inflammatory infiltrate, but no aberrant I-A Ag expression was found on endothelial cells of coronary vessels or on myofibers. Similarly, no increased MHC class I Ag expression was seen on myofibers on day 14. However, on day 21 the infiltrated myofibers did show an increase in surface MHC class I Ag expression, thereby suggesting that this phenomenon is a consequence of the inflammatory process. Furthermore, in vivo administration of monoclonal antibodies to either CD4 or CD8 protected cardiac myosin-immunized mice from myocarditis, and a similar effect was achieved by monoclonal antibody to I-A Ag. Thus, cardiac myosin-induced myocarditis is mediated by a cooperation between CD8+ cells and MHC class II restricted, i.e., CD4+ cells.

Animals↗