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Biomedical subjects

M Svinhufvud

Publications and source records attributed to M Svinhufvud.

6 recordsLinked to original sources

Active immunisation and resistance to experimental acute pneumococcal otitis media.

The middle ear mucosal system and the humoral systemic immune factors are the two immunological systems whose involvement in the defence against acute otitis media (AOM) have been most intensively studied. However, their respective importance and their mutual influence is not clear. In the present study, a rat model for pneumococcal AOM was used to further elucidate the involvement of systemic immunity in protection against pneumococcal AOM. Six groups of male Sprague-Dawley rats were immunised with pneumococcal vaccine (PneumovaxRN) or live pneumococci (type 3) via one of three different routes: intraperitoneally, into the gastrointestinal tract (GIT) or into the right middle ear. A subsequent middle ear challenge (re-challenge in one group) with the same pneumococcal strain was performed after 4 days to 8 weeks in the different groups. Systemic immunity was found to be triggered, not only by systemic immunisation, but also by antigenic stimulation of the mucosa in the middle ear and in the GIT. In all groups but that immunised in the GIT, no new peak of specific IgG antibody response was demonstrated in serum after middle ear challenge/re-challenge. In contrast, half of the rats immunised in the GIT showed such a response not only after the inoculation into the GIT but also after a later performed middle ear challenge. Though a faster resolution of pus from the middle ear was observed in rats from all but one group, a significant reduction in the number of rats who developed AOM occurred exclusively among those rats that had previously manifested serological response to immunisation in the GIT.

Animals↗

Mucosal immunoreactivity in experimental pneumococcal otitis media.

A rat model was used to investigate immunological events in the middle ear mucosa during pneumococcal acute otitis media (AOM). Twelve healthy male Sprague-Dawley rats were challenged in the right middle ear with Streptococcus pneumoniae type 3, the presence of AOM being confirmed by otomicroscopy. Randomly selected rats, four at a time, were sacrificed on days 7, 14 and 56 after bacterial challenge. Immunohistochemical staining for IgG, secretory IgA (SIgA), and IgM was performed on tissue specimens from four separate locations in the middle ear and tubal mucosa. Immunoglobulins, especially IgG, were found around blood vessels in the middle ear mucosa. Immunoreactive lymphoid cells of all three Ig classes investigated, undetectable before bacterial challenge, appeared within 7-14 days after middle ear challenge, and the location of these cells in the middle ear mucosa suggests the presence of IgG, SIgA, and IgM, respectively. On the other hand, reactivity with anti-SIgA (but not with anti-IgG or anti-IgM) in Eustachian epithelial cells, and also in the subepithelial glands of tubal mucosa was present both before and after challenge. The results suggest that the middle ear mucosa is an immunoreactive site only after it has been activated with pathogens. In contrast, the tubal mucosa exhibits immunological activity also prior to the antigenic stimulation of present interest.

Animals↗

Occurrence of antibodies to pneumococcal protein antigens in experimental acute otitis media.

To study serological antibody response to pneumococcal protein antigens, experimental pneumococcal (type 3) acute otitis media (AOM) was induced in 6 rats, sera being analysed with the Western blot technique at different intervals after bacterial challenge. The most striking finding was a distinct antibody response to a protein of about 35 kDa visible in 5 of the rat sera within 14 days, and persisting throughout the remainder of the study (i.e., 56 days in all). Moreover, appear to be a phenomenon restricted to type 3 pneumococci. Both the pathogenetic importance of this protein and the immunological response it evokes are still unclear. However, as antibodies to protein antigens may contribute to inflammatory reactions in the middle ear (e.g., otitis media with effusion), this 35-kDa protein might be important for the development of sequelae to AOM.

Acute Disease↗

Western blot analysis of immunoglobulin G antibodies to pneumococcal protein antigens in healthy adults.

Using the Western Blot technique, sera from apparently healthy individuals were shown to contain antibodies against pneumococcal protein antigens of different molecular weights. A remarkable correlation was found to exist between the number of protein bands stained and the level of antibodies to type-specific carbohydrate antigens and C-polysaccharide. The findings suggest that the presence of antibodies against protein antigens reflects past infection with pneumococci.

Adult↗

Experimental recurrent pneumococcal otitis media. Protection and serum antibodies.

To elucidate immune mechanisms in otitis media, middle ear infection was induced in 12 rats by intratympanic inoculation of Streptococcus pneumoniae type 3, either the ipsilateral or the contralateral middle ear being re-challenged 4 weeks later. Otomicroscopy inspection confirmed the presence of acute otitis media (AOM) in all rats after the first challenge. After re-challenge, protection against AOM was noted both in the ipsilateral and contralateral ears. Serum antibody concentrations increased after the initial challenge, reaching a maximum at 4-7 days, but had decreased to pre-immune levels at re-challenge, after which no new increase was noted. Serum IgG-antibodies to pneumococcal type 3-polysaccharide were triggered following the initial induction of unilateral pneumococcal AOM, but mucosal immune mechanisms are argued to be a more probable explanation of the ipsilateral protection seen after re-challenge.

Animals↗

Surfactant and isoprenaline effect on eustachian tube opening in rats with acute otitis media.

Purulent otitis media was induced in 12 middle ears of Sprague-Dawley rats by inoculation of pneumococci type 3. The pressure required to open the eustachian tube was recorded 4 days later and was found to be 3.05 +/- 0.10 kPa (mean +/- SEM), which was 1.08 +/- 0.15 kPa lower than the mean value obtained in a control group of healthy rats (P less than or equal to .001). We also measured the effects of pulmonary surfactant instilled into the middle ear as well as isoprenaline injected intravenously. The presence of surfactant further reduced the pressure opening level by 0.72 +/- 0.05 kPa; this reduction did not differ from that found in the control group (P greater than .8). Isoprenaline reduced the pressure opening level in the control group by 0.20 +/- 0.03 kPa (P less than or equal to .001), and no reduction was found in the rats with otitis media. Although the part played by surface tension-lowering factors in eustachian tube function is still uncertain, such factors apparently also exert an effect in the inflamed tube. However, isoprenaline, which is considered to act by the secretion of surface tension-lowering substances, did not facilitate opening of the eustachian tube in rats with acute otitis media.

Animals↗