The effect of rabbit alveolar macrophage (AM) on the antibody secretion of bronchoalveolar lymphocytes was investigated in vitro, using a plaque-forming cell assay. Animals were intratracheally primed and reimmunized with 10(10) sheep red blood cells (SRBC). Free alveolar cells were obtained by lung lavage and broncho-alveolar lymphocyte-enrichment was achieved through Sephadex G-10 columns. Cell suspensions with various macrophage-to-lymphocyte ratios (AM:L from 1:25 to 3:1) were prepared using appropriate numbers of plastic adherent alveolar cells. After a 4 day in vitro co-culture of 5 X 10(6) alveolar cells (AM plus lymphocytes) with 3 X 10(6) SRBC, IgM and IgG antibody-forming cells (AFC) were counted. A significant suppressive effect (p less than 0.05) of AM on both IgM and IgG-AFC was observed when AM:L ratio was increased from 1:25 to 1:10. This effect was slightly accentuated with higher AM:L values, required viable AM, and was not affected by adding indomethacin in the culture medium. Moreover, a preliminary co-culture of AM with bronchoalveolar lymphocytes and the antigen was necessary for the expression of this suppressive effect. These data suggest that the suppressive activity of primed AM on alveolar lymphocytes may be of physiologic significance in vivo in the regulation of one of the pulmonary immune responses to airborne antigens, namely local antibody production.

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PubMedDate not supplied

Immunologic competence of the bronchi in the rabbit: the IgA-mediated plaque-forming response to intratracheally injected sheep erythrocytes.

Immune responses to intratracheally injected sheep erythrocytes in rabbits were investigated in bronchi, thoracic lymph nodes (TLN), mesenteric lymph nodes (MLN) and spleen using an IgA-mediated haemolytic plaque-assay. The time-course appearance of specific IgA antibody forming cells (IgA-AFC) was studied in each tissue after primary and secondary immunizations. Overall low splenic and MLN responses suggest weak systemic and intestinal immunizations, respectively. Peak IgA-AFC concentrations occurred in TLN five days after priming and, in a lesser extent, three days after the booster. Conversely, the bronchial response was delayed, progressive and enhanced by the re-immunization. These results strongly suggest that bronchial-derived, IgA-precommitted cells are the major source of these specific IgA-AFC which concentrate in bronchi and that, before homing in the submucosa, they accumulate transiently in the TLN.

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PubMedDate not supplied

[Prognostic elements in respiratory insufficiency. Analytical and prospective study].

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