Assessment of chemokinetic behavior of inflammatory lung macrophages in a linear under-agarose assay.

Migration of cells in response to a chemoattractant gradient is influenced by directed migration (chemotaxis) and stimulated random motility (chemokinesis). The present study quantitated the chemokinetic motility of normal and inflammatory lung macrophages by performing the linear under-agarose assay in the presence of uniform concentrations of chemoattractant. Under these conditions, cell motility can be likened to a molecular diffusion process.

Pathogenesis of acute pulmonary inflammation in strain 2 and strain 13 guinea pigs.

An acute inflammatory response was elicited in the lungs of strain 2 and 13 guinea pigs following immunization and aerosol challenge with ovalbumin. The pulmonary inflammatory response, characterized by hemorrhage and influx of inflammatory cells, progressed from initiation at 12-hours postchallenge through resolution at 96-hours postchallenge. Inflammatory and immunoregulatory cells, recovered by bronchoalveolar lavage, showed quantitative changes in their relative contribution to the bronchoalveolar cell infiltrate over the course of inflammation.

Cellular immunoregulation of acute pulmonary inflammation in strain 2 guinea pigs.

Subclasses of lung immunoregulatory T cells were analyzed during acute pulmonary inflammation in strain 2 guinea pigs and compared with T cell subpopulations in the peripheral circulation. Immunized animals were aerosol-challenged with specific antigen and sacrificed at 12-, 24-, 48-, 72-, and 96-hours postchallenge. Mononuclear cells, isolated from peripheral blood and bronchoalveolar lavage, were enriched for T cells.

Splenic regulation of the murine pulmonary lymph node response.

Exposure to intratracheal immunization and aerosolization with soluble antigen plus murmayl-dipeptide (MDP) induces the development of plaque-forming cells in the pulmonary draining lymph nodes of two of three inbred mouse strains. Splenectomy before immunization led to a heightened plaque-forming cell response in the two responder mouse strains. Adoptive transfer of spleen cells from one strain exposed to sperm whale myoglobin via the respiratory tract revealed the presence of antigen-specific suppressor cells.

Hemolytic plaque inhibition by synthetic antigenic peptides of sperm whale myoglobin.

We have investigated the systemic antibody response to sperm whale myoglobin (SWMb) antigenic sites in three strains of inbred mice using an inhibition of plaque assay. Sperm whale myoglobin was attached to sheep red blood cells (SRBC) via rabbit anti-SRBC Fab' fragments. Inhibition of lysis was obtained with synthetic peptides representing the purported five antigenic sites but not with a peptide whose sequence was unrelated to SWMb and synthetic peptides of SWMb from outside the antigenic sites gave minimal or no inhibition.

Pulmonary immune effector cells: II. Antigen-specific blastogenic responsiveness of lymphocyte populations during pulmonary immune complex disease in guinea pigs.

A guinea pig pulmonary immune complex disease was used to evaluate local antigen (ovalbumin)-specific lymphoproliferative responses in lung tissue, bronchoalveolar spaces, and hilar lymph nodes (HLN) at various time intervals after challenge. The responses of lung tissue and bronchoalveolar lymphocytes appear to be mediated by T cells, whereas the response of HLN lymphocytes was mediated by B and/or T cells, depending on the stage of the disease. The blastogenic response of HLN lymphocytes to concanavalin A was much greater than that observed in lung tissue or bronchoalveolar lymphocyte preparations, even after the removal of adherent cells, suggesting a possible inherent difference between these cell populations in their response to mitogen.

Pulmonary immune effector cells in guinea pigs with immune complex disease. I. Changes in T- and B-lymphocyte populations after exposure to antigen.

Changes in immunologic effector cell populations in lung tissue, bronchoalveolar spaces, tracheobronchial lymph nodes, spleen, and peripheral blood were evaluated during the course of a pulmonary immune complex disease in guinea pigs. The number of macrophages, lymphocytes, and neutrophils present in each cell population were determined. T and B lymphocytes were identified by E and EAC rosette formation, respectively.

Immune complex disease in guinea pig lungs: elicitation with pigeon serum.

Immune complex- and T cell-mediated reactions to organic antigens appear to contribute to the pathogenesis of hypersensitivity pneumonitis in humans. Because pigeon serum is one of the reagents used by clinicians to diagnose this disease, we assessed its potential to elicit immune complex-mediated pulmonary inflammation in guinea pigs. Animals were immunized with different concentrations of pigeon serum protein emulsified in complete Freund's adjuvant, and serums were collected at 4-day intervals after the booster injection.

Immunologically induced lung disease in guinea pigs. A comparison of ovalbumin and pigeon serum as antigens.

This study was conducted to compare the capacity of pigeon serum (PS), an antigen (Ag) associated with hypersensitivity pneumonitis (HP), and ovalbumin (OA) in the induction of immunologic lung disease in guinea pigs (gp). Whereas OA was very effective in inducing a severe pneumonitis, PS failed to produce significant disease. A determination of the antibody (Ab) responses in OA- or PS-sensitized GP revealed that total Ab activity, as well as specific IgG1, and IgG2 responses, were not significantly different in the two groups.