A novel 37-Kd adhesive membrane protein from cloned murine bone marrow stromal cells and cloned murine hematopoietic progenitor cells

The adhesion of hematopoietic progenitor cells to bone marrow stromal cells is critical to hematopoiesis and involves multiple effector molecules. Stromal cell molecules that participate in this interaction were sought by analyzing the detergent-soluble membrane proteins of GBI/6 stromal cells that could be adsorbed by intact FDCP-1 progenitor cells. A single-chain protein from GBI/6 cells having an apparent molecular weight of 37 Kd was selectively adsorbed by FDCP-1 cells. This protein, designated p37, could be surface-radiolabeled and thus appeared to be exposed on the cell membrane. An apparently identical 37- Kd protein was expressed by three stromal cell lines, by Swiss 3T3 fibroblastic cells, and by FDCP-1 and FDCP-2 progenitor cells. p37 was selectively adsorbed from membrane lysates by a variety of murine hematopoietic cells, including erythrocytes, but not by human erythrocytes. Binding of p37 to cells was calcium-dependent, and was not affected by inhibitors of the hematopoietic homing receptor or the cell-binding or heparin-binding functions of fibronectin. It is proposed that p37 may be a novel adhesive molecule expressed on the surface of a variety of hematopoietic cells that could participate in both homotypic and heterotypic interactions of stromal and progenitor cells.     

Parasitism by Virulent Treponema pallidum of Host Cell Surfaces

The interaction between virulent Treponema pallidum extracted from infected rabbit testes and animal cells in culture was examined. The extent of treponemal attachment to monolayers of normal rabbit testicular and HEp-2 cells was dependent upon the incubation temperature and retained motility of the spirochetes. The specific orientation of treponemes to host cell surfaces was demonstrated by dark-field microscopic examination of wet-mount preparations and scanning and transmission electron microscopy. Once attached, T. pallidum organisms remained actively motile yet anchored in place by their terminal tapered structures. After several hours of co-incubation, maximal attachment was attained, and the degree of parasitism seemed regulated not only by available surface sites on individual host cells but also by the proposed membrane response of parasitized cells to continued exposure to treponemes. The avirulent strain, Treponema phagedenis biotype Reiter, did not adhere to monolayer cultures. Characterization of host cell determinants that permitted surface colonization by T. pallidum was attempted. Also, properties of virulent treponemes that enabled surface parasitism were monitored by measuring the effects of enzymes, detergents, and metabolic inhibitors on the host-parasite interaction. Results reinforced the specific nature of the treponemal attachment mechanism. Furthermore, the ability of convalescent rabbit sera to reduce attachment of treponemes to host cells suggested that surface structures on T. pallidum could be masked or inactivated by host components, thus providing a potentially effective research approach for investigating the pathogenesis of syphilis and screening appropriate vaccine candidates.     

Absence of Mycoplasma pneumoniae cytadsorption protein P1 in Mycoplasma genitalium and Mycoplasma gallisepticum

Polyclonal and monoclonal antibodies to Mycoplasma pneumoniae protein P1 were nonreactive with whole-cell or soluble preparations of M. genitalium and M. gallisepticum. However, radioimmunoprecipitation performed with hyperimmune rabbit sera raised against each mycoplasma species indicated antigenic cross-reactivity between M. pneumoniae and M. genitalium.     

Hemadsorption and virulence are separable properties of Mycoplasma pneumoniae.

A selective enrichment technique was used to isolate a hemadsorption-positive revertant of a hemadsorption-negative mutant strain of Mycoplasma pneumoniae. This hemadsorption-positive revertant was shown to have simultaneously regained both the ability to attach to neuraminidase-sensitive receptors on the tracheal ring respiratory epithelium in vitro and the ability to synthesize three virulent-strain-specific proteins which were not synthesized by the hemadsorption-negative mutant. Despite the persistence of the revertant in hamster lung tissue for 9 to 12 weeks postinfection, no cytopathology was observed. Intranasal inoculation of the revertant provided limited protection against a challenge dose of virulent M. pneumoniae.