An extended release for surfactant

An extended release for surfactant ost think of exocytosis as an instantaneous process that once started cannot be fine-tuned. But on page 279, Haller et al. describe the exocytosis of surfactant from specialized lung cells (alveolar type II cells), and find that the degree and rate of pore expansion can be modified, thus controlling the rate of release of this vital agent from open pores. The authors gauge the extent of pore opening by adding a dye, and comparing the rate of its accumulation in either free surfactant or surfactant that remains trapped in open pores. The relative rates give a measure of the opening of the pores, and indicate that opening can be slow initially before a later expansion or, occasionally, retraction. Pores can remain open for as long as several hours. Continuous measurements of pore behavior were made by using an M Pore opening controls surfactant release. close relative of Lassa fever virus (LFV) may sneak into cells by displacing the extracellular matrix molecule laminin from its normal binding partner, ␣-dystroglycan, according to Kunz et al. (page 301). A mutant virus with a lower binding affinity for ␣-dystroglycan fails to displace laminin and cannot infect the same cell types. This changes the course of the disease. A The infection with the mouse virus, lymphocytic choriomeningitis virus (LCMV), is played out primarily in the spleen. The high affinity virus infects mostly ␣-dystroglycan– producing dendritic cells, which normally migrate from the peripheral zone into the white pulp, where they present antigen to naive B and T cells. An infection of the dendritic cells with high affinity LCMV interferes with antigen presentation and causes immunosuppression. To infect dendritic cells and establish a persistent infection, it appears that LCMV must wrest its cellular intermediate laser strength that balances photobleaching of dye with replenishment by new dye accumulation. Surfactant comes in a big hydrophobic glob, so it is perhaps not surprising that it takes some time to unspool it through a fusion pore. But post-fusion regulation might be relevant to other exocytic cargos, such as those that are only slowly released from proteoglycan tethers or other matrices, or even untethered cargos present in vesicles that flicker open and closed only briefly. Haller et al. point to calcium as a major regulator of post-fusion pore behavior. Calcium is released by both of the two stimuli that are known to potentiate surfactant release from alveolar …