PubMed · 4610208
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T Suchi. 1974. [Reticulosarcoma--various problems concerning reticulosarcoma].. https://pubmed.ncbi.nlm.nih.gov/4610208/
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Surfactant protein A (SP-A) has been shown to bind to and regulate the functions of both alveolar type II cells and immune cells including alveolar macrophages. The interaction of SP-A with type II cells has been shown in vitro to inhibit lipid secretion and to promote the uptake of lipid by these cells and these observations led to the hypothesis that SP-A plays an important role in regulating surfactant turnover and metabolism. The finding that mice made deficient in SP-A by homologous recombination (SP-A -/- mice) have relatively normal surfactant pool sizes has raised the possibility that either redundant mechanisms function in vivo to keep pool sizes normal in the absence of SP-A or that the in vitro findings are not significant in the context of the whole, unstressed animal. The interaction of SP-A with immune cells has been shown to affect a variety of responses which, in general, function to promote host defense against infection. Although SP-A receptors have been identified, additional studies will be required to elucidate the mechanism of interaction of SP-A with these cells and the relative importance of the different receptors in SP-A mediated regulation of cell function.
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The pathogenic Neisseria species constitute a multi-faceted infection model of a highly adapted pathogen-host relationship. Several bacterial and host-cell factors involved in the cellular cross-talk have been recently unraveled. Using Neisseria gonorrhoeae as a prototype, several structurally variable surface proteins, including pili and Opa proteins, have been revealed as adhesins recognizing distinct host-cell receptors. The Opa proteins, in particular, are important in facilitating interaction with heparan sulfate proteoglycan receptors and members of the CD66 and integrin receptor families. These interactions not only enable the pathogens' anchoring, and penetration into, the human mucosa but also stimulate cellular signaling cascades involving the phosphatidylcholine-dependent phospholipase C, acidic sphingomyelinase and protein kinase C in epithelial cells, and Src-related kinases, Rac1, p21-activated kinase and Jun N-terminal kinase in phagocytic cells. Activation of these pathways is essential for the entry and intracellular accommodation of the pathogens but also leads to an early induction of cytokine release, thus priming the immune response. It is believed that detailed knowledge of cellular signaling cascades activated by infection will aid us in applying known and novel interfering drugs, in addition to classical antibiotic therapy, to the therapeutic and prophylactic treatment of persistent or otherwise difficult-to-treat bacterial infections.