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Surveillance and Countermeasures in Innate Immunity

lation factors represent an additional mechanism by which S. aureus can corrupt host defense. This is best exemplified by the extracellular complement-binding protein that impairs complement activation by binding to the C3d domain of C3 while its homolog, the extracellular fibrinogen-binding protein, blocks both complement activation and neutrophil adhesion to fibrinogen [7] . While the complement system is part of the humoral arm of the innate immune system, tissue macrophages and dendritic cells are involved in cellular responses. Both cell types are thought to derive from hematopoietic stem cells. They exist in the bone marrow and generate intermediate precursor populations with increasingly restricted lineage potentials, making these cells able to respond to different stimuli [8] . Flagellins are globular proteins that form the bacterial flagellum. These are recognized by both Toll-like receptor (TLR5) and NAIP5/ NLRC4 inflammasome receptors. Yang et al. [9] elegantly demonstrate that flagellins of the pathogen Salmonella typhi and non-pathogenic Escherichia coli both activated the TLR5 pathway. The latter pathogen induced significantly less interleukin-1β production and pyroptotic cell death in peritoneal macrophages and also showed markedly lower efficiency in activating caspase-1 through the NLRC4 pathway than flagellins of S. typhi . Thus, the authors concluded that macrophages may differentially recognize flagellins by intracellular sensors and thereby disIn the first 2014 issue of the Journal of Innate Immunity , aspects on the activation of innate immune responses by several major human pathogens are discussed. Notably, bacterial infections may present the major target for innate immunity in an evolutionary perspective [1] . In the current issue of the journal, it is shown how staphylococcal proteases aid in evasion of the complement system. The four major extracellular proteases of Staphylococcus aureus , staphopain A and staphopain B, the serine protease V8 and the metalloproteinase aureolysin, inhibit all pathways of complement due to degradation of several crucial components, such as the complement factors C3 and C5 [2] . This may be important both during local and systemic infection. S. aureus sometimes occurs as an airway pathogen, not least in cystic fibrosis and chronic obstructive pulmonary disease [3] . In this environment, collectins, e.g. surfactant protein (SP)-A and SP-D, are important in host defense of the alveoli against both viral and bacterial pathogens [4] . Recently, it was shown that the S. aureus protease staphopain A degrades SP-A, thus compromising host defense of the alveoli [5] . In a recent review, the importance of staphylococcal coagulases was discussed [6] . The canonical coagulase as well as the von Willebrand factor binding protein modify the coagulation cascade during infection. Thus, the extracellular proteases of S. aureus are important virulence factors. However, released proteins that bind complement and coaguPublished online: December 17, 2013 Journal of Innate Immunity