Abstract
There is evidence that many pathogens co-evolve with their hosts. This is often reflected in species specific virulence factors that can selectively interfere with host defense mechanisms, innate and acquired as well as a range of interactions with host homeostatic pathways that contribute to the course and severity of an infection. In this review, we highlight a number of select examples of these interactions and suggest that understanding of molecular pathogenesis requires a broad systems approach that can evaluate the multiple and dynamic interactions that are occurring during infection.
Keywords: Bacteria, homeostasis, blood coagulation, fibrinolysis, innate immunity, acquired immunity, homeostatic pathways, molecular pathogenesis, homeostatic systems, immune system, coagulation, pathogenesis, Koch's postulates, Salmonella typhimurium, immunocompetent host, transgenic, infectious agents, microbe, bacteria colonize, inflammatory response, plasmin(ogen), plasminogen activation, chemotactic signaling, zymogen substrates, firbrinopeptides, monocytes, granulocytes, Borellia burgdorefri, Yersinia pestis, Streptococcus pyogenes, Plasminogen, streptokinase (SK), streptokinase-plasminogen complex, Yersinia pestis model, Staphylococcus aureus, symbiotic relationship, spirochetes, spirochetemia, bacterial endocarditis, zymogen proteins, Staphylocoagulase, bacteria-fibrin-platelet, sepsis syndrome, microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), zymogen activator and adhesion protein, myelopoiesis, leukocytosis
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