Pneumococcal pathogenesis: "innate invasion" yet organ-specific damage.
Streptococcus pneumoniae encounters a variety of unique cellular situations during colonization of the nasopharynx or invasion into the lungs, the bloodstream, or the central nervous system. The ligand/receptor pairings that enable this progression of disease appear to be shared by many respiratory pathogens suggesting that a primitive "innate invasion" mechanism may underlie the well-known species-specific mechanisms of pathogenesis. That the acute phase of the innate immune response includes elements to interrupt this path supports this concept. However, it also appears that each cell type or organ responds differently to activation of this innate invasion pathway leaving some organs, such as the lung, intact post-infection but others, such as the brain, largely destroyed. This review posits a concept of innate invasion but cautions that organ-specific responses complicate opportunities for a simple approach to protect from organ damage.
Thornton
Justin A
JA
Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.
Durick-Eder
Kelly
K
Tuomanen
Elaine I
EI
D006801:Humans; D007113:Immunity, Innate; D009928:Organ Specificity; D010767:Phosphorylcholine; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D011008:Pneumococcal Infections / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D013296:Streptococcus pneumoniae / Q000276:immunology / Q000472:pathogenicity*
D010980:Platelet Membrane Glycoproteins; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D010767:Phosphorylcholine