Abstract
Innate immunity is expected to play a primary role in conferring resistance to novel infectious diseases, but few studies have attempted to examine its role in the evolution of resistance to emerging pathogens in wild vertebrate populations. Here, we used experimental infections and cDNA microarrays to examine whether changes in the innate and/or acquired immune responses likely accompanied the emergence of resistance in house finches (Carpodacus mexicanus) in the eastern United States subject to a recent outbreak of conjunctivitis-causing bacterium (Mycoplasma gallisepticum-MG). Three days following experimental infection with MG, we observed differences in the splenic transcriptional responses between house finches from eastern U.S. populations, with a 12-year history of MG exposure, versus western U.S. populations, with no history of exposure to MG. In particular, western birds down-regulated gene expression, while eastern finches showed no expression change relative to controls. Studies involving poultry have shown that MG can manipulate host immunity, and our observations suggest that pathogen manipulation occurred only in finches from the western populations, outside the range of MG. Fourteen days after infection, eastern finches, but not western finches, up-regulated genes associated with acquired immunity (cell-mediated immunity) relative to controls. These observations suggest population differences in the temporal course of the response to infection with MG and imply that innate immune processes were targets of selection in response to MG in the eastern U.S. population.
Highlights
Novel pathogens are powerful selective agents in humans (Diamond 1997) and other animals (Grenfell & Dobson 1995; Haldane 1949), and can have devastating effects on biodiversity (Benning et al 2002; Lips et al 2006)
Despite the potential for innate immunity to play a key role in the response to novel pathogens, the vast majority of studies in ecological immunology in vertebrates have focused on the acquired immune system (Acevedo-Whitehouse & Cunningham 2006; van der Most et al 2011)
Experimental infection In January and February 2007, we captured male house finches from two geographically distant locations: southeastern Arizona in the western U.S which was outside the 2007-range of MG; and southern Alabama in the eastern U.S, where finches had co-existed with MG for years
Summary
Novel pathogens are powerful selective agents in humans (Diamond 1997) and other animals (Grenfell & Dobson 1995; Haldane 1949), and can have devastating effects on biodiversity (Benning et al 2002; Lips et al 2006). Studies simultaneously monitoring the emergence of an infectious disease in the wild and the associated changes in host populations are rare, leading to a reduced understanding of how hosts evolve immunity to novel pathogens, in vertebrates. Emerged, apparently mediated through escape from pathogen-induced immunosuppression which facilitated the development of an enhanced innate and a specific cell-mediated immune response (Best & Kerr 2000). Populations can evolve resistance to novel pathogens rapidly Despite the potential for innate immunity to play a key role in the response to novel pathogens, the vast majority of studies in ecological immunology in vertebrates have focused on the acquired immune system (Acevedo-Whitehouse & Cunningham 2006; van der Most et al 2011). Of particular interest in host-parasite co-evolution has been the role of the polymorphic Mhc genes in detecting foreign antigens and triggering pathogen-specific T-lymphocyte cytotoxicity and humoral immune responses
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