Activation of innate immune-response genes in little brown bats (Myotis lucifugus) infected with the fungus Pseudogymnoascus destructans.
Recently bats have been associated with the emergence of diseases, both as reservoirs for several new viral diseases in humans and other animals and, in the northern Americas, as hosts for a devastating fungal disease that threatens to drive several bat species to regional extinction. However, despite these catastrophic events little Information is available on bat defences or how they interact with their pathogens. Even less is known about the response of bats to infection during torpor or long-term hibernation. Using tissue samples collected at the termination of an experiment to explore the pathogenesis of White Nose Syndrome in Little Brown Bats, we determined if hibernating bats infected with the fungus Pseudogymnoascus destructans could respond to infection by activating genes responsible for innate immune and stress responses. Lesions due to fungal infection and, in some cases, secondary bacterial infections, were restricted to the skin. However, we were unable to obtain sufficient amounts of RNA from these sites. We therefore examined lungs for response at an epithelial surface not linked to the primary site of infection. We found that bats responded to infection with a significant increase in lungs of transcripts for Cathelicidin (an anti-microbial peptide) as well as the immune modulators tumor necrosis factor alpha and interleukins 10 and 23. In conclusion, hibernating bats can respond to experimental P. destructans infection by activating expression of innate immune response genes.
Department of Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Noreen
N
Rapin
Department of Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Kirk
K
Johns
Department of Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Lauren
L
Martin
Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada.
Lisa
L
Warnecke
Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada.
James M
JM
Turner
Department of Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Trent K
TK
Bollinger
Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada.
Craig K R
CK
Willis
Department of Biology, New Mexico Tech, Socorro, New Mexico, United States of America.
Jamie
J
Voyles
Department of Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Vikram
V
Misra
D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000235:genetics / Q000378:metabolism; D001203:Ascomycota / Q000502:physiology*; D002685:Chiroptera / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology; D005786:Gene Expression Regulation / Q000276:immunology*; D007113:Immunity, Innate / Q000235:genetics*; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D053759:Interleukin-23 / Q000235:genetics / Q000378:metabolism; D008168:Lung / Q000378:metabolism / Q000382:microbiology; D009181:Mycoses / Q000276:immunology* / Q000382:microbiology; D060888:Real-Time Polymerase Chain Reaction; D012867:Skin / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D054804:Cathelicidins
D023181:Antimicrobial Cationic Peptides; D053759:Interleukin-23; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D054804:Cathelicidins