
handle: 10138/346536
Hibernation, a period where bats have suppressed immunity and low body temperatures, provides the psychrophilic fungus Pseudogymnoascus destructans the opportunity to colonise bat skin, leading to severe disease in susceptible species. Innate immunity, which requires less energy and may remain more active during torpor, can control infections with local inflammation in some bat species that are resistant to infection. If infection is not controlled before emergence from hibernation, ineffective adaptive immune mechanisms are activated, including incomplete Th1, ineffective Th2, and variable Th17 responses. The Th17 and neutrophil responses, normally beneficial antifungal mechanisms, appear to be sources of immunopathology for susceptible bat species, because they are hyperactivated after return to homeothermy. Non-susceptible species show both well-balanced and suppressed immune responses both during and after hibernation.
Peer reviewed
PATHOLOGY, COMMENSALISM, INFLAMMATION, Ecology, evolutionary biology, WHITE-NOSE SYNDROME, SYNDROME FUNGUS, CELLS, ta1181, DISEASE TOLERANCE, PSEUDOGYMNOASCUS-DESTRUCTANS, LECTIN RECEPTORS, HIBERNATION
PATHOLOGY, COMMENSALISM, INFLAMMATION, Ecology, evolutionary biology, WHITE-NOSE SYNDROME, SYNDROME FUNGUS, CELLS, ta1181, DISEASE TOLERANCE, PSEUDOGYMNOASCUS-DESTRUCTANS, LECTIN RECEPTORS, HIBERNATION
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