Exploring the link between ultraviolet B radiation and immune function in amphibians: implications for emerging infectious diseases

Abstract

Amphibian populations the world over are under threat of extinction, with as many as 40% of assessed species listed as threatened under IUCN Red List criteria (a significantly higher proportion than other vertebrate group). Amongst the key threats to amphibian species is the emergence of novel infectious diseases, which have been implicated in the catastrophic amphibian population declines and extinctions seen in many parts of the world. The recent emergence of these diseases coincides with increased ambient levels of ultraviolet B radiation (UVBR) due to anthropogenic thinning of the Earth's protective ozone layer, raising questions about potential interactions between UVBR exposure and disease in amphibians. While reasonably well documented in other vertebrate groups (particularly mammals), the immunosuppressive capacity of UVBR and the potential for it to influence disease outcomes has been largely overlooked in amphibians. Herein, we review the evidence for UVBR-associated immune system disruption in amphibians and identify a number of direct and indirect pathways through which UVBR may influence immune function and disease susceptibility in amphibians. By exploring the physiological mechanisms through which UVBR may affect host immune function, we demonstrate how ambient UVBR could increase amphibian susceptibility to disease. We conclude by discussing the potential implications of elevated UVBR for inter and intraspecific differences in disease dynamics and discuss how future research in this field may be directed to improve our understanding of the role that UVBR plays in amphibian immune function.

Keywords: Batrachochytrium dendrobatidis; adaptive; chytridiomycosis; embryo; innate; larvae.

Figure 1:

Schematic representation of the potential direct and indirect pathways through which UVBR can influence immune function in amphibian early life stages. UVBR can directly kill and damage cells in the outer skin layers, disrupting the physical integrity of the skin, compromising the function of cutaneous dendritic cells (D) and leucocytes (L), and triggering exposed keratinocytes (K) to release a cascade of immunosuppressive molecules that inhibit innate and adaptive immune functions of the systemic immune system. UVBR can disrupt the innate immune function of the cutaneous ‘secretome’ (mucus, antimicrobial peptides, complement, lysozyme, etc.) and influence the composition of the host microbiome. Indirectly, UVBR may influence immune function via its impact on interrelated physiological systems. For example, UVBR can affect immune function by disrupting energy production and/or distribution pathways, by influencing neuroendocrine signalling pathways controlling immune system maturation or inducing a physiological stress response (involving glucocorticoids). UVRB-associated damage to DNA and other biomolecules may also have a lasting impact on immune function by influencing gene expression patterns in subsequent life stages. Image: Cameron Baker©.