Most hosts contain few parasites, whereas few hosts contain many. This pattern, known as aggregation, is well-documented in macroparasites where parasite intensity distribution among hosts affects host-parasite dynamics. Infection intensity also drives fungal disease dynamics, but we lack a basic understanding of host-fungal aggregation patterns, how they compare to macroparasites, and if they reflect biological processes.
View Article and Find Full Text PDFHistorically, amphibians have been essential to our understanding of vertebrate biology and animal development. Because development from egg to tadpole to adult frog can be directly observed, amphibians contributed greatly to our understanding of not only vertebrate animal development but also the development of the immune system. The South African clawed frog (Xenopus laevis) has been key to many of these findings.
View Article and Find Full Text PDFAntimicrobial peptides (AMPs) play a fundamental role in the innate defense against microbial pathogens, as well as other immune and non-immune functions. Their role in amphibian skin defense against the pathogenic fungus Batrachochytrium dendrobatidis (Bd) is exemplified by experiments in which depletion of host's stored AMPs increases mortality from infection. Yet, the question remains whether there are generalizable patterns of negative or positive correlations between stored AMP defenses and the probability of infection or infection intensity across populations and species.
View Article and Find Full Text PDFGlobal amphibian declines are compounded by deadly disease outbreaks caused by the chytrid fungus, (). Much has been learned about the roles of amphibian skin-produced antimicrobial components and microbiomes in controlling , yet almost nothing is known about the roles of skin-resident immune cells in anti- defenses. Mammalian mast cells reside within and serve as key immune sentinels in barrier tissues like skin.
View Article and Find Full Text PDFThe collagen IV (Col-IV) scaffold, the major constituent of the glomerular basement membrane (GBM), is a critical component of the kidney glomerular filtration barrier. In Alport syndrome, affecting millions of people worldwide, over two thousand genetic variants occur in the COL4A3, COL4A4, and COL4A5 genes that encode the Col-IV scaffold. Variants cause loss of scaffold, a suprastructure that tethers macromolecules, from the GBM or assembly of a defective scaffold, causing hematuria in nearly all cases, proteinuria, and often progressive kidney failure.
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