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PLoS One
2008 Jul 16;37:e2692. doi: 10.1371/journal.pone.0002692.
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Major histocompatibility complex based resistance to a common bacterial pathogen of amphibians.
Barribeau SM
,
Villinger J
,
Waldman B
.
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Given their well-developed systems of innate and adaptive immunity, global population declines of amphibians are particularly perplexing. To investigate the role of the major histocompatibility complex (MHC) in conferring pathogen resistance, we challenged Xenopus laevis tadpoles bearing different combinations of four MHC haplotypes (f, g, j, and r) with the bacterial pathogen Aeromonas hydrophila in two experiments. In the first, we exposed ff, fg, gg, gj, and jj tadpoles, obtained from breeding MHC homozygous parents, to one of three doses of A. hydrophila or heat-killed bacteria as a control. In the second, we exposed ff, fg, fr, gg, rg, and rr tadpoles, obtained from breeding MHC heterozygous parents and subsequently genotyped by PCR, to A. hydrophila, heat-killed bacteria or media alone as controls. We thereby determined whether the same patterns of MHC resistance emerged within as among families, independent of non-MHC heritable differences. Tadpoles with r or g MHC haplotypes were more likely to die than were those with f or j haplotypes. Growth rates varied among MHC types, independent of exposure dose. Heterozygous individuals with both susceptible and resistant haplotypes were intermediate to either homozygous genotype in both size and survival. The effect of the MHC on growth and survival was consistent between experiments and across families. MHC alleles differentially confer resistance to, or tolerance of, the bacterial pathogen, which affects tadpoles' growth and survival.
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18629002
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Figure 1. Mortality as a function of bacterial dose and MHC genotype among families.(A) Percent mortality of tadpoles exposed to the control (3.0×106 cfu/ml heat-killed), low (1.0×106 cfu/ml), medium (2.5×106 cfu/ml), and high (3.0×106 cfu/ml) doses of A. hydrophila. N = 90 in each treatment. (B) Percent mortality of tadpoles from each MHC genotype that were exposed to each dose of live A. hydrophila or the control. N = 15 in each condition.
Figure 2. Survival with time as a function of bacterial dose, MHC genotype, and clutch order among families.Kaplan-Meier plots showing the survival of (A) tadpoles exposed to the control (3.0×106 cfu/ml heat-killed), low (1.0×106 cfu/ml), medium (2.5×106 cfu/ml), and high (3.0×106 cfu/ml) doses of A. hydrophila; (B) tadpoles exposed to the control or A. hydrophila (all doses combined); (C) tadpoles from each MHC genotype; and (D) tadpoles from early and late clutches.
Figure 3. Growth as a function of MHC genotype among families.Body length (X̅±SE) at day 25 of tadpoles from each genotype exposed to the pathogen A. hydrophila and the control.
Figure 4. Mortality as a function of bacterial exposure and MHC genotype within families.(A) Percent mortality of tadpoles exposed to live (exposed) and heat-killed (control) A. hydrophila. N = 120 for each treatment. (B) Percent mortality of tadpoles with each MHC genotype from 3 different families. Sample sizes differed among families; see Table 1.
Figure 5. Survival with time as a function of bacterial exposure and MHC genotype within families.Kaplan-Meier plots showing the survival of (A) tadpoles exposed to live (exposed) or heat-killed (control) A. hydrophila, and (B) tadpoles with different MHC genotypes. Vertical lines indicate exposure days.
Figure 6. Growth as a function of bacterial exposure.Body length (X̅±SE) of tadpoles exposed to live A. hydrophila, heat-killed bacteria and no bacteria (controls) over time.
Figure 7. Growth as a function of MHC genotype within families.(A) Total and (B) body length (X̅±SE) of tadpoles on day 18 with different MHC genotypes that were either exposed to live or heat-killed A. hydrophila as a control.
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