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Primary research by Brian D. Corbin and coauthors, Science 319(5865), 962–965 (15 February 2008). The abstract reports calprotectin-dependent restriction of manganese and zinc in Staphylococcus aureus abscesses, inhibition of bacterial growth by metal chelation, and metal enrichment and increased bacterial proliferation in mice lacking calprotectin.

Nutritional immunity is a host-defense strategy that limits the supply of nutrients available to a pathogen. Restricting access to needed metal ions is one example: a host protein can bind a metal so that its presence in tissue does not imply that invading bacteria can acquire it.

A concrete experimental example is calprotectin in Staphylococcus aureus abscesses. Brian D. Corbin and colleagues found that neutrophil-derived calprotectin inhibited bacterial growth through chelation of manganese and zinc. Abscesses in mice lacking calprotectin contained more metal and supported greater bacterial proliferation. The combination of growth inhibition and the comparison with deficient animals connects metal sequestration to a host defense, rather than merely showing that a binding protein is present at an infection site.^[ref]

A simple two-pool model makes the distinction between total amount and accessibility explicit. Write the total metal concentration as $M_T=M_{\mathrm{free}}+M_{\mathrm{bound}}$. If $M_T=1\mu \mathrm{mol}{\mathrm{L}}^{-1}$ and $99\%$ is bound, the free concentration is only $0.01\mu \mathrm{mol}{\mathrm{L}}^{-1}$: one hundredth of the value if all the metal were free. These are illustrative numbers, not measurements from the experiment. Actual microbial access also depends on whether a bacterium can obtain metal from the bound pool; total metal concentration alone therefore does not measure nutrient availability.