Peschel et al. reply:

Colonization of the anterior nares of healthy individuals by S. aureus leads to an increased risk of nosocomial infections. We have recently shown that WTA polymers on the staphylococcal cell surface are essential for nasal colonization in a cotton rat model and mediate specific interaction with human nasal epithelial cells1. A WTA-deficient mutant was rapidly and completely lost from the nares, and preinstillation with purified WTA interfered with nasal colonization.

Foster suggests that nasal colonization should be regarded as a multifactorial process, and that surface-exposed staphylococcal proteins such as the keratin-10 binding protein ClfB (ref. 2) might also have a significant role in the process. We agree with this possibility and would like to emphasize that the Brief Communications format of our paper did not allow a more detailed discussion of other studies and further factors contributing to nasal colonization.

Bacterial binding to human cells has been shown in several cases to rely on more than one interaction, and may involve loose initial attachment followed by tighter binding. Future experiments may explain how WTA and surface proteins contribute to nasal colonization. It will be very interesting to study nasal colonization of clfB or similar mutants in the cotton rat model.

We cannot rule out that WTA deficiency compromises the keratin-binding capacity of surface proteins such as ClfB, but our preliminary experiments do not support such a conclusion (data not shown). The inhibition of nasal colonization by preinstillation of cotton rat nares with purified WTA, and the dose-dependent binding of WTA-coated microspheres to nasal cells, instead point strongly toward a WTA-mediated attachment of S. aureus to human cells. Elucidating the cognate interaction partner and its role in nasal colonization will be an interesting subject for future research.

See Nasal colonization by Staphylococcus aureus by Peschel et al.