Wounding in lizards results in the release of beta-defensins at the wound site and formation of an antimicrobial barrier.

After tail loss in lizards no infections occur indicating the presence of an effective anti-microbial barrier in the exposed tissues of the tail stump. Previous molecular studies on the lizard Anolis carolinensis have identified some beta-defensin-like genes and the deduced peptides that may be involved in anti-infective protection. The present study has analyzed the tissues of wounded and normal tails in lizards in order to immune-localize one of the beta-defensins previously found (AcBD15) and to detect variation in its gene expression during wounding. No immunoreactivity for this beta-defensin is present in normal tissues or in the epidermis of lizards, except for some sparse granulocytes. The latter are seen during the first 1-6days after tail amputation and AcBD15 immunoreactivity is present in their granules. Degenerating granulocytes are incorporated, together with dead erythrocytes, platelets and keratinocytes into the scab. Real time RT-PCR and western blotting analysis indicates up-regulation of AcBD15 expression during wounding with respect to normal tissues, indicating that production, storage and release of this beta-defensin from granulocytes are active following wounding. The production of beta-defensins from granulocytes would allow protection of exposed tissues from microbial invasion avoiding a persistent inflammation, a process that leads to tissue regeneration.