Purpose of review: The purpose of the present review is to describe the involvement of neurogenic inflammation in ocular surface diseases and to outline recent advances in understanding the complex interaction of neuromediators and inflammatory cells in the conjunctiva.
Recent findings: Evidence indicates that all clinical forms of ocular surface disease, including allergic and autoimmune, share the involvement of a neurogenic inflammation triggered by nociceptive stimuli and resulting in plasma extravasation and local activation of immune cells. Players of this complex mechanism are neuropeptides, including substance P, calcitonine gene-related peptide, neuropeptide Y, and vasoactive intestinal peptide. These neuropeptides are, however, only a minor component of a complex neuroimmune cross-talk capable of modulating local inflammation.
Summary: As already shown in other mucosal surfaces, neurogenic inflammation and innate immunity may work together to protect the ocular surface. In this review, we present the most recent advances in the understanding of the roles played by nerve endings and neuropeptides in local inflammatory processes of the ocular surface, in order to better clarify their function in physiologic and pathologic conditions and to open new research, diagnostic, and therapeutic perspectives.