PURPOSE: We report a rare case of eyelid neuroma, discovered nine years after external levator advancement, presenting with recalcitrant ocular foreign body sensation and pain, persistent corneal epithelial defect, followed by corneal scarring, and ptosis. OBSERVATIONS: An 85-year-old man with a history of multiple skin cancers presented with left ptosis, epiphora and recalcitrant eye pain. Nine years prior to presentation, he underwent excision of melanoma in situ of the left forehead, followed by simultaneous forehead reconstruction and left external ptosis repair. At presentation, he had left ptosis and left superior corneal scarring. Eversion of the eyelid demonstrated the presence of a nodule at the superior border of the tarsus. The patient underwent simultaneous excisional biopsy of the lesion and posterior ptosis repair by Müller muscle conjunctival resection (MMCR). He experienced postoperative resolution of pain, ptosis and epiphora. Histopathologic examination demonstrated the presence of a foreign body granuloma alongside a neuroma. CONCLUSIONS: This case highlights the importance of thorough eyelid exam in individuals with ocular surface disease. We review herein the pathophysiology and histopathology of eyelid neuroma.

Chlamydia pneumoniae (CP) is associated with induction and exacerbation of asthma. CP infection can induce allergic airway sensitization in mice in a dose- and time-dependent manner. Allergen exposure 5 days after a low dose (mild-moderate), but not a high dose (severe) CP infection induces antigen sensitization in mice. Innate immune signals play a critical role in controlling CP infection induced allergic airway sensitization, however these mechanisms have not been fully elucidated. Wild-type, TLR2−/−, and TLR4−/− mice were infected intranasally (i.n.) with a low dose of CP, followed by i.n. exposure to human serum albumin (HSA) and challenged with HSA 2 weeks later. Airway inflammation, immunoglobulins, eosinophils, and goblet cells were measured. Low dose CP infection induced allergic sensitization in TLR2−/− mice, but not in TLR4−/− mice, due to differential Treg responses in these genotypes. TLR2−/− mice had reduced numbers of Tregs in the lung during CP infection while TLR4−/− mice had increased numbers. High dose CP infection resulted in an increase in Tregs and pDCs in lungs, which prevented antigen sensitization in WT mice. Depletion of Tregs or pDCs resulted in allergic airway sensitization. We conclude that Tregs and pDCs are critical determinants regulating CP infection-induced allergic sensitization. Furthermore, TLR2 and TLR4 signaling during CP infection may play a regulatory role through the modulation of Tregs.