Lymphangitis occurring after intralesional Candida antigen injection for verruca vulgaris.

Verruca vulgaris is a common dermatological disease with many treatment options including destructive modalities and more recently, immunotherapy. Intralesional injections of Candida antigen have been described as a safe and effective treatment with the most common adverse reactions including local reactions (burning, blistering, peeling), local erythema, and pain at the injection site. We describe the first reported case of lymphangitis after intralesional Candida antigen injection for verruca vulgaris in a healthy 18-year-old woman. The lymphangitis rapidly resolved with ibuprofen and cold compresses. Physicians should be aware of this potential adverse reaction when using this treatment modality and should be familiar with appropriate treatment of subsequent lymphangitis.

Chromium(VI) stimulates Fyn to initiate innate immune gene induction in human airway epithelial cells.

Mechanisms for pathogenic metal signaling in airway injury or disease promotion are poorly understood. It is widely believed that one mechanism for pathogenic and possible carcinogenic effects of inhaled chromium (Cr(VI)) is inhibition of inducible gene transactivation. However, we recently reported that Cr(VI) inhibition of Sp1-dependent transactivation required signal transducer and activator of transcription 1 (STAT1)-dependent expression of an inhibitory protein in airway epithelium. Thus, Cr(VI) exposures can induce genes, and we hypothesized that this induction resulted from Cr(VI) signaling through an innate immune-like STAT1-dependent pathway initiated by Fyn. Exposure of human airway epithelial (BEAS-2B) cells to Cr(VI) selectively transactivated the STAT-responsive interferon-stimulated response element (ISRE) and induced ISRE-driven transactivation of interferon regulatory factor 7 (IRF7), without affecting the gamma interferon-activated site (GAS)-driven IRF1 expression. Cr(VI)-induced IRF7 was absent or greatly reduced in cells that lacked STAT1, were treated with the Src family kinase inhibitor, PP2, or lacked Fyn. Expressing Fyn, but not Src, in mouse embryonic fibroblasts cells null for Src, Yes, and Fyn restored Cr(VI)-stimulated STAT1 tyrosine phosphorylation and IRF7 expression. Finally, shRNA knockdown of Fyn in BEAS-2B cells prevented Cr(VI)-activated STAT1 transactivation of IRF7. These data support a novel mechanism through which Cr(VI) stimulates Fyn to initiate interferon-like signaling for STAT1-dependent gene transactivation.