CD4+ T cells apoptosis and conversion of Th1/Th2-type cytokines promote the progress of sporotrichosis.

Sporotrichosis is a fungal disease of the human and other mammals, caused by a complex of Sporothrix schenckii. The disease follows the traumatic inoculation to lead to fixed lesions, regional lymphangitic lesions, or even disseminated lesions including internal involvement, which depends on host immunological status and strain virulence. In this work, we observed the role of CD4+ T cells apoptosis and conversion of Th1/Th2-type cytokines in the cellular immunity regulation on mice model sporotrichosis. The experiments showed that there was more CD4+ T cells apoptosis, by endogenous apoptosis signaling pathway (P < .05), and more conversions of Th1/Th2-type cytokines in more severe and longer duration groups (P < .05). Meanwhile, the trends of the conversions of Th1/Th2-type cytokines were almost consistent with the CD4 + T cell's apoptosis in the corresponding groups. These findings suggest that CD4+ T cells apoptosis and conversion of Th1/Th2-type cytokines are contributing to promoting the progress of sporotrichosis.

A novel case of cutaneous squamous cell carcinoma at the site of previous sporotrichosis.

BACKGROUND: Cutaneous squamous cell carcinoma (cSCC) is a malignant tumor of epithelial keratinocytes, with a relatively reduced frequency of lymph node metastasis. Despite the fact that this tumor type is largely preventable, the incidence of cSCC is rising every year. Ultraviolet exposure is a major cause of cSCC and directly contributes to cSCC. Other known environmental risk factors include ionizing radiation, cigarette smoking, and certain chemical exposures. AIMS: In this study, we report a clinical case of cSCC with a novel causative factor. PATIENT/METHODS: The report describes a 72-year-old male who was seen for a dermatosis condition initially. Later, epidermal hyperplasia and granulomatous inflammation of the dermis was diagnosed based on skin biopsy. Fungal culture revealed the presence of Sporothrix schenckii which led to the diagnosis of fixed-type sporotrichosis. RESULTS: Four months of oral terbinafine (250 mg once a day) administration partially resolved the lesions. Patient was subsequently diagnosed with cSCC, and surgical resection with wider margins was performed. CONCLUSION: After a careful and rigorous exclusion of known risk factors, we confirmed that this incidence of cSCC was caused by chronic inflammation which followed fixed-type sporotricosis.

A secondary discoid lupus erythematosus induced by scald of edible oil: An illustration of Koebner phenomenon.

BACKGROUND: Discoid lupus erythematosus (DLE) is a most well-known clinical variation of chronic cutaneous lupus erythematosus inside the spectrum of lupus erythematosus (LE). Cutaneous trauma remains a significant and peculiar causative factor for DLE. AIMS: We present a case wherein the patient demonstrated unilateral distribution of DLE on a clinically normal appearing occult facial scald of edible oil, representing Koebner phenomenon (KP) i.e. occurrence of a new skin disease at the site of an unrelated and already healed one. PATIENT/METHODS: The 53 years old female patient was unique because she experienced DLE on the nasal back. RESULTS: The injury was totally settled following a month treatment of oral hydroxychloroquine and topical 0.03% tacrolimus ointment. After three months, she encountered an accidental edible oil scald on the right upper cheek. Several small vesicles appeared on a soybean-sized erythema base with a burning sensation. CONCLUSION: We review the literature and conclude by discussing important histologic highlights to think about while endeavoring to perceive the fundamental character and pathogenicity of such sores.

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms.

Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 ß1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4+/CD8+ T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions.