Evaluation of Epithelial-Mesenchymal Transition Markers in Autoimmune Thyroid Diseases.

A state of chronic inflammation is common in organs affected by autoimmune disorders, such as autoimmune thyroid diseases (AITD). Epithelial cells, such as thyroid follicular cells (TFCs), can experience a total or partial transition to a mesenchymal phenotype under these conditions. One of the major cytokines involved in this phenomenon is transforming growth factor beta (TGF-ß), which, at the initial stages of autoimmune disorders, plays an immunosuppressive role. However, at chronic stages, TGF- ß contributes to fibrosis and/or transition to mesenchymal phenotypes. The importance of primary cilia (PC) has grown in recent decades as they have been shown to play a key role in cell signaling and maintaining cell structure and function as mechanoreceptors. Deficiencies of PC can trigger epithelial-mesenchymal transition (EMT) and exacerbate autoimmune diseases. A set of EMT markers (E-cadherin, vimentin, α-SMA, and fibronectin) were evaluated in thyroid tissues from AITD patients and controls through RT-qPCR, immunohistochemistry (IHC), and western blot (WB). We established an in vitro TGF-ß-stimulation assay in a human thyroid cell line to assess EMT and PC disruption. EMT markers were evaluated in this model using RT-qPCR and WB, and PC was evaluated with a time-course immunofluorescence assay. We found an increased expression of the mesenchymal markers α-SMA and fibronectin in TFCs in the thyroid glands of AITD patients. Furthermore, E-cadherin expression was maintained in these patients compared to the controls. The TGF-ß-stimulation assay showed an increase in EMT markers, including vimentin, α-SMA, and fibronectin in thyroid cells, as well as a disruption of PC. The TFCs from the AITD patients experienced a partial transition to a mesenchymal phenotype, preserving epithelial characteristics associated with a disruption in PC, which might contribute to AITD pathogenesis.

Cytologic features of a pleural effusion after silicone breast implant rupture.

Pleural effusion is an extremely rare complication of ruptured breast silicone implants. Rupture may be related to a recent trauma or occur spontaneously, making its diagnosis more difficult. In the few reported cases, cytology did not play a relevant role in its diagnosis. We describe and illustrate a silicone foreign body reaction in a pleural effusion. Cytologic findings were so remarkable as to permit a specific diagnosis. The patient, a 37-year-old female with a history of previous bilateral breast implant surgery was admitted because of a pleural effusion. Computed tomography scan showed a left effusion with secondary atelectasis and bilateral breast rupture with lymph node "siliconomas." Cytologic analysis of the effusion showed well-defined droplets or globules of transparent material, in addition to a microvacuolized background. Where abundant silicone droplets induced a staining artifact of the smears. These were cellular with numerous macrophages containing large vacuoles displacing the nuclei to the periphery. Some had a signet cell ring appearance, while others showed multinucleation. Flow cytometry revealed a predominant macrophagic cell population. With the increasing use of silicone breast implants, rare complications such as pleural effusion may become more common. The pathologist must consider this possibility when extracellular transparent droplets or evidence of a foreign body-type reaction are present. The artifact appearance of the smears may help to suspect it. This rare complication must be always considered when evaluating effusions in patients with silicone breast implants.