Inducible nitric oxide synthase (iNOS) expression in autoimmune thyroid disorders (AITD) [Expresión de la enzima óxido nítrico sintetasa inducible en las enfermedades tiroideas autoinmunitarias]
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Introduction: Nitric oxide is synthesized by different cell types through the action of the enzyme nitric oxide synthase (NOS). There are four isoforms of this enzyme: the neuronal, the endothelial, the mitochondrial, and the inducible (iNOS) forms. Although NO production may play an important role in the pathogenesis of inflammation and tissue damage, its possible role in autoimmune thyroiditis has not been adequately explored. Objective: To study protein and mRNA expression of iNOS in human autoimmune thyroid disorders (AITD). Patients and method: We evaluated the expression of iNOS in thyroid gland specimens from 10 patients with Graves%27 disease (GD), from five patients with Hashimoto%27s thyroiditis (HT) and from 10 controls by immunohistochemical and reverse transcription-polymerase chain reaction (RT-PCR). Results: Both immunohistochemistry and PCR techniques showed up-regulated expression of iNOS in the thyroid glands of patients with GD and HT. iNOS expression was higher in GD than in HT. In contrast, no iNOS expression was detected in normal thyroid tissue. In both GD and HT, iNOS was detected in thyrocytes, mainly in those localized in areas close to the inflammatory cell infiltrate. In addition, upregulated expression of iNOS was observed in endothelial cells and thyroid-infiltrating mononuclear cells in both GD and HT. Conclusions: The enhanced expression of iNOS in autoimmune thyroiditis suggests that NO synthesis may play an important role in the inflammatory phenomena and tissue damage observed in this disease.
Introduction: Nitric oxide is synthesized by different cell types through the action of the enzyme nitric oxide synthase (NOS). There are four isoforms of this enzyme: the neuronal, the endothelial, the mitochondrial, and the inducible (iNOS) forms. Although NO production may play an important role in the pathogenesis of inflammation and tissue damage, its possible role in autoimmune thyroiditis has not been adequately explored. Objective: To study protein and mRNA expression of iNOS in human autoimmune thyroid disorders (AITD). Patients and method: We evaluated the expression of iNOS in thyroid gland specimens from 10 patients with Graves' disease (GD), from five patients with Hashimoto's thyroiditis (HT) and from 10 controls by immunohistochemical and reverse transcription-polymerase chain reaction (RT-PCR). Results: Both immunohistochemistry and PCR techniques showed up-regulated expression of iNOS in the thyroid glands of patients with GD and HT. iNOS expression was higher in GD than in HT. In contrast, no iNOS expression was detected in normal thyroid tissue. In both GD and HT, iNOS was detected in thyrocytes, mainly in those localized in areas close to the inflammatory cell infiltrate. In addition, upregulated expression of iNOS was observed in endothelial cells and thyroid-infiltrating mononuclear cells in both GD and HT. Conclusions: The enhanced expression of iNOS in autoimmune thyroiditis suggests that NO synthesis may play an important role in the inflammatory phenomena and tissue damage observed in this disease.
