Transcellular thiocyanate transport by human airway epithelia

Fragoso, Miryam A.; Fernandez, Vania E.; Forteza, Rosanna; Randell, Scott H.; Salathé, Matthias; Conner, Gregory E.

doi:10.1113/jphysiol.2004.071548

Cited by 102 publications

(100 citation statements)

References 33 publications

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“…Since previous studies showed that CFTR played a role in SCN À transport from the serosal to mucosal compartments [17], we evaluated the possible contribution of CFTR anion channel activity to the SCN À transport observed in cultures. Non-CF cultures showed the expected increase in SCN À transport after stimulation of PKA by apical addition of dibutyryl cAMP (0.5 mM) and forskolin (10 lM), while CF cultures did not (Fig.…”

Section: Thiocyanate Transportmentioning

confidence: 99%

“…We have previously shown that normal human bronchial epithelial cells actively transport SCN À from the basolateral to apical surfaces and that the transport was regulated by CFTR as it was stimulated by cAMP analogs and by forskolin, and inhibited by apical glibenclamide, diphenylamine-2-carboxylic acid and 5-nitro-2-(3-phenylpropylamino)-benzoate [17]. Since a loss of SCN À in the airway lumen might result in a loss of LPO antibacterial activity and perhaps also affect neutrophil MPO antibacterial activity, we assessed whether SCN À transport was defective in CF bronchial epithelial cells compared to normal epithelia.…”

Section: Thiocyanate Transportmentioning

confidence: 99%

“…Normal human airway epithelia transport SCN À from the basolateral to the apical surface and concentrate it in airway secretions [17]. This transport utilizes the sodium/iodide symporter at the basolateral surface to mediate uptake of SCN À or I À into the cells followed by release to the apical surface that is regulated by CFTR [17].…”

Section: Introductionmentioning

confidence: 99%

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The lactoperoxidase system links anion transport to host defense in cystic fibrosis

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Section: Thiocyanate Transportmentioning

confidence: 99%

Section: Thiocyanate Transportmentioning

confidence: 99%

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The lactoperoxidase system links anion transport to host defense in cystic fibrosis

et al. 2006

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“…(40), providing oxidants to support the lactoperoxidase-H 2 O 2 -thiocyanate antimicrobial system (41,42). Defective thiocyanate transport in cystic fibrosis subverts optimal activity of this system and contributes in part to the frequent respiratory infections seen in patients with this disorder.…”

Section: Nox3-p22mentioning

confidence: 99%

Biological Roles for the NOX Family NADPH Oxidases

Nauseef

2008

Journal of Biological Chemistry

285

225

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Linking the phagocyte defect in patients with chronic granulomatous disease (CGD) 2 with the biochemical basis for oxygen consumption by stimulated neutrophils (1) represented a seminal advance in understanding the molecular basis for a key component of innate immunity. In subsequent decades, the catalytic and regulatory elements of the "respiratory burst oxidase" were elucidated, tacitly assuming all along that the NADPH-dependent oxidase under study represented a system uniquely expressed in phagocytic cells and dedicated to generating relatively large amounts of reactive oxygen species (ROS) destined to destroy invading microbes. Development of more sensitive analytical systems for ROS detection revealed that some physiological and pathophysiological events in non-phagocytic cells were associated with ROS generation, although the subcellular source of oxidants remained uncertain. With the identification of mox1 in 1999 (2) as a homolog of gp91 phox , the catalytic component of the phagocyte oxidase, came the birth of the NADPH oxidase (NOX) protein family and the eventual identification of its seven members. With remarkable rapidity, many features of the structure, activity, cell biology, and physiology of the NOX proteins have been described, as summarized in several excellent and comprehensive recent reviews (3)(4)(5). This more circumscribed minireview provides an overview of the organizing features of the protein family, a summary of the physiology and pathophysiology in which NOX proteins participate (or might participate), and identification of some of the remaining unanswered questions in the field.

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“…Moreover, recent studies have shown that iodide may play an important role in the innate immune system of the pulmonary tree by acting as a substrate for an oxidative microbicidal system [6,7]. Iodine accumulation in bronchopulmonary secretions, while acting to defend against respiratory viruses and bacteria in inflammatory lung states [6][7][8][9][10], may also lead to false-positive post-RAI scans resulting in erroneous diagnoses.…”

mentioning

confidence: 99%

False-Positive Radioactive Iodine Uptake Mimicking Miliary Lung Metastases in a Patient Affected by Papillary Thyroid Cancer and IgA Deficiency

Demidowich

Kundu

Reynolds

et al. 2015

Nucl Med Mol Imaging

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A 42-year-old female with immunoglobulin A deficiency and recurrent sinopulmonary infections underwent thyroidectomy for papillary thyroid cancer (PTC). I scintigraphy demonstrated diffuse pulmonary uptake, suggesting metastatic disease. However, subsequent pathologic, biochemical and radiographic testing proved that she was in fact disease free, and the initial 123 I pulmonary uptake was identified as a false positive. Inflammatory conditions may rarely cause iodine uptake in non-thyroidal tissues due to local retention, organification, and/or immunologic utilization. To avoid exposing patients to unnecessary treatments, it is critical for clinicians to recognize that comorbid pulmonary conditions may mimic metastatic PTC on radioiodine scintigraphy.Keywords Radionuclide imaging . Scintigraphy . Papillary thyroid carcinoma . False-positive reactions . IgA deficiency A 42-year-old female, with a past medical history of IgA deficiency and recurrent sinopulmonary infections, underwent total thyroidectomy for a 1.1-cm follicular variant PTC. Preoperative ultrasound (US) found no abnormal lymph nodes, and pathology demonstrated a welldifferentiated unifocal cancer with no capsular or lymphovascular invasion. At 3-month follow-up, the rhTSH-stimulated Tg level was low at 1.7 ng/ml with negative Tg antibodies. However, the 123 I whole-body scan demonstrated focal increased uptake in the left thyroid bed and diffuse uptake in both lungs, suggestive of metastatic disease (Fig. 1a). At the time of testing, the patient was taking oral prednisone, inhaled mometasone/formoterol, and oral amoxicillin/clavulanate for a bronchitis flare. Given her conflicting results, the possibility of a false-positive radioiodine uptake result in the setting of active pulmonary inflammation was raised. In view of these findings, the patient was scheduled for 131 I dosimetry after levothyroxine withdrawal. Imaging at 48 h confirmed the thyroid bed findings, but the lungs had only minimal uptake (Fig. 1b). Labwork demonstrated an appropriately elevated TSH of 67.3 mcIU/ml, with a low Tg of 4.6 ng/ml, and negative Tg antibodies. These results suggested that the initial pulmonary uptake was a false positive. The patient was subsequently treated with 100 mCi of 131 I. The post-treatment scan (Fig. 1c) confirmed the pretreatment findings.At 1-year follow-up, the rhTSH-stimulated 123 I scan again showed faint diffuse uptake in both lungs. Stimulated Tg and Tg antibody levels were undetectable, neck US was negative for residual or recurrent disease, and CT of the lungs demonstrated bilateral bronchiectasis with no obvious metastatic lesions (Fig. 2). Thus, the persistent radioiodine uptake in the lungs was confirmed to be a spurious finding due to her underlying pulmonary disease rather than metastatic thyroid cancer.

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Transcellular thiocyanate transport by human airway epithelia

Abstract: Human airway mucosa synthesizes and secretes lactoperoxidase (LPO).

Cited by 102 publications

References 33 publications

The lactoperoxidase system links anion transport to host defense in cystic fibrosis

The lactoperoxidase system links anion transport to host defense in cystic fibrosis

Biological Roles for the NOX Family NADPH Oxidases

False-Positive Radioactive Iodine Uptake Mimicking Miliary Lung Metastases in a Patient Affected by Papillary Thyroid Cancer and IgA Deficiency

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