Oxidative Stress in Sarcoidosis

Dhooria, Sahajal; Gupta, Dheeraj

doi:10.1007/978-1-4939-0497-6_11

Cited by 2 publications

(2 citation statements)

References 56 publications

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“…Both VOCs are considered pollutants [57,58], but it is also hypothesized that these compounds are produced due to alterations in oxidative stress levels [59,60]. However, since oxidative stress is increased in sarcoidosis [61] higher concentrations of branched alkanes were expected in the patients compared to the controls. Additionally, both compounds are found in increased concentrations indoors compared to outdoors (two-fold for 2-methylpentane and three-fold for 3-methylhexane) [62], suggesting that patients are exposed to higher concentrations than controls as they would spend more time indoors due to sarcoidosis-associated fatigue [13].…”

Section: Branched Alkanesmentioning

confidence: 99%

The necessity of external validation in exhaled breath research: a case study of sarcoidosis

et al. 2017

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Section: Branched Alkanesmentioning

confidence: 99%

The necessity of external validation in exhaled breath research: a case study of sarcoidosis

et al. 2017

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“…Previous studies reported elevated levels of oxidative stress markers in serum and respiratory samples along with increased apoptotic cells within the granuloma and in the bronchoalveolar lavage (BAL) cells of sarcoidosis patients [ 16 , 17 , 18 ]. In recent studies of the murine model, we demonstrated that MWCNT instilled C57BL/6 wild-type mice also have apoptotic cells in the BAL and granulomas, and this effect is accompanied by an increase in reactive oxygen species (ROS) in BAL cells, BAL fluid, and lung tissues, suggesting the role of oxidative stress and apoptosis in granuloma formation [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Myeloid ABCG1 Deficiency Enhances Apoptosis and Initiates Efferocytosis in Bronchoalveolar Lavage Cells of Murine Multi-Walled Carbon Nanotube-Induced Granuloma Model

Soliman

Bhalla

Elhassanny

et al. 2021

IJMS

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The use of carbon nanotubes has increased in the past few decades. Carbon nanotubes are implicated in the pathogenesis of pulmonary sarcoidosis, a chronic granulomatous inflammatory condition. We developed a murine model of chronic granulomatous inflammation using multiwall carbon nanotubes (MWCNT) to investigate mechanisms of granuloma formation. Using this model, we demonstrated that myeloid deficiency of ATP-binding cassette (ABC) cholesterol transporter (ABCG1) promotes granuloma formation and fibrosis with MWCNT instillation; however, the mechanism remains unclear. Our previous studies showed that MWCNT induced apoptosis in bronchoalveolar lavage (BAL) cells of wild-type (C57BL/6) mice. Given that continual apoptosis causes persistent severe lung inflammation, we hypothesized that ABCG1 deficiency would increase MWCNT-induced apoptosis thereby promoting granulomatous inflammation and fibrosis. To test our hypothesis, we utilized myeloid-specific ABCG1 knockout (ABCG1 KO) mice. Our results demonstrate that MWCNT instillation enhances pulmonary fibrosis in ABCG1 KO mice compared to wild-type controls. Enhanced fibrosis is indicated by increased trichrome staining and transforming growth factor-beta (TGF-β) expression in lungs, together with an increased expression of TGF-β related signaling molecules, interleukin-13 (IL-13) and Smad-3. MWCNT induced more apoptosis in BAL cells of ABCG1 KO mice. Initiation of apoptosis is most likely mediated by the extrinsic pathway since caspase 8 activity and Fas expression are significantly higher in MWCNT instilled ABCG1 KO mice compared to the wild type. In addition, TUNEL staining shows that ABCG1 KO mice instilled with MWCNT have a higher percentage of TUNEL positive BAL cells and more efferocytosis than the WT control. Furthermore, BAL cells of ABCG1 KO mice instilled with MWCNT exhibit an increase in efferocytosis markers, milk fat globule-EGF factor 8 (MFG-E8) and integrin β3. Therefore, our observations suggest that ABCG1 deficiency promotes pulmonary fibrosis by MWCNT, and this effect may be due to an increase in apoptosis and efferocytosis in BAL cells.

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Oxidative Stress in Sarcoidosis

Cited by 2 publications

References 56 publications

The necessity of external validation in exhaled breath research: a case study of sarcoidosis

The necessity of external validation in exhaled breath research: a case study of sarcoidosis

Myeloid ABCG1 Deficiency Enhances Apoptosis and Initiates Efferocytosis in Bronchoalveolar Lavage Cells of Murine Multi-Walled Carbon Nanotube-Induced Granuloma Model

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