Chronic Obstructive Pulmonary Disease and Cigarette Smoke Lead to Dysregulated Mucosal-associated Invariant T-Cell Activation

Huber, Megan E.; Larson, Emily A.; Lust, Taylor N; Heisler, Chelsea M; Harriff, Melanie J.

doi:10.1165/rcmb.2022-0131oc

Cited by 9 publications

(9 citation statements)

References 65 publications

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“… 7 , 26 Furthermore, CS increases the severity of disease‐causing agents and promotes the risk of pulmonary infections. 27 The fine and ultrafine PM reported in this work are potent because they can be inhaled deeper into the respiratory landscape, as earlier reported by Kwon et al 28 Particulate emissions having an aerodynamic diameter ≤2.5 μm can cross the biological respiratory filters and are precursors for alveoli injury and irreversible damage to the lung microphages. 28 , 29 Moreover, ultrafine PM initiates upper and lower respiratory inflammation, malignant lung growth, rib cage malfunctions, and, ultimately, cancer of the lungs.…”

Section: Discussionsupporting

confidence: 75%

“…CS induces oxidative stress resulting in chronic inflammation and recruitment of inflammatory cells to the airways by activation of epithelial cells, neutrophils, and lymphocytes 7,26 . Furthermore, CS increases the severity of disease‐causing agents and promotes the risk of pulmonary infections 27 . The fine and ultrafine PM reported in this work are potent because they can be inhaled deeper into the respiratory landscape, as earlier reported by Kwon et al 28 Particulate emissions having an aerodynamic diameter ≤2.5 μm can cross the biological respiratory filters and are precursors for alveoli injury and irreversible damage to the lung microphages 28,29 .…”

Section: Discussionmentioning

confidence: 99%

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The impact of puff frequency on respirable particulate matter in mainstream cigarette smoke

Maiyo

Korir

Kibet

2023

Clinical Respiratory J

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Background Inhalation of particulate matter (PM) from cigarette smoke is hazardous to smokers and non‐smokers. This contribution simulates the deposition of cigarette PM on the lung surface by trapping tobacco smoke particulates on Croton megalocarpus biochar. This study investigated one commercial cigarette (MM) and one local cigarette (RR). Methodology Biochar was incorporated into the filters of MM and RR cigarettes in order to adsorb PM from mainstream cigarette smoke. A weighed 5 mg of biochar with adsorbed cigarette PM was analyzed using a scanning electron microscope and a Fourier transform infrared spectrometer. The size distribution of cigarette smoke particulates was processed using ImageJ software. Results At 15 s puff time, the mean particulate diameters for the commercial and the local cigarettes, respectively, can be classified as coarse ≈ PM 10 . Conversely, the mean particulate diameter at 2 s puff time for the commercial cigarette falls under the ultrafine classification of ≤PM 2.5 , whereas at the same puff time, the mean particulate diameter for the local cigarette was approximately PM 2.5 . Data from Fourier transform infrared spectroscopy indicate the PM in the two model cigarettes contains aromatic structures that feature the C=C bond characterized by an intense absorption band at δs (1600 cm −1 ). Conclusions This study found that PM in mainstream cigarette smoke depends on puff time. Although cigarette smoking was conducted for two model cigarettes, this study can be extended to any other form of cigarette. Moreover, this study emphasizes the need for comprehensive studies on real‐world cigarette smoking conditions, taking into account cigarette smokers who use larger puff volumes.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

The impact of puff frequency on respirable particulate matter in mainstream cigarette smoke

Maiyo

Korir

Kibet

2023

Clinical Respiratory J

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“…In this issue of the Journal , Huber and colleagues (pp. 90–102 ) describe their investigations into the impact of both smoking and COPD on the interaction between epithelial cells and mucosal-associated invariant T (MAIT) cells ( 6 ). MAIT cells are innate-like T cells that play a role in controlling bacterial infection by recognizing nonpeptide antigens derived from the bacterial vitamin B2 pathway presented by the MR1 (major histocompatibility complex–related protein 1) ( 7 ).…”

mentioning

confidence: 99%

“…Huber and colleagues first demonstrate that unstimulated bronchial epithelial cells (BECs) from patients with COPD drive more IFNγ expression from a MAIT cell clone (D426 G11) than do BECs from both healthy and currently smoking control subjects ( 6 ). These investigators go on to show that this increase was mediated directly via interaction between the MAIT cell and epithelial-expressed MR1, using blocking antibodies, rather than by increases in soluble cytokines released by the COPD epithelium.…”

mentioning

confidence: 99%

“…Huber and colleagues ( 6 ) then proceeded to investigate the effects of 30% (vol/vol) SC extract (CSE) on the ability of the epithelial cells to activate the MAIT cell clone by incubating the BECs with CSE for 3 hours before removing the CSE media and incubating the BECs with the MAIT cell clone. Exposure of healthy control and COPD BECs to CSE had no effect on MAIT cell activation, whereas CSE caused a reduction in MAIT cell activation by BECs from smokers.…”

mentioning

confidence: 99%

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Breaching the Defenses? Mucosal-associated Invariant T Cells, Smoking, and Chronic Obstructive Pulmonary Disease

Staples

2023

Am J Respir Cell Mol Biol

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MAIT cells are associated with responsiveness to neoadjuvant immunotherapy in COPD‐associated NSCLC

Yin,

Zeng,

Abuduwayiti

et al. 2024

Cancer Medicine

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BackgroundPatients with non‐small cell lung cancer (NSCLC) and chronic obstructive pulmonary disease (COPD) experience worse clinical outcomes but respond better to immunotherapy than patients with NSCLC without COPD. Mucosal‐associated invariant T (MAIT) cells, a versatile population of innate immune T lymphocytes, have a crucial function in the response to infection and tumors. This study investigated the distribution of MAIT cells in COPD‐associated NSCLC and their involvement in the immune response.MethodsFlow cytometry, immunohistochemistry, and immunofluorescence were performed on tissue samples of patients with NSCLC, with or without COPD, treated with or without anti‐programmed death 1 (PD1) immunotherapy. MAIT cells were stimulated with 5‐OP‐RU using a mouse subcutaneous tumor model.ResultsTumors contained significantly more MAIT cells than paraneoplastic tissues, and CD8+ MAIT cells accounted for more than 90% of these cells. Patients with NSCLC and COPD had higher CD8+ MAIT cell counts than those with NSCLC without COPD. Additionally, patients with NSCLC and COPD displayed reduced expression of the activation marker, CD69, and functional markers, granzyme B (GZMB) and interferon γ (IFNγ), and higher expression of the immune exhaustion marker, PD1. Among patients who received immunotherapy, the proportion with a complete or partial response was higher in those with COPD than in those without COPD. In patients with NSCLC and COPD, the major pathologic response (MPR) group had higher MAIT levels than those in the no major pathologic response (NPR) group. In the mouse subcutaneous tumor model stimulation of MAIT cells using 5‐OP‐RU enhanced the antitumor effects of anti‐PD1.ConclusionsIn patients with NSCLC and COPD, response to immunotherapy is associated with accumulation of CD8+ MAIT cells showing immune exhaustion. These findings may contribute to innovative approaches for immunotherapy targeting CD8+ MAIT cells.

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Chronic Obstructive Pulmonary Disease and Cigarette Smoke Lead to Dysregulated Mucosal-associated Invariant T-Cell Activation

Cited by 9 publications

References 65 publications

The impact of puff frequency on respirable particulate matter in mainstream cigarette smoke

The impact of puff frequency on respirable particulate matter in mainstream cigarette smoke

Breaching the Defenses? Mucosal-associated Invariant T Cells, Smoking, and Chronic Obstructive Pulmonary Disease

MAIT cells are associated with responsiveness to neoadjuvant immunotherapy in COPD‐associated NSCLC

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