Increased <scp>CD8 T</scp>‐cell granzyme <scp>B</scp> in <scp>COPD</scp> is suppressed by treatment with low‐dose azithromycin

Hodge, Sandra; Hodge, Greg; Holmes, Mark; Jersmann, Hubertus; Reynolds, Paul N.

doi:10.1111/resp.12415

Cited by 16 publications

(5 citation statements)

References 33 publications

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“…Some studies have suggested that the increase of CD8+ T cells is a negative factor for COPD patients, and even in some studies, it has been suggested that the application of small dose of azithromycin can reduce the number of CD8+ T cells in the alveolar lavage fluid of COPD patients, reduce the level of granulosin B released by CD8+ T cells in the peripheral blood, and improve the cellular immunity of COPD patients [ 30 ]. In this study, CD8+ T level was upregulated after autoimmune cell therapy, which has not been seen in other previous studies on the treatment of COPD, and the literature on autoimmune cell therapy of COPD is limited, so the reasons for the increase of CD8+ T level and the advantages and advantages of the increase of CD8+ T level on COPD still need to be further studied.…”

Section: Discussionmentioning

confidence: 99%

Effect of Autoimmune Cell Therapy on Immune Cell Content in Patients with COPD: A Randomized Controlled Trial

Zhou

et al. 2022

Computational and Mathematical Methods in Medicine

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Objective. To explore the effect of autoimmune cell therapy on immune cells in patients with chronic obstructive pulmonary disease (COPD) and to provide a reference for clinical treatment of COPD. Methods. Sixty patients with stable COPD were randomly divided into control group and treatment group ( n = 30 ). The control group was given conventional treatment, and the treatment group was given one autoimmune cell therapy on the basis of conventional treatment. The serum levels of CD3+ T cells, CD4+ T cells, CD8+ cells, B cells, and NK cells in the peripheral blood were detected by flow cytometry. Possible adverse reactions were detected at any time during treatment. Results. There were no significant differences in the contents of CD3+ T cells, CD4+ T cells, CD8+ cells, B cells, and NK cells in the serum of the control group ( P > 0.05 ). Compared with before treatment, the contents of CD3+ T cells, CD4+ T cells, CD8+ cells, B cells, and NK cells in the serum of the treatment group were significantly increased ( P < 0.05 ). The ratio of CD 4 + / CD 8 + T cells in both control and treatment groups did not change significantly during treatment ( P > 0.05 ). There were no significant differences in serum CD3+ T cells, CD4+ T cells, CD8+ cells, B cells, and NK cells in the treatment group at 30 days and 90 days after treatment ( P > 0.05 ), but they were significantly higher than those in the control group ( P < 0.05 ). Conclusion. Autoimmune cell therapy can significantly increase the level of immune cells in the body and can be maintained for a long period of time, which has certain clinical benefits for recurrent respiratory tract infections and acute exacerbation in patients with COPD.

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Section: Discussionmentioning

confidence: 99%

Effect of Autoimmune Cell Therapy on Immune Cell Content in Patients with COPD: A Randomized Controlled Trial

Zhou

et al. 2022

Computational and Mathematical Methods in Medicine

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“…The granzyme B pathway is a major mediator of cytotoxic T cell induced apoptosis and DNA fragmentation in target cells including airway epithelial cells. A 12 week study by Hodge and colleagues found that low‐dose azithromycin can reduce production of the cytotoxic mediator granzyme B by CD8 + T cells from both airway and intra‐epithelial compartments. This suggested that low‐dose azithromycin may be an adjunct treatment option for controlling epithelial cell apoptosis, abnormal airway repair and chronic inflammation in COPD, although the possible development of microbial resistance and long term benefit needs to be addressed in larger studies.…”

Section: Copdmentioning

confidence: 99%

Year in review 2015: Asthma and chronic obstructive pulmonary disease

et al. 2016

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Asthma continues to cause substantial morbidity and mortality, affecting some 300 million people worldwide, with a large proportion of those poorly controlled.1-3 In the last year, Respirology published a broad-based range of papers focusing on this important disease, ranging from questionnaire studies to molecular biology in mouse models. 4,5 This range of papers emphasizes the breadth of asthma research underway and the role of Respirology in disseminating these advances.

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“…Treatment with erythromycin has been found to decrease neutrophil and lymphocyte counts, lower levels of IL-8 and TNF-α in the BALF, and downregulate keratinocyte-derived chemokine and TNF-α transcription in CS-exposed mice 21,26. Emerging evidence shows that macrolides could play an immunomodulatory role in addition to the known antibiotic role, including the regulation of innate and adaptive immune cells 40,41. We previously showed that erythromycin modulated inflammatory immune cells in the airway and restored the decrease of Treg through immunomodulation in rats exposed to cigarette smoke 26.…”

Section: Discussionmentioning

confidence: 99%

<p>Erythromycin Prevents Elastin Peptide-Induced Emphysema and Modulates CD4<sup>+</sup>T Cell Responses in Mice</p>

Tang

Zhang

et al. 2019

COPD

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Elastin peptides (EP) can induce lung inflammation and emphysema. Erythromycin has been shown to decrease acute exacerbation frequency and delay lung function decline in chronic obstructive pulmonary disease patients and ameliorate emphysema in murine models; however, the mechanism remains unclear. We aimed to observe the preventive and immunomodulatory effects of erythromycin in a mouse model of EP-induced emphysema. Methods: In the in vivo study, Balb/c mice were treated with EP intranasally on day 0, and then administered erythromycin (100 mg/kg) or vehicle orally on day 1, which was continued every other day. Mice exposed to cigarette smoke were used as an emphysema positive control. The severity of emphysema and inflammation in the lungs of EP-exposed mice with or without erythromycin treatment were observed on day 40 after EP administration. In the in vitro study, naïve CD4 + T cells were isolated from healthy mice spleens and stimulated by EP with or without erythromycin incubation. Flow cytometry was used to measure the proportions of Th1, Th17, and Treg cells. ELISA was used to detect cytokine levels of IFN-γ, IL-17, IL-6, and TGF-β. Transcript levels of Ifnγ, IL17a, and Foxp3 were evaluated by qRT-PCR. Results: After exposure to EP, Th1 and Th17 cell percentages and the levels of inflammatory cytokines increased in vivo and in vitro, while Treg cells decreased in vivo. Erythromycin reduced IFN-γ, IL-17, IL-6 inflammatory cytokines, MLI, and the inflammation score in the lungs of EP-exposed mice. In vitro, erythromycin also limited Th17 and Th1 cell differentiation and downregulated transcript levels of Ifnγ and IL17a in the EPstimulated CD4 + T cells. Conclusion: The Th1 and Th17 cell responses were increased in EP-induced emphysema. Prophylactic use of erythromycin effectively ameliorated emphysema and modulated CD4 + T cells responses in EP-induced lung inflammation in mice.

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Increased CD8 T‐cell granzyme B in COPD is suppressed by treatment with low‐dose azithromycin

Abstract: We provide further evidence for the application of low-dose azithromycin as an attractive adjunct treatment option for controlling epithelial cell apoptosis, abnormal airway repair and chronic inflammation in COPD.

Cited by 16 publications

References 33 publications

Effect of Autoimmune Cell Therapy on Immune Cell Content in Patients with COPD: A Randomized Controlled Trial

Effect of Autoimmune Cell Therapy on Immune Cell Content in Patients with COPD: A Randomized Controlled Trial

Year in review 2015: Asthma and chronic obstructive pulmonary disease

<p>Erythromycin Prevents Elastin Peptide-Induced Emphysema and Modulates CD4<sup>+</sup>T Cell Responses in Mice</p>

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