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Immune Regulation in Respiratory Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 1775

Special Issue Editors


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Guest Editor
Institut Necker Enfants Malades, CNRS UMR 8253, Inserm 1151, Université de Paris Cité, 75015 Paris, France
Interests: asthma inflammation; asthma; human allergies; innate-like T cells
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Guest Editor
AP-HP, Hôpital Necker-Enfants Malades, Service de Pneumologie et Allergologie Pédiatriques, 75015 Paris, France
Interests: pulmonary medicine; spirometry; respiratory physiology; bronchoalveolar lavage; asthma management; allergic diseases

Special Issue Information

Dear Colleagues, 

Respiratory diseases are among the most common disorders in the world and represent a significant health and economic burden. Abnormal immune regulation and persistent inflammation are hallmarks of asthma, chronic obstructive pulmonary disease (COPD), chronic bronchitis, cystic fibrosis, and pneumonia. Several types of immune cells contribute to the inflammation of the airways in these pathologies, including neutrophils, eosinophils, macrophages, innate lymphoid cells, dendritic cells, and B and T lymphocytes. Despite major advances in this area, a better understanding of the immune mechanisms involved in respiratory diseases, both at the cellular and molecular level, is still necessary to propose a “personalized medicine” approach for the treatment of these pathologies. This Special Issue will collect research and review articles focusing on novel studies employing human cells or animal models to investigate immune regulatory mechanisms in respiratory diseases. Research revealing new molecular mechanisms is especially encouraged.

Dr. Maria Leite de Moraes
Dr. Guillaume Lezmi
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • asthma
  • COPD
  • lung infection
  • immunoregulation
  • lung innate immunity
  • lung adaptive immunity
  • animal models
  • cytokines

Published Papers (1 paper)

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Research

15 pages, 1680 KiB  
Article
COPD Patients Exhibit Distinct Gene Expression, Accelerated Cellular Aging, and Bias to M2 Macrophages
by Camila Oliveira da Silva, Jeane de Souza Nogueira, Adriana Paulino do Nascimento, Tatiana Victoni, Thiago Prudente Bártholo, Cláudia Henrique da Costa, Andrea Monte Alto Costa, Samuel dos Santos Valença, Martina Schmidt and Luís Cristóvão Porto
Int. J. Mol. Sci. 2023, 24(12), 9913; https://doi.org/10.3390/ijms24129913 - 8 Jun 2023
Cited by 1 | Viewed by 1412
Abstract
COPD, one of world’s leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease severity can be classified as mild, moderate, severe, and very severe. The [...] Read more.
COPD, one of world’s leading contributors to morbidity and mortality, is characterized by airflow limitation and heterogeneous clinical features. Three main phenotypes are proposed: overlapping asthma/COPD (ACO), exacerbator, and emphysema. Disease severity can be classified as mild, moderate, severe, and very severe. The molecular basis of inflammatory amplification, cellular aging, and immune response are critical to COPD pathogenesis. Our aim was to investigate EP300 (histone acetylase, HAT), HDAC 2 (histone deacetylase), HDAC3, and HDAC4 gene expression, telomere length, and differentiation ability to M1/M2 macrophages. For this investigation, 105 COPD patients, 42 smokers, and 73 non-smoker controls were evaluated. We identified a reduced HDAC2 expression in patients with mild, moderate, and severe severity; a reduced HDAC3 expression in patients with moderate and severe severity; an increased HDAC4 expression in patients with mild severity; and a reduced EP300 expression in patients with severe severity. Additionally, HDAC2 expression was reduced in patients with emphysema and exacerbator, along with a reduced HDAC3 expression in patients with emphysema. Surprisingly, smokers and all COPD patients showed telomere shortening. COPD patients showed a higher tendency toward M2 markers. Our data implicate genetic changes in COPD phenotypes and severity, in addition to M2 prevalence, that might influence future treatments and personalized therapies. Full article
(This article belongs to the Special Issue Immune Regulation in Respiratory Diseases)
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