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Biomedicines
Special Issues
Innate Immunity Orchestration in Lung Health and Diseases
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Innate Immunity Orchestration in Lung Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 16069

Special Issue Editors

Dr. Meraj Alam Khan

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Guest Editor
Program in Translational Medicine, Peter Gilgan Centre for Research and Learning, The Hospital for SickChildren, Toronto, ON M5G 0A4, Canada
Interests: molecular and cellular innate immunity; iPS cell differentiation to neutrophils; Neutrophils Extracellular Traps (NETs); kinase mediated cell signaling; large scale transcriptomics; respiratory infection; chronic lung infection and inflammation; COPD; asthma; Cystic Fibrosis; in vivo lung infection and inflammation model; lung transplant, post lung transplant diseases; NETs-mediated metastasis; long chain fatty acid (Furanoic acid) role in innate immunity; wound healing; chemotherapy drug screening and validation; endometriosis; reproductive biology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Anjana Talwar

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Co-Guest Editor
Department of Physiology Respiratory Research Laboratory All India Institute of Medical Sciences (AIIMS), New Delhi 110029, India
Interests: to understand the role of immune cells in underlying mechanisms of COPD by high throughput array-based comparative genomic hybridization (aCGH ) and micro array-based gene expression profiling of mononuclear cells; non-invasive techniques to assess airway inflammatory cells; exercise capacity by cardio-pulmonary exercise testing in patients with airway inflammatory diseases
Dr. Soumen Manna

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Co-Guest Editor
Department of Physiology, VMMC & Safdarjung Hospital, New Delhi 110029, India
Interests: human physiology; respiratory diseases; innate immunity; role of Nitric oxide (NO); oxidant/antioxidant in lung development

Special Issue Information

Dear Colleagues,

The lungs act as an interface between innate immunity and inhaled components. On average, ten thousand liters of inhaled air pass through the respiratory tract daily, exposing the lungs to a plethora of microbes, pathogens, chemicals, toxins, and other unwanted compounds. Respiratory tract infections, chronic inflammation, and injuries (pathogen or sterile) are not only a major cause of morbidity but affect quality of life.

Healthy innate and adaptive immune systems not only combat pathogen attack but help to maintain healthy lung function. Innate immunity provides the first line of immune defense against pathogens and promotes the resolution of inflammation. To counter pathogenic attack, a complex interplay occurs between host cells, infiltrating innate immune cells, secreted innate immune proteins, and innate lymphoid cells, producing various cytokines and chemokines within the airway microenvironment. Innate immune cell neutrophils are the first to arrive at the site of infection or injury and play a pivotal role against infectious pathogens either through phagocytosis, degranulation, or by releasing NETs (neutrophil extracellular traps), a unique mechanism to trap and kill pathogens. Recent literature suggests that NETs are a beneficial mechanism to combat pathogens but the presence of dysregulated or excessive NETs can exacerbate diseases including cystic fibrosis, COPD, asthma, ARDS, acute lung injury, pneumonia as well as several chronic pulmonary diseases.

The aim of this Special Issue of Biomedicines is to provide a comprehensive overview of the roles of innate immune cells, innate immune proteins, lymphoid cells, and the microenvironment during lung pathologies. The discussion of underlying mechanisms and regulatory interactions between innate immune components and effectors will aid in the development of new therapeutic options for lung-associated disorders. We invite authors to submit relevant original research articles, mini and full reviews, and perspectives for inclusion in this Special Issue.

Dr. Meraj Alam Khan
Prof. Dr. Anjana Talwar
Dr. Soumen Manna
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • innate immune cells
  • neutrophils
  • NETs
  • NETosis
  • macrophages
  • phagocytosis
  • Innate lymphoid cells
  • epithelial cells
  • lung inflammation
  • lung cancer
  • immunotherapy

Published Papers (4 papers)

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Research

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12 pages, 1464 KiB  
Article
SEZ6L2 Is an Important Regulator of Drug-Resistant Cells and Tumor Spheroid Cells in Lung Adenocarcinoma
by Jang-Seok Lee, Hee Yeon Kim, Bomyi Won, Sang Won Kang, Yong-Nyun Kim and Hyonchol Jang
Biomedicines 2020, 8(11), 500; https://doi.org/10.3390/biomedicines8110500 - 13 Nov 2020
Cited by 7 | Viewed by 3197
Abstract
Many lung cancer deaths result from relapses in distant organs, such as the brain or bones, after standard chemotherapy. For cancer cells to spread to other organs, they must survive as circulating tumor cells (CTCs) in blood vessels. Thus, reducing distant recurrence after [...] Read more.
Many lung cancer deaths result from relapses in distant organs, such as the brain or bones, after standard chemotherapy. For cancer cells to spread to other organs, they must survive as circulating tumor cells (CTCs) in blood vessels. Thus, reducing distant recurrence after chemotherapy requires simultaneously inhibiting drug resistance and CTC survival. Here, we investigated the molecular pathways and genes that are commonly altered in drug-resistant lung cancer cells and lung tumor spheroid (TS) cells. First, RNA sequencing was performed in drug-resistant cells and TS cells originating from H460 and A549 lung cancer cells. Bioinformatic pathway analysis showed that cell cycle-related pathways were downregulated in drug-resistant cells, and cholesterol biosynthesis-related pathways were upregulated in TS cells. Seizure-related 6 homolog-like 2 (SEZ6L2) was selected as a gene that was commonly upregulated in both drug-resistant cells and TS cells, and that showed elevated expression in samples from lung adenocarcinoma patients. Second, the protein expression of SEZ6L2 was analyzed by flow cytometry. The proportions of SEZ6L2 positive cells among both drug-resistant cells and TS cells was increased. Finally, as SEZ6L2 is a transmembrane protein with an extracellular region, the function of SEZ6L2 was disrupted by treatment with an anti-SEZ6L2 antibody. Treatment with the anti-SEZ6L2 antibody reduced drug resistance and TS formation. Overall, our data showed that SEZ6L2 plays an important role in drug resistance and TS formation and may be a therapeutic target for reducing distant recurrence of lung adenocarcinoma. Full article
(This article belongs to the Special Issue Innate Immunity Orchestration in Lung Health and Diseases)
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16 pages, 2060 KiB  
Article
Nrf2 Lowers the Risk of Lung Injury via Modulating the Airway Innate Immune Response Induced by Diesel Exhaust in Mice
by Ying-Ji Li, Takako Shimizu, Yusuke Shinkai, Tomomi Ihara, Masao Sugamata, Katsuhito Kato, Maiko Kobayashi, Yukiyo Hirata, Hirofumi Inagaki, Makoto Uzuki, Toshio Akimoto, Masakazu Umezawa, Ken Takeda, Arata Azuma, Masayuki Yamamoto and Tomoyuki Kawada
Biomedicines 2020, 8(10), 443; https://doi.org/10.3390/biomedicines8100443 - 21 Oct 2020
Cited by 6 | Viewed by 2588
Abstract
In the present study, we investigated the role of Nrf2 in airway immune responses induced by diesel exhaust (DE) inhalation in mice. C57BL/6J Nrf2+/+ and Nrf2−/− mice were exposed to DE or clean air for 8 h/day and 6 days/week for [...] Read more.
In the present study, we investigated the role of Nrf2 in airway immune responses induced by diesel exhaust (DE) inhalation in mice. C57BL/6J Nrf2+/+ and Nrf2−/− mice were exposed to DE or clean air for 8 h/day and 6 days/week for 4 weeks. After DE exposure, the number of neutrophils and macrophage inflammatory protein (MIP)-2 level in bronchoalveolar lavage fluid (BALF) and interleukin (IL)-17 level in the lung tissue increased in Nrf2−/− mice compared with Nrf2+/+ mice; however, the lack of an increase in the level of tumor necrosis factor (TNF)-α in the lung tissue in Nrf2+/+ mice and mild suppression of the level of TNF-α in Nrf2−/− mice were observed; the level of granulocyte macrophage colony-stimulating factor (GM-CSF) in the lung tissue decreased in Nrf2−/− mice than in Nrf2+/+ mice; the number of DE particle-laden alveolar macrophages in BALF were larger in Nrf2−/− mice than in Nrf2+/+ mice. The results of electron microscope observations showed alveolar type II cell injury and degeneration of the lamellar body after DE exposure in Nrf2−/− mice. Antioxidant enzyme NAD(P)H quinone dehydrogenase (NQO)1 mRNA expression level was higher in Nrf2+/+ mice than in Nrf2−/− mice after DE exposure. Our results suggested that Nrf2 reduces the risk of pulmonary disease via modulating the airway innate immune response caused by DE in mice. Full article
(This article belongs to the Special Issue Innate Immunity Orchestration in Lung Health and Diseases)
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15 pages, 2578 KiB  
Article
Discovery of Hordenine as a Potential Inhibitor of Pyruvate Dehydrogenase Kinase 3: Implication in Lung Cancer Therapy
by Saleha Anwar, Taj Mohammad, Anas Shamsi, Aarfa Queen, Shahnaz Parveen, Suaib Luqman, Gulam Mustafa Hasan, Khalid A. Alamry, Naved Azum, Abdullah M. Asiri and Md. Imtaiyaz Hassan
Biomedicines 2020, 8(5), 119; https://doi.org/10.3390/biomedicines8050119 - 14 May 2020
Cited by 78 | Viewed by 5112
Abstract
Design and development of potential pyruvate dehydrogenase kinase 3 (PDK3) inhibitors have gained attention because of their possible therapeutic uses in lung cancer therapy. In the present study, the binding affinity of naturally occurring alkaloids, hordenine, vincamine, tryptamine, cinchonine, and colcemid was measured [...] Read more.
Design and development of potential pyruvate dehydrogenase kinase 3 (PDK3) inhibitors have gained attention because of their possible therapeutic uses in lung cancer therapy. In the present study, the binding affinity of naturally occurring alkaloids, hordenine, vincamine, tryptamine, cinchonine, and colcemid was measured with PDK3. The molecular docking and fluorescence binding studies suggested that all these compounds show a considerable binding affinity for PDK3. Among them, the affinity of hordenine to the PDK3 was excellent (K = 106 M−1) which was further complemented by isothermal titration calorimetric measurements. Hordenine binds in the active site pocket of PDK3 and forms a significant number of non-covalent interactions with functionally important residues. All-atom molecular dynamics (MD) simulation study suggested that the PDK3-hordenine complex is stabilized throughout the trajectory of 100ns and leads to fewer conformational changes. The enzyme inhibition studies showed that hordenine inhibits the activity of PDK3 with an IC50 value of 5.4 µM. Furthermore, hordenine showed a cytotoxic effect on human lung cancer cells (A549 and H1299) with an admirable IC50 value. However, it did not inhibit the growth of HEK293 cells up to 200 µM, indicating its non-toxicity to non-cancerous cell lines. In summary, our findings provide the basis for the therapeutic implication of hordenine and its derivatives in lung cancer and PDK3-related diseases after required in vivo validation. Full article
(This article belongs to the Special Issue Innate Immunity Orchestration in Lung Health and Diseases)
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Review

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25 pages, 3233 KiB  
Review
Orchestration of Neutrophil Extracellular Traps (Nets), a Unique Innate Immune Function during Chronic Obstructive Pulmonary Disease (COPD) Development
by Anjali Trivedi, Meraj A. Khan, Geetanjali Bade and Anjana Talwar
Biomedicines 2021, 9(1), 53; https://doi.org/10.3390/biomedicines9010053 - 08 Jan 2021
Cited by 30 | Viewed by 4632
Abstract
Morbidity, mortality and economic burden caused by chronic obstructive pulmonary disease (COPD) is a significant global concern. Surprisingly, COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030. It is characterized by persistent [...] Read more.
Morbidity, mortality and economic burden caused by chronic obstructive pulmonary disease (COPD) is a significant global concern. Surprisingly, COPD is already the third leading cause of death worldwide, something that WHO had not predicted to occur until 2030. It is characterized by persistent respiratory symptoms and airway limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles of gases. Neutrophil is one of the key infiltrated innate immune cells in the lung during the pathogenesis of COPD. Neutrophils during pathogenic attack or injury decide to undergo for a suicidal death by releasing decondensed chromatin entangled with antimicrobial peptides to trap and ensnare pathogens. Casting neutrophil extracellular traps (NETs) has been widely demonstrated to be an effective mechanism against invading microorganisms thus controlling overwhelming infections. However, aberrant and massive NETs formation has been reported in several pulmonary diseases, including chronic obstructive pulmonary disease. Moreover, NETs can directly induce epithelial and endothelial cell death resulting in impairing pulmonary function and accelerating the progression of the disease. Therefore, understanding the regulatory mechanism of NET formation is the need of the hour in order to use NETs for beneficial purpose and controlling their involvement in disease exacerbation. For example, DNA neutralization of NET proteins using protease inhibitors and disintegration with recombinant human DNase would be helpful in controlling excess NETs. Targeting CXC chemokine receptor 2 (CXCR2) would also reduce neutrophilic inflammation, mucus production and neutrophil-proteinase mediated tissue destruction in lung. In this review, we discuss the interplay of NETs in the development and pathophysiology of COPD and how these NETs associated therapies could be leveraged to disrupt NETopathic inflammation as observed in COPD, for better management of the disease. Full article
(This article belongs to the Special Issue Innate Immunity Orchestration in Lung Health and Diseases)
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