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Biomolecules
Special Issues
Inflammation and Immunity in Lung Disease
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Inflammation and Immunity in Lung Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 20 December 2026 | Viewed by 2355

Special Issue Editor

Dr. Xuexian Yang

E-Mail Website
Guest Editor
Department of Molecular Genetics and Microbiology, School of Medicine, University of New Mexico, Albuquerque, NM, USA
Interests: cytokine signaling; unfolded protein response; transcriptional control; T helper cell; immunity and inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Many pathogenic, environmental, and genetic factors lead to lung inflammation, affecting lung function. This Specific Issue covers a variety of lung diseases, including but not limited to pulmonary infection, asthma, bronchiectasis, chronic obstructive pulmonary disease, pulmonary fibrosis, interstitial lung disease, and lung cancer. These conditions can affect different parts of the lungs and cause breathing difficulties, coughing, and chest pain. Specified immune responses to pathogenic invasion and environmental agents play an important role in host defense and pathology, where excessive, inappropriate, and/or prolonged inflammation damages lung tissue and impairs lung function. Genetic deficiencies (such as the CFTR gene mutation that causes cystic fibrosis) and lung cancer compromise the host defense machinery and harm lung tissue integrity. Cytokine release syndrome, seen in uncontrolled systemic inflammation, e.g., systemic lupus erythematosus, impacts the functionality of multiple organs, including the lungs. Local and remote signals from the nervous, metabolic, intestinal, and endocrine systems influence pulmonary immunity, attracting broad interest.

Dr. Xuexian Yang
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules 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 2700 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

  • lung
  • infection
  • inflammation
  • host defense
  • cytokine release syndrome
  • genetic deficiency

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Published Papers (3 papers)

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Research

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22 pages, 6337 KB  
Article
Cigarette Smoke Induces Canonical Stress Granule Formation in Human Bronchial Epithelial Cells in Reactive Oxygen Species- and PERK-Dependent Manners
by Mousumi Bhowmik, Chenkun Zheng, Bisrat Bekele, Jessica Failler, Carlie Klatt, Souren Farimani, Bryant Jones, Chung-Chun Tyan and Asmahan Abu-Arish
Biomolecules 2026, 16(4), 615; https://doi.org/10.3390/biom16040615 - 21 Apr 2026
Viewed by 480
Abstract
Cigarette smoke (CS) is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD). Investigating the impact of CS on human airway epithelium is important for understanding COPD development and combating its effects. While some studies show that long exposure [...] Read more.
Cigarette smoke (CS) is the primary risk factor for the development of chronic obstructive pulmonary disease (COPD). Investigating the impact of CS on human airway epithelium is important for understanding COPD development and combating its effects. While some studies show that long exposure to CS activates inflammasome formation in airway epithelium, leading to cytokines’ maturation and release, its acute effect on inflammation regulation requires further elucidation. Due to the importance of acute cellular responses in modulating cell survival and controlling inflammatory outcomes, we examined the effect of acute cigarette smoke extract exposure on human bronchial epithelial cells. Due to the high reactive oxygen species content in CS, we hypothesize that acute CS exposure activates the integrated stress response (ISR) pathway leading to stress granules (SG) formation to facilitate oxidative stress resolution and promote cell survival. Immunostaining, fluorescence confocal imaging, quantitative analyses, and immunoblotting were performed to test our hypothesis. We report here that acute exposure to CS extract triggers canonical SG formation by activating the ISR pathway via the PERK/eIF2α arm in a reactive oxygen species-dependent manner. SG formation is abolished upon inhibiting PERK or eIF2α function, or by scavenging oxidants prior to smoke exposure. Characterizing SG formation in terms of measuring SG size and abundance and the sequestration of the SG marker G3BP1 reveals that SG formation is maximal at 15% CS extract exposure for 2 h and undergoes gradual disassembly at longer exposure times. This is closely dependent on cytoplasmic p-eIF2α levels. These results demonstrate that acute exposure to CS activates the protective ISR pathway to potentially reduce the detrimental effects of CS and promote stress resolution and cell survival. Full article
(This article belongs to the Special Issue Inflammation and Immunity in Lung Disease)
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20 pages, 4476 KB  
Article
Notch Signaling Exacerbates Pulmonary Fibrosis by Regulating the Differentiation of CD4+ Tissue-Resident Memory T Cells
by Jia Shi, Ruiting Su, Lili Zhuang, Zhangmei Lin, Xinyuan Ruan, Yichao Qian, Jieying Zhu, Shuyi Wang and Niansheng Yang
Biomolecules 2026, 16(2), 328; https://doi.org/10.3390/biom16020328 - 20 Feb 2026
Viewed by 702
Abstract
The involvement of the immune system in pulmonary fibrosis is established, the precise contributions of tissue-resident memory T (TRM) cells are still poorly defined. This study sought to define the contribution of CD4+ TRM cells to pulmonary fibrosis, their [...] Read more.
The involvement of the immune system in pulmonary fibrosis is established, the precise contributions of tissue-resident memory T (TRM) cells are still poorly defined. This study sought to define the contribution of CD4+ TRM cells to pulmonary fibrosis, their origin, and regulatory mechanisms. We combined bioinformatic analysis of human fibrotic lung single-cell RNA-sequencing data with experiments in a bleomycin-induced C57BL/6 mouse model. Flow cytometry, targeted in vivo depletion, lymphocyte trafficking blockade, cell co-culture, and pharmacological inhibition were employed. CD4+ TRM cells were observed at higher frequencies within fibrotic lung tissue. Their presence correlated with disease severity, and they were found to exhibit a pro-inflammatory and pro-fibrotic phenotype. Their specific depletion alleviated fibrosis. These cells primarily originated from recruited circulating lymphocytes, as blocking this recruitment reduced TRM accumulation and attenuated disease. Furthermore, the Notch signaling pathway was activated in fibrotic lung CD4+ TRM cells, and its inhibition suppressed their differentiation and impaired their pro-fibrotic function. We conclude that CD4+ TRM cells are pathogenic drivers in pulmonary fibrosis, originating from circulating precursors and being regulated by Notch signaling, underscoring their relevance for therapeutic intervention. Full article
(This article belongs to the Special Issue Inflammation and Immunity in Lung Disease)
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Review

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24 pages, 873 KB  
Review
The Neutrophil–NET Axis in Immune Checkpoint Inhibitor Resistance in Non-Small Cell Lung Cancer: Roles, Biomarkers and Therapeutic Opportunities
by Geng Xu, Bing Wang and Elisa Giovannetti
Biomolecules 2026, 16(3), 400; https://doi.org/10.3390/biom16030400 - 8 Mar 2026
Viewed by 747
Abstract
Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related death. Although molecular stratification and multimodal therapy have improved outcomes in selected patients, overall prognosis is still limited by late diagnosis, heterogeneity, and treatment resistance. Immune checkpoint inhibitors (ICIs) have substantially improved [...] Read more.
Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related death. Although molecular stratification and multimodal therapy have improved outcomes in selected patients, overall prognosis is still limited by late diagnosis, heterogeneity, and treatment resistance. Immune checkpoint inhibitors (ICIs) have substantially improved survival outcomes in a subset of patients; however, the overall benefit remains limited, and both primary and acquired resistance are common. Neutrophils, as key effectors of innate immune responses, can be activated by diverse stimuli and release neutrophil extracellular traps (NETs). Growing evidence indicates that neutrophils and NETs contribute to remodeling of the tumor microenvironment (TME) in NSCLC, promoting resistance to ICIs. This review systematically summarizes the biological features, key molecular pathways, and inducing factors of neutrophils and NETs in lung cancer and synthesizes evidence supporting their roles as biomarkers of ICI efficacy and prognosis. We further focus on the mechanisms by which NETs mediate immunosuppression and foster an immune-excluded TME, thereby driving resistance to immunotherapy. In addition, we outline potential therapeutic and combination strategies targeting neutrophils and NETs, providing a theoretical basis for developing optimized immunotherapy approaches for NSCLC that target neutrophils and NETs. Full article
(This article belongs to the Special Issue Inflammation and Immunity in Lung Disease)
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