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Advanced Research in Pulmonary Pathophysiology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 2481

Special Issue Editors


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Guest Editor
Laboratory of Human Pathophysiology, Department of Nursing, University of Thessaly, Larissa, Greece
Interests: small airway disease; airway diseases; pleural pathophysiology; fibrotic diseases; microrna profiling

E-Mail Website
Guest Editor
Department of Nursing, University of Thessaly, 41500 Larissa, Greece
Interests: study of lung and pleural diseases through in silico, immunological, and molecular analyses

Special Issue Information

Dear Colleagues,

It is our pleasure to announce a Special Issue of Biomedicines, entitled “Advance Research in Pulmonary Pathophysiology”. To make meaningful progress in the field of lung-related illnesses, it is crucial to take a constructive approach towards advancing research in pulmonary pathophysiology. With lung pathology posing a significant threat to public health globally, we must work towards fostering a positive and collaborative research environment that encourages innovation and creativity. By investigating the pathophysiology of lung-related illnesses, we can obtain a deeper understanding of the underlying mechanisms that contribute to these diseases and develop more effective treatments. Through careful examination of the molecular, cellular, and physiological processes involved in lung diseases, it is possible to uncover new therapeutic targets and develop novel treatments that improve patient outcomes and quality of life.

This Biomedicines SI is dedicated to showcasing key areas of research in pulmonary pathophysiology. In particular, we aim to offer insights into the latest advancements of and innovative approaches in the spectrum of respiratory diseases, such as airway diseases, including the role of small airway disease in the development, progression and clinical outcomes of these conditions. Additionally, we aim to focus on allergy and its underlying neuroimmune pathways. Our goal is to delve into the role of microbiota in lung diseases, such as in occupational disorders, pulmonary fibrotic diseases, and molecular mechanisms influencing the pathogenesis of these entities. Moreover, we aim to present innovation-based research approaches in the field of lung cancer in order to revolutionize diagnosis and treatment, and among others recognize biomarkers regarding pleural pathophysiology, pulmonary infections, COVID-19, vascular respiratory diseases, sleep medicine, critical care, adult and pediatric medicine by presenting recent research on the changes that occur in normal mechanical, physical, and biochemical functions. Overall, this Special Issue has the goal of revealing new ideas by inspired collaborations and present recent advances in the area of respiratory pathophysiology.

Dr. Ourania S. Kotsiou
Dr. Erasmia Rouka
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

  • pathophysiology
  • aging
  • disease
  • injury
  • microbiome
  • small airways
  • pleura
  • lung cancer
  • infections
  • critical care

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Published Papers (1 paper)

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Research

15 pages, 3498 KiB  
Article
The Gut–Lung Axis During Ethanol Exposure and a Pseudomonas aeruginosa Bacterial Challenge
by Anthony Santilli, Yingchun Han, Hannah Yan, Naseer Sangwan and Gail A. M. Cresci
Biomedicines 2024, 12(12), 2757; https://doi.org/10.3390/biomedicines12122757 - 3 Dec 2024
Viewed by 958
Abstract
Background: Susceptibility to and severity of pulmonary infections increase with ethanol consumption. We have previously shown that ethanol-induced changes in the gut microbiome disrupt gut homeostasis, allowing for the translocation of proinflammatory mediators into the circulation and eliciting an immune response in the [...] Read more.
Background: Susceptibility to and severity of pulmonary infections increase with ethanol consumption. We have previously shown that ethanol-induced changes in the gut microbiome disrupt gut homeostasis, allowing for the translocation of proinflammatory mediators into the circulation and eliciting an immune response in the lung. Additionally, targeting the gut with butyrate supplementation not only rescues ethanol-induced disruptions to gut health but also reverses aspects of immune dysregulation in the lungs. Here, we assessed the impact of this connection on a subsequent infectious challenge. Methods: To assess if ethanol-induced alterations to the gut microbiome could also impact the host response to a pulmonary infectious challenge, we employed a chronic-binge ethanol-feeding mouse model followed by a nasal instillation of Pseudomonas aeruginosa. Results: In addition to altering gut microbiome composition and metabolism, ethanol consumption also disrupted the local immune response as demonstrated by suppressed cecal SIgA levels, a decreased presence of CD3+CD8a+ cytotoxic T cells in the proximal colon mucosa, and depleted CD3+CD8a+ T cells and CD11c+CD8a+ dendritic cells in the mesenteric lymph nodes. Circulatory Ly6G+CD11b+ neutrophils increased, indicating a systemic change in immune-cell presence with ethanol exposure. Ethanol exposure increased CD11c+CD64+ macrophages and Ly6G+CD11b+ neutrophils in the lungs, with neutrophil populations being further exacerbated during a bacterial challenge with Pseudomonas aeruginosa. Lipocalin 2, a marker of oxidative stress, was also elevated with ethanol consumption, though not with infection. Conclusions: These data suggest that ethanol-induced changes in the gut microbiome and immune environment are linked to dysfunctional immune responses in the intestine, blood, and the lungs, compromising the pulmonary immune response during an infectious challenge in mice. Full article
(This article belongs to the Special Issue Advanced Research in Pulmonary Pathophysiology)
Show Figures

Figure 1

Figure 1
<p>Alterations to cecal microbiome induced by ethanol consumption. Cecal gDNA contents underwent shotgun metagenomic sequencing analysis. (<b>A</b>) Simpson index alpha diversity between treatment groups. (<b>B</b>) PCoA graph depicting Bray–Curtis dissimilarity. Ellipses were used to visually highlight differences between ethanol-fed and pair-fed groups and do not represent any statistical analysis. (<b>C</b>) Venn diagram displaying taxa overlap between treatment groups. (<b>D</b>) Stacked graph depicting relative abundance of top species identified in cecal contents. PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P. aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa</span>.</p>
Full article ">Figure 2
<p>Alterations to microbial metabolic pathways in murine cecal contents identified using shotgun metagenomic sequencing. PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P. aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa</span>. Differential abundance analysis among all groups was performed using metagenomeSeq followed by Tukey’s honest significant difference (HSD) test to assess if each of the features (pathway) that were predicted in the differential abundance analysis could individually differentiate the pathways.</p>
Full article ">Figure 3
<p>Loss of butyrate-producing taxa during ethanol exposure. (<b>A</b>) CCXIVa gDNA expression in cecal contents at 6 h post ethanol binge via qRT-PCR. (<b>B</b>) <span class="html-italic">F. prausnitzii</span> gDNA expression in cecal contents at 6 h post ethanol binge via qRT-PCR. (<b>C</b>) CCXIVa gDNA expression in cecal contents via qRT-PCR at 48 h post ethanol binge and ±<span class="html-italic">P. aeruginosa</span> nasal instillation. (<b>D</b>) <span class="html-italic">F. prausnitzii</span> gDNA expression via qRT-PCR in cecal contents at 48 h post ethanol binge and ±<span class="html-italic">P. aeruginosa</span> nasal instillation. (<b>E</b>) <span class="html-italic">P. aeruginosa</span> gDNA expression via qRT-PCR in cecal contents at 48 h post ethanol binge and ±<span class="html-italic">P. aeruginosa</span> nasal instillation. There were 6–12 mice per treatment group. PF: control diet; EF: ethanol diet; PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P. aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa</span>. * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01.</p>
Full article ">Figure 4
<p>Ethanol feeding reduces cecal SIgA levels and T cells in the proximal colon. (<b>A</b>) SIgA concentrations in mouse cecal contents as measured by ELISA. Data are presented as a fold change relative to PF-S mice. (<b>B</b>) The abundance of positive staining (area) for CD3<sup>+</sup> cells in the proximal colon was assessed using immunohistochemical analysis. (<b>C</b>) The abundance of positive staining (area) of CD3<sup>+</sup>CD8a<sup>+</sup> co-positive cells in the proximal colon was assessed using immunohistochemical analysis. (<b>D</b>) Representative images using a 20× field for proximal colon tissue stained for CD3 (green), CD8a (red), and DAPI (blue), with 4–6 mice per treatment group. PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P. aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa</span>. * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001.</p>
Full article ">Figure 5
<p>Ethanol treatment suppresses immune-cell presence in MLN but elevates neutrophils in plasma. (<b>A</b>) The percentage of CD3<sup>+</sup>CD8a<sup>+</sup> cells present in the MLN was assessed using flow cytometry. (<b>B</b>) The percentage of CD11c<sup>+</sup>CD8a<sup>+</sup> cells present in the MLN was assessed using flow cytometry. (<b>C</b>) The percentage of Ly6G<sup>+</sup>CD11b<sup>+</sup> cells present in whole blood was assessed using flow cytometry. There were 4–6 mice per treatment group. PF: control diet; EF: ethanol diet; PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P.</span> <span class="html-italic">aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa</span>. * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01.</p>
Full article ">Figure 6
<p>Ethanol-induced changes in lung immunity both with and without <span class="html-italic">P. aeruginosa</span>. (<b>A</b>) Ly6G<sup>+</sup>CD11b<sup>+</sup> neutrophils from lung homogenate were assessed using flow cytometry. (<b>B</b>) CD11c<sup>+</sup>CD64<sup>+</sup> macrophages from lung homogenate were assessed using flow cytometry. (<b>C</b>) LCN2 mRNA expression in lung tissue obtained via RT-PCR. There were 4–6 mice per treatment group. PF-S: control diet + intranasal saline; EF-S: ethanol diet + intranasal saline; PF-Pseudo: control diet + intranasal <span class="html-italic">P. aeruginosa</span>; EF-Pseudo: ethanol diet + intranasal <span class="html-italic">P. aeruginosa.</span> * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01; **** <span class="html-italic">p</span> &lt; 0.0001. ns: not significant.</p>
Full article ">
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