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Molecular Research in Acute Lung Injury
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Molecular Research in Acute Lung Injury

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 28 February 2027 | Viewed by 2683

Editor

Dr. Emilia Lecuona

E-Mail Website
Guest Editor
Feinberg School of Medicine, Northwestern University, Simpson Querrey 5-407, 303 E Superior Street, Chicago, IL 60611, USA
Interests: lung; transplant; monocytes; neutrophils; primary graft dysfunction; sodium transport; Toll-like receptors; signaling transduction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As we know, Acute Lung Injury (ALI) is a disorder of acute inflammation that causes the disruption of the lung endothelial and epithelial barriers. It is characterized by the loss of alveolar–capillary membrane integrity, excessive transepithelial neutrophil migration, and the release of pro-inflammatory mediators. The acute phase of ALI and its more severe form—acute respiratory distress syndrome (ARDS)—are characterized by the influx of protein-rich edema fluid into the alveolar spaces as a consequence of the increased permeability of the alveolar–capillary barrier. All these factors can lead to respiratory failure.

The ethiology of Acute Lung Injury (ALI) is diverse, from pneumonia and aspiration to sepsis and trauma. In particular, a form of ALI called primary graft dysfunction occurs frequently after lung transplantation. Importantly, the treatement options for ALI are scarce and mainly supportive.

This Special Issue is focused on the molecular mechanisms involved in the development and resolution of ALI. Despite the body of work published relating to this subject, the precise mechanisms regulating ALI development and resolution remain unclear. Morover, more research involving pharmacological interventions is paramount. This Special Issue aims to consolidate current knowledge on ALI, highlighting molecular mechanisms and clinical relevance through original research and review articles.

Dr. Emilia Lecuona
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-anonymized 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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • acute lung injury
  • ARDS
  • primary graft dysfunction
  • immune cells
  • neutrophils
  • pulmonary edema
  • alveolar epithelium
  • lung endothelium

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Published Papers (3 papers)

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Research

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19 pages, 10374 KB  
Article
Plasma Lipidomics Identify Pathways Linked to Acute Lung Injury in a Porcine One-Lung Ventilation Surgery Model
by Simone C. da Silva Rosa, Evan Gauvin, Dagem Chernet, Jay Kormish, Catherine Giffin, Martha Hinton, Shyamala Dakshinamurti, Ruth Graham, Christopher D. Pascoe, Amir Ravandi and Biniam Kidane
Int. J. Mol. Sci. 2026, 27(12), 5219; https://doi.org/10.3390/ijms27125219 - 9 Jun 2026
Viewed by 410
Abstract
One-lung ventilation (OLV) is performed during lung surgeries by ventilating a single lung, while collapsing the operative lung to provide surgical exposure within the thoracic cavity. While a lung-protective ventilation strategy is recommended during OLV, increasing the fraction of inspired oxygen (FiO2 [...] Read more.
One-lung ventilation (OLV) is performed during lung surgeries by ventilating a single lung, while collapsing the operative lung to provide surgical exposure within the thoracic cavity. While a lung-protective ventilation strategy is recommended during OLV, increasing the fraction of inspired oxygen (FiO2) or tidal volume (VT) may be required to prevent hypoxemia during surgery. Unfortunately, these increases are associated with postoperative lung injury. Using a porcine model of OLV, our project aims to determine if high FiO2 or VT during OLV contributes to elevation of pro-inflammatory lipid mediators postoperatively. Fifteen three-month-old farm-bred pigs underwent left upper lobectomy requiring OLV. Pigs were exposed to one of three ventilation parameters: normoxic low VT lung-protective ventilation LPV-NO, n = 5, FiO2 < 50%, VT = 6 mL/kg), hyperoxic lung-protective ventilation (LPV-HO, n = 5, FiO2 >100%, VT = 6 mL/kg), or normoxic high VT (injurious mechanical ventilation) (IMV, n = 5, FiO2 < 50%, VT = 10–12 mL/kg). Arterial plasma was collected before and after OLV, and lipids were detected via LC-MS-MS. Lipidomic analysis demonstrated a statistically significant increase (FC = 2, p ≤ 0.05) in lysophosphatidylethanolamines (LPE 18:3, LPE 20:4, LPE 18:2, LPE 22:6), free fatty acids (FFA 20:4), phosphatidylserine (PS 38:5), lysophosphatidylcholine (LPC 18:1, LPC 18:3, LPC 22:6), triglyceride (TG 18:2-18:2-20:4), free fatty acids (FFA 20:5), linoleyl-carnitine molecules (C18-2 Linoleoyl Carnitine), and phosphatidylethanolamines (PE 36:5) in LPV-HO. IMV resulted in a significant increase (FC = 2, p ≤ 0.05) in triglyceride (TG 18:2-18:2-20:4), diglyceride (DG 18:1-20:4, DG 16:0-20:4), linoleyl-carnitine molecules (C18-2 Linoleoyl Carnitine), and free fatty acids (FFA 20:5). There was no significant change in lipid biomarker levels following LPV-NO post-surgery. Our lipidomic analysis supports that both high FiO2 and VT contribute to systemic lipid metabolic derangements. Lipids that were elevated in LPV-HO and IMV are associated with multiple inflammatory pathways implicated in lung injury. This suggests that intra-operative anti-inflammatory therapies targeted to these lipid pathways may reduce or prevent postoperative pulmonary complications after lung surgery. Full article
(This article belongs to the Special Issue Molecular Research in Acute Lung Injury)
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Review

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29 pages, 1206 KB  
Review
Sedation as an Immunomodulator of Inflammatory Responses in the Lung–Brain Axis of ARDS
by Cassian-Gabriel Gălbenușe, Andreea Doriana Stănculescu and Nicoleta Alice Drăgoescu
Int. J. Mol. Sci. 2026, 27(11), 4700; https://doi.org/10.3390/ijms27114700 - 23 May 2026
Viewed by 778
Abstract
Acute respiratory distress syndrome (ARDS) is characterized by systemic inflammation, immune dysregulation, oxidative stress, and frequent extrapulmonary organ involvement. Neurological complications of ARDS, such as neuroinflammation, cognitive impairment and delirium, are common and worsen outcomes. Early evidence highlights bidirectional communication between the lungs [...] Read more.
Acute respiratory distress syndrome (ARDS) is characterized by systemic inflammation, immune dysregulation, oxidative stress, and frequent extrapulmonary organ involvement. Neurological complications of ARDS, such as neuroinflammation, cognitive impairment and delirium, are common and worsen outcomes. Early evidence highlights bidirectional communication between the lungs and brain, the lung–brain axis, through which inflammation may amplify both pulmonary and cerebral injury. This narrative review synthesizes recent experimental and clinical data on the immunomodulatory and neuroprotective effects of commonly used sedative agents in ARDS, focusing on their influence on inflammatory mediators (IL-1β, IL-6, IL-8, IL-10, TNF-α) and neuronal injury biomarkers (S100B, neuron-specific enolase). Sedative agents seem to exert effects beyond sedation by modulating systemic and neuroinflammatory responses. Evidence suggests they can influence cytokine profiles and reduce biomarkers associated with neuronal injury, potentially mitigating neuroinflammation and delirium in ARDS patients. Sedatives may modulate lung–brain crosstalk in ARDS through immunoinflammatory pathways, integrating sedative and neuroprotective effects. Mechanistic clarification may enable targeted sedation strategies to improve pulmonary and neurological outcomes. Full article
(This article belongs to the Special Issue Molecular Research in Acute Lung Injury)
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14 pages, 381 KB  
Review
The Anti-Inflammatory Role of GLP-1 RAs in Acute Lung Injury and Acute Respiratory Distress Syndrome
by Paul Dumitrescu and Beata Kosmider
Int. J. Mol. Sci. 2026, 27(7), 2922; https://doi.org/10.3390/ijms27072922 - 24 Mar 2026
Cited by 2 | Viewed by 1028
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) pose a significant burden on the healthcare system. The mechanisms underlying the pathophysiology of ALI/ARDS are widely studied. However, currently, there are no clinically approved drugs that can effectively reduce the high mortality [...] Read more.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) pose a significant burden on the healthcare system. The mechanisms underlying the pathophysiology of ALI/ARDS are widely studied. However, currently, there are no clinically approved drugs that can effectively reduce the high mortality of patients. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are an increasingly popular class of medications. Their FDA approval was driven by the beneficial effects in patients with type 2 diabetes mellitus. Notably, recent studies are beginning to recognize the role of GLP-1 RAs in immunomodulation and anti-inflammatory responses across various organs, including the lungs. Animal models of ALI demonstrate the potential of these medications for treatment and prophylaxis. Observational studies suggest that patients taking GLP-1 RAs experienced fewer pulmonary complications. Here, we reviewed reports on their impact on the respiratory system in animal models of ALI and in clinical trials. Their effects in the intensive care unit setting and conditions predisposing to ALI/ARDS were also summarized. The mechanisms of action of GLP-1 RAs were reviewed based on in vitro studies using various lung cell types, and experimental approaches. Moreover, the roles of the pharmaceutical industry and patent law in extending the scope of GLP-1 RAs beyond obesity and diabetes were also described. Full article
(This article belongs to the Special Issue Molecular Research in Acute Lung Injury)
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