---
title: "Resolvin D5 reduces lung inflammation and boosts antibacterial defense in severe pneumococcal pneu"
id: "pubmed-42581796"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42581796"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42581796/"
doi: "10.1042/CS20261424"
published_at: "2026-09-09T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Resolvin D5 reduces lung inflammation and boosts antibacterial defense in severe pneumococcal pneu
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42581796
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42581796/)
- **DOI:** [10.1042/CS20261424](https://doi.org/10.1042%2FCS20261424)
- **Published At:** 2026-09-09T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Streptococcus pneumoniae remains a leading cause of lower respiratory tract infection and pneumonia mortality; neutrophil recruitment is required for containment but excessive neutrophilic inflammation can cause severe lung injury and ARDS. - Specialized pro-resolving mediators, including **Resolvin D5 (RvD5)**, are produced in lungs and may both promote pathogen clearance and limit inflammatory injury. - This study used a mouse model of severe pneumococcal pneumonia to test exogenous RvD5 given at infection or post-infection with the antibiotic **ceftriaxone**. - Outcomes assessed were lung neutrophil accumulation, bacterial burden, neutrophil activation markers, and alveolar barrier integrity; complementary in vitro assays tested effects on human neutrophil phagocytosis and activation by LTB4. - When given at the time of infection, RvD5 reduced neutrophil accumulation in BAL and lung tissue, enhanced clearance of S. pneumoniae, decreased neutrophil activation marker expression, and lowered BAL total protein consistent with less inflammatory lung injury. - When administered after infection together with ceftriaxone, RvD5 further reduced lung neutrophil numbers and barrier disruption compared with antibiotic alone. - In vitro, RvD5 increased phagocytic uptake and intracellular bacterial killing by human neutrophils and blunted secondary calcium mobilization responses to **LTB4**. - Overall, RvD5 engaged pro-resolving mechanisms that were adjunctive to antibiotics to enhance bacterial clearance and limit inflammation-driven lung injury in severe pneumococcal pneumonia. - Keywords and key mechanistic themes: **neutrophils**, **specialized pro-resolving mediators**, alveolar barrier integrity, bacterial clearance, and adjunctive therapy with **ceftriaxone**.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A. * 2 Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A. * PMID: **42581796** * DOI: [ 10.1042/CS20261424 ](https://doi.org/10.1042/cs20261424) Item in Clipboard # Resolvin D5 limits inflammatory lung injury and enhances antibacterial host defense in severe pneumococcal pneumonia Henry H Gong et al. Clin Sci (Lond). 2026. Show details Display options Display options Format Abstract PubMed PMID Clin Sci (Lond) Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Clin+Sci+%28Lond%29%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Clin+Sci+%28Lond%29%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42581796/) . 2026 Sep 9;140(9):1937-1951. doi: 10.1042/CS20261424. ### Authors [Henry H Gong](https://pubmed.ncbi.nlm.nih.gov/?term=Gong+HH&cauthor_id=42581796)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-1 "Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Stephanie Pons](https://pubmed.ncbi.nlm.nih.gov/?term=Pons+S&cauthor_id=42581796)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-1 "Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Jasmine Ji](https://pubmed.ncbi.nlm.nih.gov/?term=Ji+J&cauthor_id=42581796)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-2 "Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Robert Nshimiyimana](https://pubmed.ncbi.nlm.nih.gov/?term=Nshimiyimana+R&cauthor_id=42581796)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-2 "Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Charles N Serhan](https://pubmed.ncbi.nlm.nih.gov/?term=Serhan+CN&cauthor_id=42581796)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-2 "Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Luciana P Tavares](https://pubmed.ncbi.nlm.nih.gov/?term=Tavares+LP&cauthor_id=42581796)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-1 "Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A."), [Bruce D Levy](https://pubmed.ncbi.nlm.nih.gov/?term=Levy+BD&cauthor_id=42581796)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42581796/#short-view-affiliation-1 "Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A.") ### Affiliations * 1 Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A. * 2 Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, U.S.A. * PMID: **42581796** * DOI: [ 10.1042/CS20261424 ](https://doi.org/10.1042/cs20261424) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Streptococcus pneumoniae remains a leading cause of lower respiratory tract infections and pneumonia-related mortality worldwide. Although neutrophil recruitment is essential for pneumococcal containment, excessive and dysregulated neutrophilic inflammation can drive severe lung injury and acute respiratory distress syndrome. Specialized pro-resolving mediators, such as Resolvin D5 (7S,17S-dihydroxy-4Z,8E,10Z,13Z,15E,19Z-docosahexaenoic acid; RvD5), are produced in the lungs and have the potential to promote pathogen clearance and limit inflammatory injury. Using a mouse model of severe pneumococcal pneumonia, we investigated the actions of RvD5 on disease progression. Exogenous RvD5 was administered either at the time of infection or post-infection together with the antibiotic ceftriaxone. Outcomes measured included lung neutrophil accumulation, bacterial burden, neutrophil activation markers, and indices of alveolar barrier integrity. Complementary in vitro assays were performed to assess the effects of RvD5 on human neutrophil phagocytosis and activation by LTB4. When administered at the time of infection, RvD5 reduced neutrophil accumulation in bronchoalveolar lavage (BAL) and lung tissue and enhanced clearance of S. pneumoniae. RvD5 decreased neutrophil activation marker expression and lowered total protein levels in BAL fluid, consistent with reduced inflammatory lung injury. When administered post-infection together with ceftriaxone, RvD5 significantly reduced lung neutrophil numbers and barrier disruption compared with antibiotic treatment alone. In vitro, RvD5 enhanced phagocytic uptake and intracellular killing of bacteria by human neutrophils, and blunted secondary calcium mobilization responses to LTB4. In summary, these findings indicate that RvD5 can initiate pro-resolving mechanisms adjunctive to antibiotics to enhance bacterial clearance and limit inflammation-driven lung injury in severe pneumococcal pneumonia. **Keywords:** acute lung injury; bacterial infections; neutrophils; pneumonia; specialized pro-resolving mediators; streptococcus pneumoniae. © 2026 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Similar articles * [ Angiotensin-(1-7) treatment improves pneumonia and prevents sepsis caused by pneumococcal infection. ](https://pubmed.ncbi.nlm.nih.gov/41296084/) Melo EM, Galvão I, Felix FB, Magalhães FMV, Rago F, Machado MG, Ascenção FR, Campagnole-Santos MJ, Dos Santos RAS, Cassali GD, Teixeira MM.Melo EM, et al.Inflamm Res. 2025 Nov 26;74(1):171. doi: 10.1007/s00011-025-02146-w.Inflamm Res. 2025.PMID: 41296084 * [ Neutrophil reduction attenuates the severity of lung injury in the early phase of pneumococcal pneumonia in mice. ](https://pubmed.ncbi.nlm.nih.gov/38772909/) Taenaka H, Fang X, Maishan M, Trivedi A, Wick KD, Gotts JE, Martin TR, Calfee CS, Matthay MA.Taenaka H, et al.Am J Physiol Lung Cell Mol Physiol. 2024 Aug 1;327(2):L141-L149. doi: 10.1152/ajplung.00113.2024. Epub 2024 May 21.Am J Physiol Lung Cell Mol Physiol. 2024.PMID: 38772909Free PMC article. * [ Aspirin-triggered resolvin D1 is produced during self-resolving gram-negative bacterial pneumonia and regulates host immune responses for the resolution of lung inflammation. ](https://pubmed.ncbi.nlm.nih.gov/26647716/) Abdulnour RE, Sham HP, Douda DN, Colas RA, Dalli J, Bai Y, Ai X, Serhan CN, Levy BD.Abdulnour RE, et al.Mucosal Immunol. 2016 Sep;9(5):1278-87. doi: 10.1038/mi.2015.129. Epub 2015 Dec 9.Mucosal Immunol. 2016.PMID: 26647716Free PMC article. * [ Inhibition of Phosphodiesterase-4 during Pneumococcal Pneumonia Reduces Inflammation and Lung Injury in Mice. ](https://pubmed.ncbi.nlm.nih.gov/26677751/) Tavares LP, Garcia CC, Vago JP, Queiroz-Junior CM, Galvão I, David BA, Rachid MA, Silva PM, Russo RC, Teixeira MM, Sousa LP.Tavares LP, et al.Am J Respir Cell Mol Biol. 2016 Jul;55(1):24-34. doi: 10.1165/rcmb.2015-0083OC.Am J Respir Cell Mol Biol. 2016.PMID: 26677751 * [ Gut Microbiota Contributes to Resistance Against Pneumococcal Pneumonia in Immunodeficient Rag-/- Mice. ](https://pubmed.ncbi.nlm.nih.gov/29755958/) Felix KM, Jaimez IA, Nguyen TV, Ma H, Raslan WA, Klinger CN, Doyle KP, Wu HJ.Felix KM, et al.Front Cell Infect Microbiol. 2018 Apr 18;8:118. doi: 10.3389/fcimb.2018.00118. eCollection 2018.Front Cell Infect Microbiol. 2018.PMID: 29755958Free PMC article. 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