---
title: "CD206 deficiency worsens paraquat-induced acute lung injury in mice"
id: "pubmed-42365825"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42365825"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42365825/"
doi: "10.1016/j.bbrc.2026.154208"
published_at: "2026-09-03T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CD206 deficiency worsens paraquat-induced acute lung injury in mice
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42365825
- **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/42365825/)
- **DOI:** [10.1016/j.bbrc.2026.154208](https://doi.org/10.1016%2Fj.bbrc.2026.154208)
- **Published At:** 2026-09-03T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Study compared C57BL/6J wild-type mice with **CD206**-deficient mice after paraquat exposure to model acute oxidant lung injury. - **CD206** deficiency was associated with increased mortality and greater body weight loss following paraquat administration. - CD206-deficient mice showed higher bronchoalveolar lavage (BAL) protein and increased total BAL cell counts, indicating worsened alveolar-capillary barrier disruption and inflammation. - Histological assessment demonstrated higher fibrosis scores in lungs from CD206-deficient mice after paraquat, signifying more severe tissue injury. - Oxidative DNA damage marker **8-OHdG** was elevated in CD206-deficient mice, consistent with increased oxidative stress. - Alveolar macrophages from CD206-deficient animals had reduced expression of **Hmox1** (heme oxygenase-1), suggesting impaired antioxidant or cytoprotective responses. - In vitro co-culture experiments showed that monocyte-derived macrophages lacking CD206 increased epithelial cell death relative to wild-type macrophages. - Treatment with **N-acetylcysteine** restored epithelial survival in co-cultures with CD206-deficient macrophages, indicating oxidative stress mediation. - Authors conclude CD206 plays a previously unrecognized protective role in macrophage-associated epithelial defense during paraquat-induced **acute lung injury**.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 27. # CD206 deficiency aggravates paraquat-induced acute lung injury in mice [Masahiro Yamashita](https://pubmed.ncbi.nlm.nih.gov/?term=Yamashita+M&cauthor_id=42365825)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-1 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan; Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. Electronic address: yamam@iwate-med.ac.jp."), [Wataru Yasuno](https://pubmed.ncbi.nlm.nih.gov/?term=Yasuno+W&cauthor_id=42365825)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-2 "Center for in Vivo Sciences, Iwate Medical University, Yahaba, Japan."), [Miyuki Niisato](https://pubmed.ncbi.nlm.nih.gov/?term=Niisato+M&cauthor_id=42365825)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-3 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan."), [Yasushi Kawasaki](https://pubmed.ncbi.nlm.nih.gov/?term=Kawasaki+Y&cauthor_id=42365825)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-4 "Department of Pharmaceutical Health Science, Faculty of Pharmacy, Iryo Sosei University, Iwaki, Japan."), [Eunsang Kwon](https://pubmed.ncbi.nlm.nih.gov/?term=Kwon+E&cauthor_id=42365825)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-5 "Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan."), [Shigeki Ito](https://pubmed.ncbi.nlm.nih.gov/?term=Ito+S&cauthor_id=42365825)[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-6 "Division of Haematology & Oncology, Department of Internal Medicine, Iwate Medical University School of Medicine, Yahaba, Japan."), [Ichiro Kawada](https://pubmed.ncbi.nlm.nih.gov/?term=Kawada+I&cauthor_id=42365825)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#full-view-affiliation-3 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan.") Affiliations Expand ### Affiliations * 1 Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan; Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. Electronic address: yamam@iwate-med.ac.jp. * 2 Center for in Vivo Sciences, Iwate Medical University, Yahaba, Japan. * 3 Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan. * 4 Department of Pharmaceutical Health Science, Faculty of Pharmacy, Iryo Sosei University, Iwaki, Japan. * 5 Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. * 6 Division of Haematology & Oncology, Department of Internal Medicine, Iwate Medical University School of Medicine, Yahaba, Japan. * PMID: **42365825** * DOI: [ 10.1016/j.bbrc.2026.154208 ](https://doi.org/10.1016/j.bbrc.2026.154208) Item in Clipboard # CD206 deficiency aggravates paraquat-induced acute lung injury in mice Masahiro Yamashita et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42365825/) . 2026 Sep 3:829:154208. doi: 10.1016/j.bbrc.2026.154208. Epub 2026 Jun 27. ### Authors [Masahiro Yamashita](https://pubmed.ncbi.nlm.nih.gov/?term=Yamashita+M&cauthor_id=42365825)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-1 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan; Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. Electronic address: yamam@iwate-med.ac.jp."), [Wataru Yasuno](https://pubmed.ncbi.nlm.nih.gov/?term=Yasuno+W&cauthor_id=42365825)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-2 "Center for in Vivo Sciences, Iwate Medical University, Yahaba, Japan."), [Miyuki Niisato](https://pubmed.ncbi.nlm.nih.gov/?term=Niisato+M&cauthor_id=42365825)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-3 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan."), [Yasushi Kawasaki](https://pubmed.ncbi.nlm.nih.gov/?term=Kawasaki+Y&cauthor_id=42365825)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-4 "Department of Pharmaceutical Health Science, Faculty of Pharmacy, Iryo Sosei University, Iwaki, Japan."), [Eunsang Kwon](https://pubmed.ncbi.nlm.nih.gov/?term=Kwon+E&cauthor_id=42365825)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-5 "Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan."), [Shigeki Ito](https://pubmed.ncbi.nlm.nih.gov/?term=Ito+S&cauthor_id=42365825)[ 6 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-6 "Division of Haematology & Oncology, Department of Internal Medicine, Iwate Medical University School of Medicine, Yahaba, Japan."), [Ichiro Kawada](https://pubmed.ncbi.nlm.nih.gov/?term=Kawada+I&cauthor_id=42365825)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42365825/#short-view-affiliation-3 "Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan.") ### Affiliations * 1 Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan; Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. Electronic address: yamam@iwate-med.ac.jp. * 2 Center for in Vivo Sciences, Iwate Medical University, Yahaba, Japan. * 3 Department of Pulmonary Medicine, Iwate Medical University School of Medicine, Yahaba, Japan. * 4 Department of Pharmaceutical Health Science, Faculty of Pharmacy, Iryo Sosei University, Iwaki, Japan. * 5 Research and Analytical Center for Giant Molecules, Graduate School of Science, Tohoku University, Sendai, Japan. * 6 Division of Haematology & Oncology, Department of Internal Medicine, Iwate Medical University School of Medicine, Yahaba, Japan. * PMID: **42365825** * DOI: [ 10.1016/j.bbrc.2026.154208 ](https://doi.org/10.1016/j.bbrc.2026.154208) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Paraquat induces acute lung injury characterized by oxidative epithelial damage. To examine the role of CD206, we compared C57BL/6J wild-type and CD206-deficient mice after paraquat exposure. CD206 deficiency increased mortality, body weight loss, bronchoalveolar lavage protein, total cells, histological fibrosis scores, and 8-OHdG levels, together with reduced Hmox1 expression in alveolar macrophages. In co-culture experiments, CD206-deficient monocyte-derived macrophages enhanced epithelial cell death compared with wild-type macrophages, whereas N-acetylcysteine restored epithelial survival. These findings identify a previously unrecognized role for CD206 in macrophage-associated epithelial protection during acute oxidant lung injury. **Keywords:** Acute lung injury; CD206; Macrophage; Oxidative stress. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [ In vivo depletion of CD206+ M2 macrophages exaggerates lung injury in endotoxemic mice. ](https://pubmed.ncbi.nlm.nih.gov/25447055/) Kambara K, Ohashi W, Tomita K, Takashina M, Fujisaka S, Hayashi R, Mori H, Tobe K, Hattori Y.Kambara K, et al.Am J Pathol. 2015 Jan;185(1):162-71. doi: 10.1016/j.ajpath.2014.09.005. Epub 2014 Oct 27.Am J Pathol. 2015.PMID: 25447055 * [ Mannose receptor modulates macrophage polarization and allergic inflammation through miR-511-3p. ](https://pubmed.ncbi.nlm.nih.gov/28629744/) Zhou Y, Do DC, Ishmael FT, Squadrito ML, Tang HM, Tang HL, Hsu MH, Qiu L, Li C, Zhang Y, Becker KG, Wan M, Huang SK, Gao P.Zhou Y, et al.J Allergy Clin Immunol. 2018 Jan;141(1):350-364.e8. doi: 10.1016/j.jaci.2017.04.049. Epub 2017 Jun 17.J Allergy Clin Immunol. 2018.PMID: 28629744Free PMC article. * [ Resveratrol decreases CD45+ CD206- subtype macrophages in LPS-induced murine acute lung injury by SOCS3 signalling pathway. ](https://pubmed.ncbi.nlm.nih.gov/31559687/) Hu L, Chen Z, Li L, Jiang Z, Zhu L.Hu L, et al.J Cell Mol Med. 2019 Dec;23(12):8101-8113. doi: 10.1111/jcmm.14680. Epub 2019 Sep 27.J Cell Mol Med. 2019.PMID: 31559687Free PMC article. * [ Role of macrophage bioenergetics in N-acetylcysteine-mediated mitigation of lung injury and oxidative stress induced by nitrogen mustard. ](https://pubmed.ncbi.nlm.nih.gov/38513841/) Malaviya R, Meshanni JA, Sunil VR, Venosa A, Guo C, Abramova EV, Vayas KN, Jiang C, Cervelli JA, Gow AJ, Laskin JD, Laskin DL.Malaviya R, et al.Toxicol Appl Pharmacol. 2024 Apr;485:116908. doi: 10.1016/j.taap.2024.116908. Epub 2024 Mar 19.Toxicol Appl Pharmacol. 2024.PMID: 38513841Free PMC article. * [ Depletion of NK cells attenuates paraquat-induced acute lung injury by manipulating macrophage polarization. ](https://pubmed.ncbi.nlm.nih.gov/32559567/) Wu M, Zhou C, Li M, Yu H, Zhao D, Xue W, Qin L, Peng A.Wu M, et al.Int Immunopharmacol. 2020 Sep;86:106698. doi: 10.1016/j.intimp.2020.106698. 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