ArticleImmunology and cell biology2017
S100A8/A9 and S100A9 reduce acute lung injury.
Article in Immunology and cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- S100A9 deletion ameliorates acute lung injury by attenuating excessive neutrophil activation via activating the NRF2/HO-1 signaling axis.Respiratory research · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Targeting S100A8/A9: a molecular gateway to oral inflammation, microglial activation and neuroinflammation.Frontiers in immunology · 2026Review
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- S100A9: The Unusual Suspect Connecting Viral Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- Deficiency of S100A8/A9 attenuates pulmonary microvascular leakage in septic mice.Respiratory research · 2023Article
- A single-cell atlas of West African lungfish respiratory system reveals evolutionary adaptations to terrestrialization.Nature communications · 2023Article
- Extracellular Vesicle ITGAM and ITGB2 Mediate Severe Acute Pancreatitis-Related Acute Lung Injury.ACS nano · 2023Article
- Deficiency of S100A9 Alleviates Sepsis-Induced Acute Liver Injury through Regulating AKT-AMPK-Dependent Mitochondrial Energy Metabolism.International journal of molecular sciences · 2023Article
- Integrative proteomic profiling of lung tissues and blood in acute respiratory distress syndrome.Frontiers in immunology · 2023Article
- S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Role of TRPC6 in kidney damage after acute ischemic kidney injury.Scientific reports · 2022Article
- Single-cell gene expression analysis of cryopreserved equine bronchoalveolar cells.Frontiers in immunology · 2022Article
- Intranasal Delivery of Recombinant S100A8 Protein Delays Lung Cancer Growth by Remodeling the Lung Immune Microenvironment.Frontiers in immunology · 2022Article
- Targeting S100A9 Reduces Neutrophil Recruitment, Inflammation and Lung Damage in Abdominal Sepsis.International journal of molecular sciences · 2021Article
- Development of anti-thrombotic vaccine against human S100A9 in rhesus monkey.Scientific reports · 2021Article
- S100A9 blockade prevents lipopolysaccharide-induced lung injury via suppressing the NLRP3 pathway.Respiratory research · 2021Article
- S100a9 Protects Male Lupus-Prone NZBWF1 Mice From Disease Development.Frontiers in immunology · 2021Article
- The Key Target and Molecular Mechanism of the Volatile Component ofFrontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several types of inflammatory lung disorders. Pro- and anti-inflammatory properties are reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can function separately, likely through distinct receptors but a systematic comparison of their effects in vivo are limited. Here we assess inflammation in murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9 promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by increased mast cell degranulation and selective upregulation of some chemokine genes, particularly CXCL-10. S100 proteins did not significantly induce proinflammatory mediators including TNF-α, interleukin-1β (IL-1β), IL-6 or serum amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury provoked by lipopolysaccharide (LPS) challenge but were somewhat less inhibitory, possibly because of differential effects on expression of some chemokines, IL-1β, SAA3 and IL-10. Novel common pathways including increased induction of an NAD
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