Ask about this productRelated genes to: SFTPB antibody
- Gene:
- SFTPB NIH gene
- Name:
- surfactant protein B
- Previous symbol:
- SFTP3
- Synonyms:
- SP-B
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-06
- Date modifiied:
- 2016-10-05
Related products to: SFTPB antibody
Related articles to: SFTPB antibody
- Neonatal lung biopsy guides management of unusually severe, diffuse lung disease with an uncertain diagnosis. Childhood interstitial lung disease (chILD) constitutes a diverse group of uncommon respiratory diseases which are associated with major morbidity and mortality. The incidence, outcome and mortality of chILD and other severe respiratory diseases in resource-limited settings (RLS) are unclear. - Source: PubMed
Goussard PierreSchubert Pawelvan Wyk LizelleBooysen LynnGie AndréUrban MichaelJanson JacquesAndronikou SavvasEber Ernst - H9N2 avian influenza virus (AIV) poses significant threats to poultry and public health, with the potential to contribute to the emergence of more virulent influenza strains. Hypoxia-inducible factor 1-alpha (HIF-1α) plays a crucial role in viral pathogenesis, immune regulation, and inflammation, making it a promising target for therapeutic intervention. Here, we explored the involvement of HIF-1α in H9N2 AIV pathogenesis and associated inflammatory responses. Our data revealed that HIF-1α exacerbates inflammation induced by H9N2 AIV infection through its regulation of mitochondrial fitness. Additionally, we investigated Sotetsuflavone (Seo), a naturally derived flavonoid, for its potential to modulate inflammatory responses following H9N2 infection. Molecular docking coupled with surface plasmon resonance assays indicated that Seo exhibits robust binding affinity to HIF-1α, implying a direct inhibitory mechanism. Subsequent studies demonstrated that Seo greatly reduced the production of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, through suppressing the HIF-1α signaling pathway in HD11 cells infected with H9N2 AIV. Correspondingly, experiments established that Seo administration significantly ameliorated pulmonary inflammation in H9N2-infected mice, while also enhancing alveolar epithelial repair, as evidenced by increased expression of type II alveolar epithelial cell markers Abca3 and Sftpb. Collectively, these findings identify Seo as a potent inhibitor of HIF-1α, highlighting its therapeutic potential in mitigating inflammation and lung damage associated with influenza virus infection.IMPORTANCEH9N2 avian influenza virus triggers inflammatory lung injury via hypoxia-inducible factor-1 alpha (HIF-1α)-mediated dysregulation of mitochondrial function. The natural flavonoid Sotetsuflavone (Seo) directly binds and inhibits HIF-1α, as confirmed by molecular docking and surface plasmon resonance assays. In H9N2-infected HD11 cells, Seo suppresses HIF-1α signaling, reducing IL-1β, IL-6, and TNF-α production. , Seo treatment attenuates pulmonary inflammation and enhances alveolar epithelial repair in mice, upregulating type II pneumocyte markers (Abca3 and Sftpb). These findings identify Seo as a promising HIF-1α-targeted therapeutic for influenza-associated immunopathology. - Source: PubMed
Publication date: 2026/08/25
Zhu SuyingLi BeibeiWang YaqiTian YuhanZhang JiayueWang Hongshan - Immune checkpoint inhibitors (ICIs) have transformed the therapeutic landscape of advanced non-small cell lung cancer (NSCLC), yet ~50% of lung adenocarcinoma (LUAD) patients exhibit primary or acquired resistance, underscoring the urgent need for predictive biomarkers. Hypoxia and metabolic reprogramming (HMR) are intertwined oncogenic hallmarks that reshape the tumor microenvironment (TME) and drive immune evasion, representing promising targets for signature development. Herein, we constructed an integrated HMR gene signature to predict clinical outcomes and therapeutic vulnerabilities in LUAD. - Source: PubMed
Publication date: 2026/06/25
Ma YuquanYang MengmengSun ZhitaoLiu FeiZheng BoyingWang YanweiLiu Junfeng - : Surfactant protein B (SFTPB) is a surfactant-associated protein secreted by alveolar type II epithelial cells that plays a critical role in maintaining alveolar stability and surface tension. Although SFTPB is closely associated with pulmonary epithelial differentiation, its clinical significance in different non-small cell lung cancer (NSCLC) subtypes remains unclear. This study investigated the clinicopathologic and prognostic significance of SFTPB expression in lung adenocarcinoma (AD) and lung squamous cell carcinoma (SCC) using The Cancer Genome Atlas (TCGA) dataset. : SFTPB mRNA expression data and clinicopathologic information were obtained from TCGA cohorts of AD and SCC patients. Patients were stratified into high- and low-expression groups according to median SFTPB expression levels. Associations between SFTPB expression and clinicopathologic variables were analyzed, and correlation analyses were performed with major oncogenic genes. Overall survival (OS) and relapse-free survival (RFS) were evaluated using Kaplan-Meier survival analysis and log-rank testing. Multivariate Cox proportional hazards regression analyses were performed after adjustment for age, sex, and pathological stage. : In AD, high SFTPB expression was significantly associated with lower pathologic stage ( = 0.011) and lower N stage ( = 0.006). SFTPB expression showed significant negative correlations with EGFR (R = -0.140, = 0.002) and BRAF (R = -0.177, < 0.001) and a positive correlation with TP53 (R = 0.128, = 0.004). Patients with high SFTPB expression demonstrated significantly improved OS compared with those with low expression ( < 0.001) while a trend toward prolonged RFS was observed without statistical significance ( = 0.089). Multivariate analysis confirmed high SFTPB expression as an independent favorable prognostic factor in AD (HR = 0.551, 95% CI = 0.405-0.748, < 0.001). In SCC, high SFTPB expression was also significantly associated with lower pathologic stage ( = 0.009) and lower N stage ( = 0.007). SFTPB expression showed significant negative correlations with SOX2 (R = -0.176, < 0.001), PIK3CA (R = -0.143, = 0.002), and TP53 (R = -0.101, = 0.026). In contrast to AD, high SFTPB expression was significantly associated with poorer OS ( = 0.026), whereas no significant difference in RFS was observed ( = 0.307). Multivariate analysis demonstrated that high SFTPB expression was an independent adverse prognostic factor in SCC (HR = 1.347, 95% CI = 1.028-1.767, = 0.031). : SFTPB expression is significantly associated with clinicopathologic characteristics and molecular signatures in both AD and SCC. However, its prognostic implications differ according to histologic subtype. High SFTPB expression independently predicts favorable survival in AD but unfavorable survival in SCC, suggesting distinct lineage-specific biological roles in NSCLC. These findings support SFTPB as a subtype-specific prognostic biomarker reflecting differential differentiation states and lineage context in NSCLC. - Source: PubMed
Publication date: 2026/06/11
Kim SoonsooHong HyowonLee Jae-Ho - Preterm birth before 28 weeks remains a leading cause of neonatal mortality and long-term morbidity. Intrauterine infection-driven chorioamnionitis is strongly associated with preterm labor, fetal inflammatory response syndrome, and neonatal lung disease. species are among the most common organisms isolated in chorioamnionitis and are frequently detected in the placenta, amniotic fluid, and respiratory tract of preterm infants. Clinical and experimental data implicate exposure in early lung inflammation, impaired alveolar development, and bronchopulmonary dysplasia (BPD), yet the pathogenic events preceding microbial invasion of the amniotic cavity or fetal tissues remain poorly defined. To characterize early intrauterine and fetal lung inflammatory responses to localized choriodecidual infection, we used a chronically catheterized pregnant rhesus macaque ( ) model. Time-mated animals underwent surgical placement of maternal, amniotic, and choriodecidual catheters and were inoculated with low-passage serovar 1 or vehicle control at approximately 117 days gestational age. Placenta, fetal membranes, fetal plasma, and fetal lungs were assessed by qRT-PCR, multiplex cytokine assays, immunoblotting, immunohistochemistry, and trichrome staining to evaluate inflammatory signaling, inflammasome activation, prostaglandin pathways, immune cell infiltration, fibrosis, and lung maturation markers. Choriodecidual infection was confirmed in all inoculated animals. Amniotic fluid remained culture-and PCR-negative, and fetal lungs were largely free of detectable bacterial DNA. Despite the absence of intra-amniotic infection, fetal lung cytokine profiling revealed broad pro-inflammatory activation, with elevated GM-CSF, IL-1β, IL-6, IL-8, MIP-1α/β, MCP-1, VEGF and reduced IL-10 contrasting with a modest systemic response limited to elevated plasma IL-18. Fetal lungs showed increased immune cell infiltration, upregulation of NLRP3, PYCARD, and CASP1, and activation of SAPK/JNK and NF-κB signaling. Histopathology demonstrated increased alveolar macrophages and intra-alveolar neutrophils with minimal fibrosis. Surfactant gene expression was altered (increased , decreased ), and elevated α-SMA indicated early myofibroblast activation. Localized choriodecidual infection induces fetal lung inflammation prior to detectable intra-amniotic infection, demonstrating that direct infection of the amniotic fluid or fetal lung is not required for the initiation of fetal pulmonary inflammation. These findings suggest that subclinical ascending infection may initiate fetal lung injury and increase susceptibility to postnatal respiratory morbidity associated with preterm birth. - Source: PubMed
Publication date: 2026/06/08
Tripathy SudeshnaCrilley NathanMorgan Terry KSchelonka Robert LKelleher Meredith A