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Last update 08 May 2025

BPIFA1

Last update 08 May 2025

Basic Info

Synonyms

bA49G10.5, BPI fold containing family A member 1, BPI fold-containing family A member 1

+ [13]

Introduction

Lipid-binding protein which shows high specificity for the surfactant phospholipid dipalmitoylphosphatidylcholine (DPPC) (PubMed:25223608). Plays a role in the innate immune responses of the upper airways (PubMed:23132494, PubMed:23499554). Reduces the surface tension in secretions from airway epithelia and inhibits the formation of biofilm by pathogenic Gram-negative bacteria, such as P.aeruginosa and K.pneumoniae (PubMed:23132494, PubMed:23499554, PubMed:27145151). Negatively regulates proteolytic cleavage of SCNN1G, an event that is required for activation of the epithelial sodium channel (ENaC), and thereby contributes to airway surface liquid homeostasis and proper clearance of mucus (PubMed:24043776, PubMed:24124190). Plays a role in the airway inflammatory response after exposure to irritants (PubMed:11425234). May attract macrophages and neutrophils (PubMed:23132494).

Drugs associated with BPIFA1

ELD-607

Target

BPIFA1 x ORAI1

Mechanism

BPIFA1 stimulators [+1]

Active Org.

Eldec Pharmaceuticals, Inc.

Originator Org.

Eldec Pharmaceuticals, Inc.

Active Indication

Enterobacter Infection [+5]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with BPIFA1

100 Translational Medicine associated with BPIFA1

0 Patents (Medical) associated with BPIFA1

287

Literatures (Medical) associated with BPIFA1

01 May 2025·Archives of Oral Biology

BPIFA1 inhibits periodontitis by regulating the NF-κB/IκB signaling pathway and macrophage M1/M2 polarization

Article

Author: Xu, Hongyan ; Yang, Ying ; Wang, Tao

BACKGROUNDPeriodontitis is a chronic inflammatory disease characterized by tissue destruction and oxidative stress, primarily driven by the imbalance of immune responses. Bactericidal/permeability-increasing fold-containing family A member 1 (BPIFA1) has emerged as a key modulator of inflammation and immune homeostasis.OBJECTIVESThis study investigates the role of BPIFA1 in periodontitis by focusing on its regulatory effects on the NF-κB/IκB signaling pathway and macrophage M1/M2 polarization.METHODSSaliva and periodontal tissue samples were collected from 20 periodontitis patients and 20 healthy volunteers. BPIFA1 expression was analyzed using qRT-PCR and Western blot. In vivo studies were conducted in wild-type and BPIFA1-knockout (KO) mice, where periodontitis was induced via ligature placement and LPS injections. Oxidative stress markers (ROS, MDA, SOD), inflammatory cytokines (TNF-α, IL-6), and macrophage polarization markers (iNOS, CD86, Arg-1, CD206) were quantified. NF-κB pathway activation was assessed through Western blot analysis.RESULTSBPIFA1 expression was significantly reduced in periodontitis patients and BPIFA1-KO mice. Loss of BPIFA1 resulted in increased oxidative stress, heightened NF-κB activation, and an imbalance in macrophage polarization, with increased M1 (pro-inflammatory) and decreased M2 (anti-inflammatory) macrophages. Additionally, BPIFA1 deficiency promoted Th17 differentiation and suppressed Treg cells, exacerbating periodontal inflammation.CONCLUSIONBPIFA1 plays a critical role in inhibiting periodontitis progression by regulating the NF-κB/IκB signaling pathway and restoring macrophage M1/M2 balance. These findings highlight BPIFA1 as a potential therapeutic target for periodontitis management.

01 Mar 2025·Journal of Ethnopharmacology

Zhichuanling injection improves bronchial asthma by attenuation airway inflammation and epithelia-mesenchymal transition

Article

Author: Liang, Huaduan ; Cao, Zhengyu ; Song, Mengmeng ; Zhao, Fang ; Niu, Bo ; Chen, Jingyi ; Ren, Kerui ; Xi, Chuchu

ETHNOPHARMACOLOGICAL RELEVANCEZhichuanling (ZCL) Injection, is a compound formulation containing extracts of mahuang (Herba Ephedrae, dried stem or aerial part of Ephedra sinica Stapf), bitter almond (Semen Armeniacae Amarum, seeds of Prunus armeniaca var. sibirica (L.) K. Koch), yangjinhua (flower of Datura metel L.) and Fructus Forsythiae (fruits of Forsythia suspensa (Thunb.) Vahl). Intramuscular injection of ZCL has been used in the clinical practice to control asthma. The aerosol inhalation of ZCL has been shown to be effective on allergic bronchial asthma. However, the underlying mechanisms remain established.AIM OF THE STUDYTo investigate the underling mechanism by which ZCL inhibits the pathogenesis of bronchial asthma.METHODSThe guinea pig tracheal rings and human bronchial epithelial (16HBE) cells were used to assess ZCL's impact on acetylcholine (Ach) induced tracheal contraction, tumor necrosis factor α (TNF-α) induced bronchial inflammation, and transforming growth factor-β1 (TGF-β1) induced airway remodeling. Cell viability and gene expression were assessed using MTT assays, qPCR. RNA-seq (gene expression analysis) was employed to explore the novel mechanisms of ZCL in OVA-induced bronchial asthma.RESULTSIn this study, we found that ZCL reduces Ach-induced contraction of isolated guinea pig trachea, suppress TNF-α-induced interleukin (IL)-1β, IL-6, and IL-8 and TGF-β1-induced E-cadherin, α-SMA, Vimentin, N-cadherin mRNA expression in the 16HBE. Transcriptomic analysis of lung tissue from mice with OVA-induced bronchial asthma suggests that ZCL may alleviate asthma symptoms by modulating BPIFA1, HIF3Α, CTXN3, GRFA3, PPEF1, KSR2, and CDSN.CONCLUSIONZCL alleviates asthma by suppressing tracheal contractions, inflammation, and epithelial-to-mesenchymal transition. ZCL effect on asthma is likely through the upregulation of BPIFA1 expression thus providing the molecular insight for the treatment of asthma. The findings suggest that ZCL holds promise as a asthma therapeutic approach, and further research is needed to explore its full clinical potential. Future studies should focus on optimizing dosage, evaluating long-term efficacy, and investigating potential synergistic effects with existing treatments to enhance asthma management and patient outcomes.

15 Jan 2025·Journal of Pathology and Translational Medicine

PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in nasopharyngeal carcinoma

Article

Author: Liu, Qingluan ; Li, Xiayu ; Feng, Ranran ; Guo, Yilin ; Jiang, Su ; Shi, Lei ; Xiong, Wei ; Liu, Yijun ; Zhou, Jieyu ; Fan, Songqing ; Chen, Meilin ; Tian, Ziying ; Li, Guiyuan ; Zhang, Wenling

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear.Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP).Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin.Conclusions: PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

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BPIFA1

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