Inhaled lysophosphatidylcholine provokes bronchoconstriction in guinea pigs in vivo

Nobata, Kouichi; Kurashima, Kazuyoshi; Fujimura, Masaki; Abo, Masahiro; Ishiura, Yoshihisa; Kondo, Kazuo; Nakao, Shinji

doi:10.1016/j.ejphar.2005.07.032

Cited by 7 publications

(8 citation statements)

References 21 publications

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“…In lungs from late stage adult respiratory distress syndrome,13 lungs challenged with antigen14 or instilled with lipopolysaccharide,15 elevated amounts of LPC are reported in the broncho-alveolar lavage fluids (BALF). Furthermore, the administration of exogenous LPC into lungs of animal models promotes eosinophil infiltration,16 increases airway resistance,16,17 and increases airway epithelial permeability 18,19. These findings suggest that elevated levels of LPC in the extracellular lung fluids can induce inflammatory injury on the airway and alveolar cell populations.…”

Section: Introductionmentioning

confidence: 89%

Bioactive Lysophosphatidylcholine 16:0 and 18:0 Are Elevated in Lungs of Asthmatic Subjects

Yoder

Zhuge

Yuan

et al. 2014

Allergy Asthma Immunol Res

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PurposeAsthma is a chronic inflammatory disease of the airways, and is associated with upregulation of phospholipase A2 (PLA2), the enzyme that hydrolyzes phosphatidylcholine, producing lysophosphatidylcholine (LPC) and free fatty acids. LPC is a lipid mediator with known pro-inflammatory and pro-atherogenic properties, and is believed to be a critical factor in cardiovascular diseases. We postulate that asthmatic subjects have an elevated content of LPC in the lung lining fluids.MethodsEight non-asthmatic controls and seven asthmatic subjects were recruited for broncho-alveolar lavage fluids (BALF) collection for analysis of LPC by high performance liquid chromatography-tandem mass spectrometry.ResultsLPC16:0 and LPC18:0 were significantly elevated in the BALF of asthmatics with impaired lung function characteristic of moderate asthma, but not mild asthma. The increased LPC content in BALF was accompanied by increased PLA2 activity. Furthermore, qRT-PCR analysis of the BALF cell fraction indicated increased secretory PLA2-X (sPLA2-X).ConclusionsThe increased LPC content in the lung lining fluids is a potential critical lipid mediator in the initiation and/or progression of airway epithelial injury in asthma.

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Section: Introductionmentioning

confidence: 89%

Bioactive Lysophosphatidylcholine 16:0 and 18:0 Are Elevated in Lungs of Asthmatic Subjects

Yoder

Zhuge

Yuan

et al. 2014

Allergy Asthma Immunol Res

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“…). They were challenged with CE (10 μg) or exposed to LPC (1-Palmitoyl-sn-glycero-3-phosphocholine) (Sigma Aldrich) (4.82 μg)12 intranasally ( i.n. ) on days 25 th , 26 th and 27 th except the CE group, which was exposed to 5% dimethylsulfoxide (DMSO) only, a vehicle control.…”

Section: Methodsmentioning

confidence: 99%

“…It involves in eosinophils infiltration and bronchoconstriction1213. These reports indicated the link of LPC and allergic airway disease like asthma.…”

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confidence: 94%

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Lysophosphatidylcholine plays critical role in allergic airway disease manifestation

Bansal

Gaur

Arora

2016

Sci Rep

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Phospholipase A2 (sPLA2), pivotal for allergic and inflammatory response, hydrolyses phosphatidylcholine (PC) to lysophosphatidylcholine (LPC). In present study, the role of LPC in allergic airway disease manifestation was studied using mouse model. Balb/c mice were immunized using cockroach extract (CE) and LPC release was blocked by sPLA2 inhibitor. Airway hyperresponse (AHR), lung-histology, total and differential leukocyte count (TLC&DLC), Th2 type cytokines, sPLA2 activity and LPC levels in bronchoalveolar lavage fluid (BALF) were measured. Exogenous LPC was given to the mice with or without CE sensitization, to demonstrate its role in allergic airway disease manifestation. Anti-CD1d antibody was given to study the involvement of natural killer T (NKT) cells in LPC induced response. AHR, lung-inflammation, TLC, DLC, Th2 type cytokines, sPLA2 activity and LPC levels were increased on CE challenge. sPLA2 activity and LPC release was blocked by sPLA2-inhibitor, which decreased AHR, and inflammatory parameters. Exogenous LPC with or without CE sensitization increased above parameters. CE challenge or LPC exposure increased LY49C+TCRβ+ NKT cells in BALF and spleen, which was reduced by anti-CD1d antibody, accompanied with reduction in AHR and allergic airway inflammation parameters. Conclusively, LPC induces allergic airway disease manifestation and it does so probably via CD1d-restricted LY49C+TCRβ+ NKT cells.

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“…Biologically, the physical barrier properties of surfactant on surface‐active phospholipid (SAPL) have been increasingly examined in the field of pulmonology (9). DPPC is the characteristic and majorconstituent of surfactant (10, 11). Although abnormalities of SAPL and its proteins have been described in asthma (12), the relationship between the DPPC component of SAPL and airway inflammation indices in children with asthma is unknown.…”

Section: Discussionmentioning

confidence: 99%

Sputum dipalmitoylphosphatidylcholine level as a novel airway inflammatory marker in asthmatic children

Shaheen

Mahmoud

Aziz

et al. 2009

Clinical Respiratory J

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Inhaled lysophosphatidylcholine provokes bronchoconstriction in guinea pigs in vivo

Cited by 7 publications

References 21 publications

Bioactive Lysophosphatidylcholine 16:0 and 18:0 Are Elevated in Lungs of Asthmatic Subjects

Bioactive Lysophosphatidylcholine 16:0 and 18:0 Are Elevated in Lungs of Asthmatic Subjects

Lysophosphatidylcholine plays critical role in allergic airway disease manifestation

Sputum dipalmitoylphosphatidylcholine level as a novel airway inflammatory marker in asthmatic children

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