Standardization of Bronchoalveolar Lavage Method Based on Suction Frequency Number and Lavage Fraction Number Using Rats

Song, Jung Sang; Yang, Hyo-Seon; Lee, Jin Soo; Kwon, Soonjin; Jung, Kyung Jin; Heo, Jeong‐Doo; Cho, Kyu-Hyuk; Song, Chang Woo; Lee, Kyuhong

doi:10.5487/tr.2010.26.3.203

Cited by 24 publications

(17 citation statements)

References 24 publications

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“…Our results likely underestimate the levels of shed MUC1-ED within the alveolar lining fluid (26) and the mucus blanket that covers the airway epithelium (27). Further, a dilutional effect is intrinsic to the BAL procedure (28), and some loss of protein is anticipated during MUC1-ED preparation (20).…”

Section: Muc1-ed Is a Shed Decoy Receptor In Vivomentioning

confidence: 82%

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Lillehoj

Guang

Hyun

et al. 2019

Journal of Biological Chemistry

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Pseudomonas aeruginosa (Pa) expresses an adhesin, flagellin, that engages the mucin 1 (MUC1) ectodomain (ED) expressed on airway epithelia, increasing association of MUC1-ED with neuraminidase 1 (NEU1) and MUC1-ED desialylation. The MUC1-ED desialylation unmasks both cryptic binding sites for Pa and a protease recognition site, permitting its proteolytic release as a hyperadhesive decoy receptor for Pa. We found here that intranasal administration of Pa strain K (PAK) to BALB/c mice increases MUC1-ED shedding into the bronchoalveolar compartment. MUC1-ED levels increased as early as 12 h, peaked at 24-48 h with a 7.8-fold increase, and decreased by 72 h. The a-type flagellin-expressing PAK strain and the b-type flagellin-expressing PAO1 strain stimulated comparable levels of MUC1-ED shedding. A flagellindeficient PAK mutant provoked dramatically reduced MUC1-ED shedding compared with the WT strain, and purified flagellin recapitulated the WT effect. In lung tissues, Pa increased association of NEU1 and protective protein/cathepsin A with MUC1-ED in reciprocal co-immunoprecipitation assays and stimulated MUC1-ED desialylation. NEU1-selective sialidase inhibition protected against Pa-induced MUC1-ED desialylation and shedding. In Pa-challenged mice, MUC1-ED-enriched bronchoalveolar lavage fluid (BALF) inhibited flagellin binding and Pa adhesion to human airway epithelia by up to 44% and flagellin-driven motility by >30%. Finally, Pa co-administration with recombinant human MUC1-ED dramatically diminished lung and BALF bacterial burden, proinflammatory cytokine levels, and pulmonary leukostasis and increased 5-day survival from 0% to 75%. We conclude that Pa flagellin provokes NEU1-mediated airway shedding of MUC1-ED, which functions as a decoy receptor protecting against lethal Pa lung infection.

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Section: Muc1-ed Is a Shed Decoy Receptor In Vivomentioning

confidence: 82%

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Lillehoj

Guang

Hyun

et al. 2019

Journal of Biological Chemistry

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“…Bronchoalveolar lavage (BAL) was collected from each rat after three suctions, as described before [ 23 ]. The levels of TNF-α and IL-6 in BAL were measured using the ELISA kits for the corresponding cytokines (R&D Systems, Minneapolis, MN, USA) following the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

et al. 2018

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BackgroundAcute lung injury (ALI) is a life-threatening lung disease where alveolar macrophages (AMs) play a central role both in the early phase to initiate inflammatory responses and in the late phase to promote tissue repair. In this study, we examined whether BML-111, a lipoxin A4 receptor agonist, could alter the phenotypes of AM and thus present prophylactic benefits for ALI.MethodsIn vitro, isolated AMs were treated with lipopolysaccharide (LPS) to induce ALI. In response to BML-111 pre-treatment, apoptosis and autophagy of AMs were examined by flow cytometry, and by measuring biomarkers for each process. The potential involvement of MAPK1 and mTOR signaling pathway was analyzed. In vivo, an LPS-induced septic ALI model was established in rats and the preventative significance of BML-111 was assessed. On the cellular and molecular levels, the pro-inflammatory cytokines TNF-α and IL-6 from bronchoalveolar lavage were measured by ELISA, and the autophagy in AMs examined using Western blot.ResultsBML-111 inhibited apoptosis and induced autophagy of AMs in response to ALI inducer, LPS. The enhancement of autophagy was mediated through the suppression of MAPK1 and MAPK8 signaling, but independent of mTOR signaling. In vivo, BML-111 pre-treatment significantly alleviated LPS-induced ALI, which was associated with the reduction of apoptosis, the dampened production of pro-inflammatory cytokines in the lung tissue, as well as the increase of autophagy of AMs.ConclusionsThis study reveals the prophylactic significance of BML-111 in ALI and the underlying mechanism: by targeting the MAPK signaling but not mTOR pathway, BML-111 stimulates autophagy in AMs, attenuates the LPS-induced cell apoptosis, and promotes the resolution of ALI.

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“…La primera muestra fue descartada, la segunda fue almacenada a 4 °C para el posterior análisis de lactato deshidrogenasa (LDH). La tercera muestra se utilizó para el recuento celular [27] .…”

Section: Lavado Broncoalveolar (Lba)unclassified

Efecto antifibrotico de Lepidium peruvianum en un modelo de fibrosis pulmonar inducida con nanosilice en ratas

Toledo¹,

Ingunza²,

Lazo³

et al. 2019

Rev. per. med. integr.

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Objetivo. Demostrar el efecto antifibrotico de Lepidium peruvianum (maca), ecotipo morado, en la fibrosis pulmonar inducida con nanoparticulas de silice en ratas. Materiales y metodos. Estudio experimental, descriptivo, analitico, transversal, realizado en la Facultad de Medicina de la Universidad Nacional Mayor de San Marcos, Lima, Peru. Se utilizaron ratas de la cepa Sprague Dawley, estos animales fueron divididos aleatoriamente en cinco grupos: Blanco (B), Control (C), Prednisona (P), Dosis 1 (D1) y Dosis 2 (D2). En los últimos cuatro grupos, se indujo la fibrosis pulmonar (20 mg de nanosilice/rata). Luego de 7 días se inició el tratamiento, durante 4 semanas se administró el extracto metanolico de Lepidium peruvianum ecotipo morado (D1: 150 mg/kg/d y D2: 1500 mg/kg/d) y prednisona (P: 6,5 mg/kg/d). El analisis estadistico fue realizado usando la prueba ANOVA seguida de la prueba de comparacion mUltiple Tukey-Kramer. Los estudios realizados incluyeron el analisis del lavado broncoalveolar (recuento celular y actividad de LDH) y del tejido pulmonar (concentracion de malondialdehido y evaluacion histopatologica). Resultados. El grado de fibrosis en el grupo D2 fue significativamente menor (P<0,01) al grupo C y P. La concentracion de malondialdehido fue significativamente mayor (P<0,01) en el grupo C en comparacion a los otros grupos. Ademas, la concentracion en el grupo D2 fue significativamente menor (P<0,01) que en el grupo P. La actividad de LDH fue significativamente menor (P<0,01) en D2 en comparacion a C y D1. No hubo diferencias significativas del numero de celulas del lavado broncoalveolar entre el grupo D2 y B. Conclusiones. Lepidium peruvianum posee un efecto antifibrotico en la fibrosis pulmonar inducida con nanoparticulas de silice en ratas.

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Standardization of Bronchoalveolar Lavage Method Based on Suction Frequency Number and Lavage Fraction Number Using Rats

Cited by 24 publications

References 24 publications

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Efecto antifibrotico de Lepidium peruvianum en un modelo de fibrosis pulmonar inducida con nanosilice en ratas

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Standardization of Bronchoalveolar Lavage Method Based on Suction Frequency Number and Lavage Fraction Number Using Rats

Cited by 24 publications

References 24 publications

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Neuraminidase 1–mediated desialylation of the mucin 1 ectodomain releases a decoy receptor that protects against Pseudomonas aeruginosa lung infection

Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling

Efecto antifibrotico de Lepidium peruvianum en un modelo de fibrosis pulmonar inducida con nanosi­lice en ratas

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Efecto antifibrotico de Lepidium peruvianum en un modelo de fibrosis pulmonar inducida con nanosilice en ratas