2020
DOI: 10.3389/fimmu.2020.579628
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CCR2 Mediates Chronic LPS-Induced Pulmonary Inflammation and Hypoalveolarization in a Murine Model of Bronchopulmonary Dysplasia

Abstract: LPS exposure, through TLR4 signaling increases lung inflammation and impairs lung alveolar growth in a CCR2-dependent manner.

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Cited by 29 publications
(19 citation statements)
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“…[87][88][89] In current study, IL1-B was overexpressed when DBMSCs were treated with 10 µg/mL LPS. This finding correlated with a study conducted by Cui et al 90 in which the authors found that several proinflammatory cytokines, such as IL1-B that were secreted by MSCs in the lungs were upregulated under exposure of chronic airway LPS. However, additional future mechanistic study is necessary to confirm this.…”
Section: Discussionsupporting
confidence: 90%
“…[87][88][89] In current study, IL1-B was overexpressed when DBMSCs were treated with 10 µg/mL LPS. This finding correlated with a study conducted by Cui et al 90 in which the authors found that several proinflammatory cytokines, such as IL1-B that were secreted by MSCs in the lungs were upregulated under exposure of chronic airway LPS. However, additional future mechanistic study is necessary to confirm this.…”
Section: Discussionsupporting
confidence: 90%
“…However, in preclinical studies, the most commonly used animal model for BPD research involves prolonged exposure to postnatal hyperoxia. Several studies have reported that antenatal injection of LPS causes impaired alveolar development and dysregulated vasculature by inducing inflammation to mimic features of human BPD, even in the absence of postnatal hyperoxia or mechanical ventilation; thus, antenatal LPS exposure may be a better model to reflect the influence of antenatal factors on BPD [16][17][18].…”
Section: Introductionmentioning
confidence: 99%
“…Intrauterine infections cause the inflammatory cells to be accumulated within the fetal lungs, resulting in the release of abundant pro-inflammatory cells, which can impair fetal lung development and lead to preterm delivery ( 47 ). Postnatal high levels of oxygen therapy, mechanical ventilation, and certain infections may cause a pulmonary inflammatory response ( 48 , 49 ). When the alveolar-capillary barrier becomes impaired, the injured alveolar tissue promptly releases inflammatory factors resulting in the dysregulated levels of pro- and anti-inflammatory factors, increased apoptosis, and decreased proliferation of lung epithelial cells, thereby affecting the differentiation of endothelial cells, lung epithelial cells, and mesenchymal cells and further hindering the alveolar development.…”
Section: Pathogenesis and Current Situation Of Bpdmentioning
confidence: 99%