CCR2 Mediates Chronic LPS-Induced Pulmonary Inflammation and Hypoalveolarization in a Murine Model of Bronchopulmonary Dysplasia

Cui, Tracy X.; Brady, A.; Fulton, Christina T.; Zhang, Yingjian; Rosenbloom, Liza M; Goldsmith, Adam M.; Moore, Bethany B.; Popova, Antonia P.

doi:10.3389/fimmu.2020.579628

Cited by 28 publications

(19 citation statements)

References 88 publications

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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%

Phenotypic and Functional Responses of Human Decidua Basalis Mesenchymal Stem/Stromal Cells to Lipopolysaccharide of Gram-Negative Bacteria

Alshareef

Mohammed

Abumaree

et al. 2021

SCCAA

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Section: Discussionsupporting

confidence: 90%

Phenotypic and Functional Responses of Human Decidua Basalis Mesenchymal Stem/Stromal Cells to Lipopolysaccharide of Gram-Negative Bacteria

Alshareef

Mohammed

Abumaree

et al. 2021

SCCAA

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“…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%

Microvesicles Derived from Human Umbilical Cord Mesenchymal Stem Cells Enhance Alveolar Type II Cell Proliferation and Attenuate Lung Inflammation in a Rat Model of Bronchopulmonary Dysplasia

You

et al. 2022

Stem Cells International

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Although it is known that exosomes derived from human umbilical cord mesenchymal stem cells (hUCMSCs) alleviate hyperoxic lung injury of bronchopulmonary dysplasia (BPD) in animal models, the role of microvesicles (MVs) derived from hUCMSCs in BPD is poorly defined. Furthermore, antenatal inflammation has been linked to high risk of BPD in preterm infants. The purpose of this study was to explore whether MVs derived from hUCMSCs can preserve lung structure and function in an antenatal lipopolysaccharide- (LPS-) induced BPD rat model and to clarify the underlying mechanism. We demonstrate that antenatal LPS induced alveolar simplification, altered lung function, and dysregulated pulmonary vasculature, which restored by hUCMSCs and MVs treatment. Furthermore, MVs were large vesicles with a diameter of 100-900 nanometers and mostly uptaken by alveolar epithelial type II cells (AT2) and macrophages. Compared with the LPS-exposed group, MVs restored the AT2 cell number and SP-C expression in vivo and promoted the proliferation of AT2 cells in vitro. MVs also restored the level of IL-6 and IL-10 in lung homogenate. Additionally, PTEN/AKT and MAPK pathways were associated with the protection of MVs. Taken together, this study suggests MVs derived from hUCMSCs improve lung architecture and function in an antenatal LPS-induced BPD rat model by promoting AT2 cell proliferation and attenuating lung inflammation; thus, MVs provide a promising therapeutic vehicle for BPD treatment.

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“…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%

Insulin‑like growth factor‑1: A potential target for bronchopulmonary dysplasia treatment (Review)

Zhang

Xue

et al. 2022

Exp Ther Med

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Bronchopulmonary dysplasia (BPD) is a common respiratory disorder among preterm infants, particularly low-birth-weight infants (LBWIs) and very-low-birth-weight infants (VLBWIs). Although BPD was first reported 50 years ago, no specific drugs or efficient measures are yet available for prevention or treatment. Insulin-like growth factor-1 (IGF-1) belongs to the insulin family. It promotes mitosis and stimulates cell proliferation and DNA synthesis, the primary factors involved in pulmonary development during the fetal and postnatal periods. Several studies have reported that IGF-1 exerts certain effects on BPD genesis and progression by regulating BPD-related biological processes. In addition, exogenous addition of IGF-1 can alleviate lung inflammation, cell apoptosis and eliminate alveolar development disorders in children with BPD. These findings suggest that IGF-1 could be a new target for treating BPD. Here, we summarize and analyze the definition, pathogenesis, and research status of BPD, as well as the pathogenesis of IGF-1 in BPD and the latest findings in related biological processes. Contents 1. Introduction 2. Definition and naming of BPD 3. Pathogenesis and current situation of BPD 4. Biological characteristics and activity of IGF-1 5. IGF-1 in lung development 6. IGF-1 and lung injury 7. Possible underlying mechanisms of IGF-1 in BPD development 8. IGF-1 as a new option for BPD treatment 9. Challenges and prospects of IGF-1 10. Conclusion

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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.

Cited by 28 publications

References 88 publications

Phenotypic and Functional Responses of Human Decidua Basalis Mesenchymal Stem/Stromal Cells to Lipopolysaccharide of Gram-Negative Bacteria

Phenotypic and Functional Responses of Human Decidua Basalis Mesenchymal Stem/Stromal Cells to Lipopolysaccharide of Gram-Negative Bacteria

Microvesicles Derived from Human Umbilical Cord Mesenchymal Stem Cells Enhance Alveolar Type II Cell Proliferation and Attenuate Lung Inflammation in a Rat Model of Bronchopulmonary Dysplasia

Insulin‑like growth factor‑1: A potential target for bronchopulmonary dysplasia treatment (Review)

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