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Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

ABSTRACT: Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

PROVIDER: PRJNA561784 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10029319.fastq.gz	Fastqsanger.gz
	SRR10029320.fastq.gz	Fastqsanger.gz
	SRR10029321.fastq.gz	Fastqsanger.gz
	SRR10029322.fastq.gz	Fastqsanger.gz
	SRR10029323.fastq.gz	Fastqsanger.gz

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Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease in which persistent injury results in scar tissue formation. As fibrosis thickens, the lung tissue becomes stiff and losses the ability to facilitate gas exchange and provide cells with needed oxygen. Currently, IPF has few treatment options and no effective therapies, aside from lung transplant. Here we present a series of studies utilizing lung spheroid cell-derived conditioned media (LSC-CM) and exosomes (LSC-EXO) to treat different rodent models of lung injury and fibrosis. Inhalation treatment was given for seven consecutive days via a nebulizer for clinical relevance. Results revealed that LSC-CM and LSC-EXO treatments could attenuate and resolve bleomycin- and silica-induced fibrosis by reestablishing normal alveolar structure, decreasing collagen accumulation, and myofibroblast proliferation. In addition, LSC-CM and LSC-EXOs exhibited superior therapeutic benefits than their counterparts derived from bone marrow mesenchymal stem cells. LSC-CM and LSC-EXOs provide promising therapeutic options for pulmonary fibrosis.

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Inhalation of ACE2-expressing lung spheroid cell exosomes provides prophylactic protection against SARS-CoV-2

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Inhalation of ACE2-expressing lung spheroid cell exosomes provides prophylactic protection against SARS-CoV-2

Project description:Continued emergence of SARS-CoV-2 variants of concern that are capable of escaping vaccine-induced immunity pose the urgency for developing new COVID-19 therapeutics. An essential mechanism for SARS-CoV-2 infection begins with the viral spike protein binding to the human ACE2. Consequently, inhibiting this interaction is a highly promising therapeutic strategy against COVID-19. Herein, we demonstrate that ACE2-expressing human lung spheroid cells (LSC)-derived exosomes (LSC-Exo) could function as a prophylactic agent to bind and neutralize SARS-CoV-2 and protect the host against SARS-CoV-2 infection. Inhalation of LSC-Exo facilitates their deposition and biodistribution throughout the whole lung in a female mouse model. We show that LSC-Exo blocks the interaction of SARS-CoV-2 with host cells in vitro and in vivo by neutralizing the virus. LSC-Exo treatment protected hamsters from SARS-CoV-2-induced disease and reduced viral loads. Furthermore, LSC-Exo intercept the entry of multiple SARS-CoV-2 variant pseudoviruses in female mice and show comparable or equal potency against the wild-type strain, demonstrating that LSC-Exo may act as broad-spectrum protectant against existing and emerging virus variants.

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Metastatic competency and tumor spheroid formation are independent cell states governed by RB in lung adenocarcinoma

Project description:Inactivation of the retinoblastoma (RB) tumor suppressor in lung adenocarcinoma is associated with the rapid acquisition of metastatic ability and the loss of lung cell lineage commitment. We previously showed that restoration of RB in advanced lung adenocarcinomas in the mouse was correlated with a decreased frequency of lineage de-committed tumors and overt metastases. To identify a causal relationship for RB and its role in reprogramming lineage commitment and reducing metastatic competency in lung adenocarcinoma, we developed multiple tumor spheroid forming lines where RB restoration could be achieved after characterization of the degree of each spheroid’s lineage commitment and metastatic ability. Surprisingly, we discovered that RB inactivation dramatically promoted tumor spheroid forming potential in tumors that arise in the KrasLSL-G12D/+; p53flox/flox lung adenocarcinoma model. However, RB reactivation had no effect on the maintenance of tumor spheroid lines once established. Additionally, we show that RB-deficient tumor spheroid lines are not uniformly metastatically competent but are equally likely to be non-metastatic. Interestingly, unlike tumor spheroid maintenance, RB restoration could functionally revert metastatic tumor spheroids to a non-metastatic cell state. Thus, strategies to reinstate RB-pathway activity in lung cancer may reverse metastatic ability and have therapeutic potential. Finally, the acquisition of tumor spheroid forming potential reflects underlying cell state plasticity, which is often predictive of, or even conflated with metastatic ability. Our data support that each is a discrete cell state restricted by RB and question the suitability of tumor spheroid models for their predictive potential of advanced metastatic tumor cell states.

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