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Article ; Online: PD-1/PD-L1 axis in organ fibrosis.

Zhao, Youliang / Qu, Yaqian / Hao, Changfu / Yao, Wu

2023 Volume 14, Page(s) 1145682

Abstract: Fibrosis is a pathological tissue repair activity in which many myofibroblasts are activated and extracellular matrix are excessively accumulated, leading to the formation of permanent scars and finally organ failure. A variety of organs, including the ... ...

Abstract	Fibrosis is a pathological tissue repair activity in which many myofibroblasts are activated and extracellular matrix are excessively accumulated, leading to the formation of permanent scars and finally organ failure. A variety of organs, including the lung, liver, kidney, heart, and skin, can undergo fibrosis under the stimulation of various exogenous or endogenous pathogenic factors. At present, the pathogenesis of fibrosis is still not fully elucidated, but it is known that the immune system plays a key role in the initiation and progression of fibrosis. Immune checkpoint molecules are key regulators to maintain immune tolerance and homeostasis, among which the programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) axis has attracted much attention. The exciting achievements of tumor immunotherapy targeting PD-1/PD-L1 provide new insights into its use as a therapeutic target for other diseases. In recent years, the role of PD-1/PD-L1 axis in fibrosis has been preliminarily explored, further confirming the close relationship among PD-1/PD-L1 signaling, immune regulation, and fibrosis. This review discusses the structure, expression, function, and regulatory mechanism of PD-1 and PD-L1, and summarizes the research progress of PD-1/PD-L1 signaling in fibrotic diseases.
MeSH term(s)	Humans ; B7-H1 Antigen/metabolism ; Programmed Cell Death 1 Receptor/metabolism ; Signal Transduction ; Fibrosis
Chemical Substances	CD274 protein, human ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2023-05-19
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1145682
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Article ; Online: Corrigendum to "A2aR inhibits fibrosis and the EMT process in silicosis by regulating Wnt/β-catenin pathway" [Ecotoxicol. Environ. Saf. 249 (2023) 114410].

Tian, Yangyang / Xia, Jiarui / Yang, Guo / Li, Chao / Qi, Yuanmeng / Dai, Kai / Wu, Chenchen / Guo, Yonghua / Yao, Wu / Hao, Changfu

Ecotoxicology and environmental safety

2024 Volume 274, Page(s) 116171

Language	English
Publishing date	2024-03-08
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2024.116171
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Zs.A 1418: Show issues

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Article ; Online: Transcriptomics Analysis Identifies the Decline in the AT2 Stem Cell Niche in Aged Human Lungs.

Liu, Xue / Zhang, Xuexi / Yao, Changfu / Liang, Jiurong / Noble, Paul W / Jiang, Dianhua

American journal of respiratory cell and molecular biology

2024

Abstract: Aging poses a global public health challenge, which is linked to the rise of age-related lung diseases. The precise understanding of the molecular and genetic changes in the aging lung that elevate the risk of acute and chronic lung diseases remains ... ...

Abstract	Aging poses a global public health challenge, which is linked to the rise of age-related lung diseases. The precise understanding of the molecular and genetic changes in the aging lung that elevate the risk of acute and chronic lung diseases remains incomplete. Alveolar type II (AT2) cells are stem cells that maintain epithelial homeostasis and repair the lung after injury. AT2 progenitor function decreases with aging. The maintenance of AT2 function requires niche support from other cell types, but little has been done to characterize alveolar alterations with aging in the AT2 niche. To systematically profile the genetic changes associated with age, we present a single-cell transcriptional atlas comprising nearly half a million cells from the healthy lungs of human subjects spanning various ages, sexes, and smoking statuses. Most annotated cell lineages in aged lungs exhibit dysregulated genetic programs. Specifically, the aged alveolar epithelial (AT2) cells demonstrate loss of epithelial identities, heightened inflammaging characterized by increased expression of AP-1 transcription factor and chemokine genes, and significantly increased cellular senescence. Furthermore, the aged mesenchymal cells display a remarkable decrease in Collagen and Elastin transcription and a loss of support to epithelial cell stemness. The decline of the AT2 niche is further exacerbated by a dysregulated genetic program in macrophages and dysregulated communications between AT2 and macrophages in aged human lungs. These findings highlight the dysregulations observed in both AT2 stem cells and their supportive niche cells, potentially contributing to the increased susceptibility of aged populations to lung diseases.
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2023-0363OC
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Zs.A 2851: Show issues

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Article ; Online: Dynamics of the inhibitory immune checkpoint TIM-3 in mouse pulmonary phagocytes after silica exposure.

Zhao, Youliang / Qu, Yaqian / Duan, Meixiu / Hao, Changfu / Yao, Wu

Ecotoxicology and environmental safety

2023 Volume 261, Page(s) 115087

Abstract: Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that silicosis is caused by an imbalance of the pulmonary immune microenvironment, in which ... ...

Abstract	Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that silicosis is caused by an imbalance of the pulmonary immune microenvironment, in which pulmonary phagocytes play a crucial role. As an emerging immunomodulatory factor, it is unclear whether T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) participate in silicosis by modulating pulmonary phagocytes function. The purpose of this study was to investigate the dynamic changes of the TIM-3 in pulmonary macrophages, dendritic cells (DCs), and monocytes during the development of silicosis in mice. The plasma levels of soluble TIM-3 in silicosis patients were also examined. Flow cytometry was used to identify alveolar macrophages (AMs), interstitial macrophages (IMs), CD11b
MeSH term(s)	Mice ; Animals ; Hepatitis A Virus Cellular Receptor 2/metabolism ; Lung/metabolism ; Silicosis/metabolism ; Phagocytes ; Silicon Dioxide/toxicity
Chemical Substances	Hepatitis A Virus Cellular Receptor 2 ; Silicon Dioxide (7631-86-9)
Language	English
Publishing date	2023-06-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2023.115087
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Zs.A 1418: Show issues

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Article ; Online: Dynamics of the inhibitory immune checkpoint TIM-3 in mouse pulmonary phagocytes after silica exposure

Youliang Zhao / Yaqian Qu / Meixiu Duan / Changfu Hao / Wu Yao

Ecotoxicology and Environmental Safety, Vol 261, Iss , Pp 115087- (2023)

2023

Abstract	Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that silicosis is caused by an imbalance of the pulmonary immune microenvironment, in which pulmonary phagocytes play a crucial role. As an emerging immunomodulatory factor, it is unclear whether T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) participate in silicosis by modulating pulmonary phagocytes function. The purpose of this study was to investigate the dynamic changes of the TIM-3 in pulmonary macrophages, dendritic cells (DCs), and monocytes during the development of silicosis in mice. The plasma levels of soluble TIM-3 in silicosis patients were also examined. Flow cytometry was used to identify alveolar macrophages (AMs), interstitial macrophages (IMs), CD11b+ DC, CD103+ DC, Ly6C+, and Ly6C- monocytes in mouse lung tissues, and further analyses were conducted on the expression of TIM-3. Results showed that soluble TIM-3 was significantly elevated in plasma of silicosis patients, and the level of which was higher in stage II and III patients than that in stage I. In silicosis mice, the protein and mRNA levels of TIM-3 and Galectin9 were significantly upregulated in lung tissues. Specific to pulmonary phagocytes, silica exposure affected TIM-3 expression in a cell-specific and dynamic manner. In macrophages, TIM-3 expression upregulated in AM after 28 days and 56 days of silica instillation, while the expression of TIM-3 in IM decreased at all observation time points. In DCs, silica exposure only caused a decrease of TIM-3 expression in CD11b+ DCs. In monocytes, TIM-3 dynamics in Ly6C+ and Ly6C- monocytes were generally consistent during silicosis development, which significant decrease after 7 and 28 days of silica exposure. In conclusion, TIM-3 may mediate the development of silicosis by regulating pulmonary phagocytes.
Keywords	Occupational silica exposure ; Silicosis ; Immune checkpoint ; TIM-3 ; Pulmonary phagocytes ; Environmental pollution ; TD172-193.5 ; Environmental sciences ; GE1-350
Subject code	570
Language	English
Publishing date	2023-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: HMGB1 coordinates with Brahma-related gene 1 to promote epithelial-mesenchymal transition via the PI3K/Akt/mTOR pathway in BEAS-2B cells.

Deng, Xuedan / Niu, Zhuoya / Hao, Changfu / Lin, Jisong / Yao, Wu

Experimental cell research

2023 Volume 424, Issue 2, Page(s) 113522

Abstract: High mobility group protein B1 (HMGB1), a highly conserved non-histone nuclear protein, is highly expressed in fibrotic diseases; however, the role of HMGB1 in pulmonary fibrosis has not been fully elucidated. In this study, an epithelial-mesenchymal ... ...

Abstract	High mobility group protein B1 (HMGB1), a highly conserved non-histone nuclear protein, is highly expressed in fibrotic diseases; however, the role of HMGB1 in pulmonary fibrosis has not been fully elucidated. In this study, an epithelial-mesenchymal transition (EMT) model was constructed using transforming growth factor-β1 (TGF-β1) to stimulate BEAS-2B cells in vitro, and HMGB1 was knocked down or overexpressed to observe its effects on cell proliferation, migration and EMT. Meanwhile, string system, immunoprecipitation and immunofluorescence analyses were applied to identify and examine the relationship between HMGB1 and its potential interacting protein Brahma-related gene 1 (BRG1), and to explore the mechanism of interaction between HMGB1 and BRG1 in EMT. The results indicate that exogenous increase in HMGB1 promotes cell proliferation and migration and facilitates EMT by enhancing the PI3K/Akt/mTOR signaling pathway, whereas silencing HMGB1 has the opposite effect. Mechanistically, HMGB1 exerts these functions by interacting with BRG1, which may enhance BRG1 function and activate the PI3K/Akt/mTOR signaling pathway, thereby promoting EMT. These results suggest that HMGB1 is important for EMT and is a potential therapeutic target for the treatment of pulmonary fibrosis.
MeSH term(s)	Humans ; Epithelial-Mesenchymal Transition ; HMGB1 Protein/genetics ; HMGB1 Protein/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Pulmonary Fibrosis/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta1/metabolism
Chemical Substances	HMGB1 Protein ; MTOR protein, human (EC 2.7.1.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Transforming Growth Factor beta1 ; SMARCA4 protein, human (EC 3.6.1.-)
Language	English
Publishing date	2023-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2023.113522
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Zs.A 563: Show issues

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Article ; Online: OxyR-regulated T6SS functions in coordination with siderophore to resist oxidative stress.

Li, Changfu / Wei, Zhiyan / He, Xinquan / He, Haiyang / Liu, Yuqi / Zuo, Yuxin / Xiao, He / Wang, Yao / Shen, Xihui / Zhu, Lingfang

Microbiology spectrum

2024 Volume 12, Issue 2, Page(s) e0323123

Abstract: The formation of reactive oxygen species is harmful and can destroy intracellular macromolecules such as lipids, proteins, and DNA, even leading to bacterial death. To cope with this situation, microbes have evolved a variety of sophisticated mechanisms, ...

Abstract	The formation of reactive oxygen species is harmful and can destroy intracellular macromolecules such as lipids, proteins, and DNA, even leading to bacterial death. To cope with this situation, microbes have evolved a variety of sophisticated mechanisms, including antioxidant enzymes, siderophores, and the type VI secretion system (T6SS). However, the mechanism of oxidative stress resistance in
MeSH term(s)	Siderophores/metabolism ; Reactive Oxygen Species/metabolism ; Oxidative Stress ; Iron/metabolism ; DNA/metabolism ; Bacterial Proteins/genetics ; Gene Expression Regulation, Bacterial
Chemical Substances	Siderophores ; Reactive Oxygen Species ; Iron (E1UOL152H7) ; DNA (9007-49-2) ; Bacterial Proteins
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.03231-23
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Article ; Online: Manganese accumulation in red blood cells as a biomarker of manganese exposure and neurotoxicity.

Deng, Xuedan / Guo, Yonghua / Jin, Xiaofei / Si, Huifang / Dai, Kai / Deng, Meng / He, Jing / Hao, Changfu / Yao, Wu

Neurotoxicology

2024 Volume 102, Page(s) 1–11

Abstract: Although overexposure to manganese (Mn) is known to cause neurotoxic damage, effective exposure markers for assessing Mn loading in Mn-exposed workers are lacking. Here, we construct a Mn-exposed rat model to perform correlation analysis between Mn- ... ...

Abstract	Although overexposure to manganese (Mn) is known to cause neurotoxic damage, effective exposure markers for assessing Mn loading in Mn-exposed workers are lacking. Here, we construct a Mn-exposed rat model to perform correlation analysis between Mn-induced neurological damage and Mn levels in various biological samples. We combine this analysis with epidemiological investigation to assess whether Mn concentrations in red blood cells (MnRBCs) and urine (MnU) can be used as valid exposure markers. The results show that Mn exposure resulted in neurotoxic damage in rats and that MnRBCs correlated well with neurological damage, showing potential as a novel Mn exposure biomarker. These findings provide a basis for health monitoring of Mn-exposed workers and the development of more appropriate biological exposure limits.
Language	English
Publishing date	2024-03-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	800820-6
ISSN	1872-9711 ; 0161-813X
ISSN (online)	1872-9711
ISSN	0161-813X
DOI	10.1016/j.neuro.2024.03.003
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Zs.A 1547: Show issues

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Article ; Online: Expression levels of key immune indicators and immune checkpoints in manganese-exposed rats.

Qi, Yuanmeng / Si, Huifang / Jin, Xiaofei / Guo, Yonghua / Xia, Jiarui / He, Jing / Deng, Xuedan / Deng, Meng / Yao, Wu / Hao, Changfu

Ecotoxicology and environmental safety

2024 Volume 272, Page(s) 116029

Abstract: Manganese is essential trace elements, to participate in the body a variety of biochemical reactions, has important physiological functions, such as stimulate the immune cell proliferation, strengthen the cellular immunity, etc. However, excessive ... ...

Abstract	Manganese is essential trace elements, to participate in the body a variety of biochemical reactions, has important physiological functions, such as stimulate the immune cell proliferation, strengthen the cellular immunity, etc. However, excessive manganese exposure can cause damage to multiple systems of the body.The immune system is extremely vulnerable to external toxicants, however manganese research on the immune system are inadequate and biomarkers are lacking. Therefore, here we applied a manganese-exposed rat model to make preliminary observations on the immunotoxic effects of manganese. We found that manganese exposure inhibited humoral immune function in rats by decreasing peripheral blood IgG (ImmunoglobulinG, IgG), IgM (ImmunoglobulinM, IgM) and complement C3 levels; It also regulates rat cellular immune activity by influencing peripheral blood, spleen, and thymus T cell numbers and immune organ ICs (Immune Checkpoints, ICs) and cytokine expression. Furthermore, it was revealed that the impact of manganese exposure on the immune function of rats exhibited a correlation with both the dosage and duration of exposure. Notably, prolonged exposure to high doses of manganese had the most pronounced influence on rat immune function, primarily manifesting as immunosuppression.The above findings suggest that manganese exposure leads to impaired immune function and related changes in immune indicators, or may provide clues for the discovery of its biomarkers.
MeSH term(s)	Rats ; Animals ; Manganese/toxicity ; T-Lymphocytes ; Immunoglobulin M ; Immunoglobulin G ; Biomarkers
Chemical Substances	Manganese (42Z2K6ZL8P) ; Immunoglobulin M ; Immunoglobulin G ; Biomarkers
Language	English
Publishing date	2024-01-30
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2024.116029
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Article ; Online: Epigenetic Changes and Functions in Pneumoconiosis.

Li, Yiping / Cheng, Zhiwei / Fan, Hui / Hao, Changfu / Yao, Wu

Oxidative medicine and cellular longevity

2022 Volume 2022, Page(s) 2523066

Abstract: Pneumoconiosis is one of the most common occupational diseases in the world, and specific treatment methods of pneumoconiosis are lacking at present, so it carries great social and economic burdens. Pneumoconiosis, coronavirus disease 2019, and ... ...

Abstract	Pneumoconiosis is one of the most common occupational diseases in the world, and specific treatment methods of pneumoconiosis are lacking at present, so it carries great social and economic burdens. Pneumoconiosis, coronavirus disease 2019, and idiopathic pulmonary fibrosis all have similar typical pathological changes-pulmonary fibrosis. Pulmonary fibrosis is a chronic lung disease characterized by excessive deposition of the extracellular matrix and remodeling of the lung tissue structure. Clarifying the pathogenesis of pneumoconiosis plays an important guiding role in its treatment. The occurrence and development of pneumoconiosis are accompanied by epigenetic factors (e.g., DNA methylation and noncoding RNA) changes, which in turn can promote or inhibit the process of pneumoconiosis. Here, we summarize epigenetic changes and functions in the several kinds of evidence classification (epidemiological investigation,
MeSH term(s)	COVID-19/genetics ; COVID-19/pathology ; DNA Methylation ; Epigenesis, Genetic ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/pathology ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Pneumoconiosis/genetics ; Pneumoconiosis/pathology ; RNA, Untranslated/metabolism ; SARS-CoV-2/isolation & purification
Chemical Substances	RNA, Untranslated
Language	English
Publishing date	2022-01-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2022/2523066
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