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Article ; Online: Amelioration of Pulmonary Fibrosis by Matrix Metalloproteinase-2 Overexpression.

Inoue, Ryo / Yasuma, Taro / Fridman D'Alessandro, Valeria / Toda, Masaaki / Ito, Toshiyuki / Tomaru, Atsushi / D'Alessandro-Gabazza, Corina N / Tsuruga, Tatsuki / Okano, Tomohito / Takeshita, Atsuro / Nishihama, Kota / Fujimoto, Hajime / Kobayashi, Tetsu / Gabazza, Esteban C

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: Idiopathic pulmonary fibrosis is a progressive and fatal disease with a poor prognosis. Matrix metalloproteinase-2 is involved in the pathogenesis of organ fibrosis. The role of matrix metalloproteinase-2 in lung fibrosis is unclear. This study evaluated ...

Abstract	Idiopathic pulmonary fibrosis is a progressive and fatal disease with a poor prognosis. Matrix metalloproteinase-2 is involved in the pathogenesis of organ fibrosis. The role of matrix metalloproteinase-2 in lung fibrosis is unclear. This study evaluated whether overexpression of matrix metalloproteinase-2 affects the development of pulmonary fibrosis. Lung fibrosis was induced by bleomycin in wild-type mice and transgenic mice overexpressing human matrix metalloproteinase-2. Mice expressing human matrix metalloproteinase-2 showed significantly decreased infiltration of inflammatory cells and inflammatory and fibrotic cytokines in the lungs compared to wild-type mice after induction of lung injury and fibrosis with bleomycin. The computed tomography score, Ashcroft score of fibrosis, and lung collagen deposition were significantly reduced in human matrix metalloproteinase transgenic mice compared to wild-type mice. The expression of anti-apoptotic genes was significantly increased, while caspase-3 activity was significantly reduced in the lungs of matrix metalloproteinase-2 transgenic mice compared to wild-type mice. Active matrix metalloproteinase-2 significantly decreased bleomycin-induced apoptosis in alveolar epithelial cells. Matrix metalloproteinase-2 appears to protect against pulmonary fibrosis by inhibiting apoptosis of lung epithelial cells.
MeSH term(s)	Mice ; Humans ; Animals ; Matrix Metalloproteinase 2/genetics ; Matrix Metalloproteinase 2/metabolism ; Lung/pathology ; Idiopathic Pulmonary Fibrosis/metabolism ; Bleomycin/adverse effects ; Mice, Transgenic ; Fibrosis ; Mice, Inbred C57BL
Chemical Substances	Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Bleomycin (11056-06-7)
Language	English
Publishing date	2023-04-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076695
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Article ; Online: Inhibition of a Microbiota-Derived Peptide Ameliorates Established Acute Lung Injury.

Fridman D'Alessandro, Valeria / D'Alessandro-Gabazza, Corina N / Yasuma, Taro / Toda, Masaaki / Takeshita, Atsuro / Tomaru, Atsushi / Tharavecharak, Suphachai / Lasisi, Isaiah O / Hess, Rebecca Y / Nishihama, Kota / Fujimoto, Hajime / Kobayashi, Tetsu / Cann, Isaac / Gabazza, Esteban C

The American journal of pathology

2023 Volume 193, Issue 6, Page(s) 740–754

Abstract: Acute lung injury (ALI) is a clinical syndrome characterized by a diffuse lung inflammation that commonly evolves into acute respiratory distress syndrome and respiratory failure. The lung microbiota is involved in the pathogenesis of ALI. Corisin, a ... ...

Abstract	Acute lung injury (ALI) is a clinical syndrome characterized by a diffuse lung inflammation that commonly evolves into acute respiratory distress syndrome and respiratory failure. The lung microbiota is involved in the pathogenesis of ALI. Corisin, a proapoptotic peptide derived from the lung microbiota, plays a role in ALI and acute exacerbation of pulmonary fibrosis. Preventive therapeutic intervention with a monoclonal anticorisin antibody inhibits ALI in mice. However, whether inhibition of corisin with the antibody ameliorates established ALI is unknown. Here, the therapeutic effectiveness of the anticorisin antibody in already established ALI in mice was assessed. Lipopolysaccharide was used to induce ALI in mice. After causing ALI, the mice were treated with a neutralizing anticorisin antibody. Mice treated with the antibody showed significant improvement in lung radiological and histopathologic findings, decreased lung infiltration of inflammatory cells, reduced markers of lung tissue damage, and inflammatory cytokines in bronchoalveolar lavage fluid compared with untreated mice. In addition, the mice treated with anticorisin antibody showed significantly increased expression of antiapoptotic proteins with decreased caspase-3 activation in the lungs compared with control mice treated with an irrelevant antibody. In conclusion, these observations suggest that the inhibition of corisin is a novel and promising approach for treating established ALI.
MeSH term(s)	Mice ; Animals ; Lung/pathology ; Acute Lung Injury/pathology ; Bronchoalveolar Lavage Fluid ; Pneumonia/metabolism ; Peptides/pharmacology ; Inflammation/pathology ; Lipopolysaccharides/pharmacology ; Mice, Inbred C57BL
Chemical Substances	Peptides ; Lipopolysaccharides
Language	English
Publishing date	2023-03-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2023.03.003
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Article: Adrenocorticotropic hormone-secreting pancreatic neuroendocrine carcinoma with multiple organ infections and widespread thrombosis: A case report.

Yoshihara, Akihiro / Nishihama, Kota / Inoue, Chisa / Okano, Yuko / Eguchi, Kazuhito / Tanaka, Soichiro / Maki, Kanako / Fridman D'Alessandro, Valeria / Takeshita, Atsuro / Yasuma, Taro / Uemura, Mei / Suzuki, Toshinari / Gabazza, Esteban C / Yano, Yutaka

World journal of clinical cases

2022 Volume 10, Issue 17, Page(s) 5723–5731

Abstract: Background: Ectopic adrenocorticotropic hormone (ACTH)-secreting neuroendocrine tumors are rare diseases. Patients with ACTH-secreting pancreatic neuroendocrine carcinomas have a poor prognosis. Infections and coagulopathies have been reported as the ... ...

Abstract	Background: Ectopic adrenocorticotropic hormone (ACTH)-secreting neuroendocrine tumors are rare diseases. Patients with ACTH-secreting pancreatic neuroendocrine carcinomas have a poor prognosis. Infections and coagulopathies have been reported as the cause of death. However, detailed clinical descriptions of the morbid complications of ACTH-secreting neuroendocrine carcinomas have not been reported. Case summary: A 78-year-old Japanese woman consulted a medical center due to systemic edema and epigastric discomfort. Laboratory analysis revealed hypercortisolemia with increased ACTH secretion without diurnal variation in serum cortisol level. An enhanced computed tomography (CT) scan revealed a 3-cm tumor in the pancreatic head. The cytological material from endoscopic ultrasound-guided fine-needle aspiration was compatible with ACTH-secreting pancreatic neuroendocrine carcinoma. The Ki-67 index was 40%. She was transferred to Mie University Hospital for surgical treatment. The patient was diagnosed with urinary tract infection, cytomegalovirus hepatitis, esophageal candidiasis, pulmonary infiltrates suspicious for Conclusion: ACTH-secreting pancreatic neuroendocrine neoplasm is a rare disease with a very poor prognosis. The clinical course and acute complications of the tumor remain unreported. Here we report the clinical course of a rapidly progressive case of ACTH-secreting pancreatic neuroendocrine tumor that developed infectious complications due to many types of pathogens in multiple organs, widespread thromboses, pulmonary embolism, and disseminated intravascular coagulation.
Language	English
Publishing date	2022-08-01
Publishing country	United States
Document type	Case Reports
ISSN	2307-8960
ISSN	2307-8960
DOI	10.12998/wjcc.v10.i17.5723
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Article ; Online: The Fairy Chemical Imidazole-4-carboxamide Inhibits the Expression of Axl, PD-L1, and PD-L2 and Improves Response to Cisplatin in Melanoma.

Inoue, Chisa / Yasuma, Taro / D'Alessandro-Gabazza, Corina N / Toda, Masaaki / Fridman D'Alessandro, Valeria / Inoue, Ryo / Fujimoto, Hajime / Kobori, Hajime / Tharavecharak, Suphachai / Takeshita, Atsuro / Nishihama, Kota / Okano, Yuko / Wu, Jing / Kobayashi, Tetsu / Yano, Yutaka / Kawagishi, Hirokazu / Gabazza, Esteban C

Cells

2022 Volume 11, Issue 3

Abstract: The leading cause of death worldwide is cancer. Many reports have proved the beneficial effect of mushrooms in cancer. However, the precise mechanism is not completely clear. In the present study, we focused on the medicinal properties of biomolecules ... ...

Abstract	The leading cause of death worldwide is cancer. Many reports have proved the beneficial effect of mushrooms in cancer. However, the precise mechanism is not completely clear. In the present study, we focused on the medicinal properties of biomolecules released by fairy ring-forming mushrooms. Fairy chemicals generally stimulate or inhibit the growth of surrounding vegetation. In the present study, we evaluated whether fairy chemicals (2-azahypoxanthine, 2-aza-8-oxohypoxanthine, and imidazole-4-carboxamide) exert anticancer activity by decreasing the expression of Axl and immune checkpoint molecules in melanoma cells. We used B16F10 melanoma cell lines and a melanoma xenograft model in the experiments. Treatment of melanoma xenograft with cisplatin combined with imidazole-4-carboxamide significantly decreased the tumor volume compared to untreated mice or mice treated cisplatin alone. In addition, mice treated with cisplatin and imidazole-4-carboxamide showed increased peritumoral infiltration of T cells compared to mice treated with cisplatin alone. In vitro studies showed that all fairy chemicals, including imidazole-4-carboxamide, inhibit the expression of immune checkpoint molecules and Axl compared to controls. Imidazole-4-carboxamide also significantly blocks the cisplatin-induced upregulation of PD-L1. These observations point to the fairy chemical imidazole-4-carboxamide as a promising coadjuvant therapy with cisplatin in patients with cancer.
MeSH term(s)	Aminoimidazole Carboxamide/analogs & derivatives ; Animals ; B7-H1 Antigen ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Humans ; Immune Checkpoint Proteins ; Melanoma/drug therapy ; Mice
Chemical Substances	B7-H1 Antigen ; Immune Checkpoint Proteins ; imidazole-4-carboxamide (26832-08-6) ; Aminoimidazole Carboxamide (360-97-4) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-01-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11030374
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Article ; Online: Protective Role of Recombinant Human Thrombomodulin in Diabetes Mellitus.

Okano, Yuko / Takeshita, Atsuro / Yasuma, Taro / Toda, Masaaki / Nishihama, Kota / Fridman D'Alessandro, Valeria / Inoue, Chisa / D'Alessandro-Gabazza, Corina N / Kobayashi, Tetsu / Yano, Yutaka / Gabazza, Esteban C

Cells

2021 Volume 10, Issue 9

Abstract: Diabetes mellitus is a global threat to human health. The ultimate cause of diabetes mellitus is insufficient insulin production and secretion associated with reduced pancreatic β-cell mass. Apoptosis is an important and well-recognized mechanism of the ... ...

Abstract	Diabetes mellitus is a global threat to human health. The ultimate cause of diabetes mellitus is insufficient insulin production and secretion associated with reduced pancreatic β-cell mass. Apoptosis is an important and well-recognized mechanism of the progressive loss of functional β-cells. However, there are currently no available antiapoptotic drugs for diabetes mellitus. This study evaluated whether recombinant human thrombomodulin can inhibit β-cell apoptosis and improve glucose intolerance in a diabetes mouse model. A streptozotocin-induced diabetes mouse model was prepared and treated with thrombomodulin or saline three times per week for eight weeks. The glucose tolerance and apoptosis of β-cells were evaluated. Diabetic mice treated with recombinant human thrombomodulin showed significantly improved glucose tolerance, increased insulin secretion, decreased pancreatic islet areas of apoptotic β-cells, and enhanced proportion of regulatory T cells and tolerogenic dendritic cells in the spleen compared to counterpart diseased mice treated with saline. Non-diabetic mice showed no changes. This study shows that recombinant human thrombomodulin, a drug currently used to treat patients with coagulopathy in Japan, ameliorates glucose intolerance by protecting pancreatic islet β-cells from apoptosis and modulating the immune response in diabetic mice. This observation points to recombinant human thrombomodulin as a promising antiapoptotic drug for diabetes mellitus.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Biomarkers/blood ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; Cell Line, Tumor ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/pathology ; Diabetes Mellitus, Experimental/prevention & control ; Hypoglycemic Agents/administration & dosage ; Injections, Intraperitoneal ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Islets of Langerhans/pathology ; Male ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-akt/metabolism ; Recombinant Proteins/administration & dosage ; Spleen/drug effects ; Spleen/immunology ; Spleen/metabolism ; Streptozocin ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Thrombomodulin/administration & dosage ; Mice
Chemical Substances	Biomarkers ; Blood Glucose ; Hypoglycemic Agents ; Recombinant Proteins ; THBD protein, human ; Thrombomodulin ; Streptozocin (5W494URQ81) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-08-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10092237
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Article ; Online: A Microbiome-Derived Peptide Induces Apoptosis of Cells from Different Tissues.

Saiki, Haruko / Okano, Yuko / Yasuma, Taro / Toda, Masaaki / Takeshita, Atsuro / Abdel-Hamid, Ahmed M / Fridman D'Alessandro, Valeria / Tsuruga, Tatsuki / D'Alessandro-Gabazza, Corina N / Katayama, Kan / Sugimoto, Masahiko / Fujimoto, Hajime / Yamanaka, Keiichi / Kobayashi, Tetsu / Cann, Isaac / Gabazza, Esteban C

Cells

2021 Volume 10, Issue 11

Abstract: Apoptosis is a programmed cell death involved in embryogenesis and tissue homeostasis under physiological conditions. However, abnormalities in the process of apoptosis are implicated in the pathogenesis of various diseases. The human microbiota may ... ...

Abstract	Apoptosis is a programmed cell death involved in embryogenesis and tissue homeostasis under physiological conditions. However, abnormalities in the process of apoptosis are implicated in the pathogenesis of various diseases. The human microbiota may release products that induce apoptosis of host cells. We recently identified a novel microbiome-derived peptide called corisin that worsens lung fibrosis by inducing apoptosis of lung epithelial cells. We hypothesized that corisin and a corisin-like peptide might also induce apoptosis of cells from different tissues. We cultured podocytes, renal tubular epithelial cells, keratinocytes, retinal and intestinal cells treated with corisin and evaluated apoptosis by flow cytometry and Western blotting. Although at different grades, flow cytometry analysis and Western blotting showed that corisin and a corisin-like peptide induced apoptosis of podocytes, keratinocytes, tubular epithelial cells, retinal, and intestinal cells. In addition, we found that corisin synergistically enhances the proapoptotic activity of transforming growth factor-β1 on podocytes. In conclusion, these results suggest that corisin and corisin-like peptides may play a role in the pathogenesis of disease in different organs by promoting apoptosis of parenchymal cells.
MeSH term(s)	Apoptosis/drug effects ; Caspase 3/metabolism ; Cell Line, Tumor ; Epithelial Cells/drug effects ; Epithelial Cells/pathology ; HaCaT Cells ; Humans ; Keratinocytes/drug effects ; Keratinocytes/pathology ; Microbiota/drug effects ; Mitochondrial Membranes/drug effects ; Mitochondrial Membranes/metabolism ; Organ Specificity/drug effects ; Peptides/pharmacology ; Podocytes/drug effects ; Podocytes/pathology ; Reactive Oxygen Species/metabolism ; Retina/pathology ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Peptides ; Reactive Oxygen Species ; Transforming Growth Factor beta1 ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2021-10-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10112885
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Article: Oral Limonite Supplement Ameliorates Glucose Intolerance in Diabetic and Obese Mice.

Uchida, Akihiro / Yasuma, Taro / Takeshita, Atsuro / Toda, Masaaki / Okano, Yuko / Nishihama, Kota / D'Alessandro-Gabazza, Corina N / Fridman D'Alessandro, Valeria / Inoue, Chisa / Takagi, Takehiro / Mukaiyama, Hiroyuki / Takagi, Norio / Shimizu, Katsumi / Yano, Yutaka / Gabazza, Esteban C

Journal of inflammation research

2021 Volume 14, Page(s) 3089–3105

Abstract: Introduction: Diabetes mellitus is a serious threat to public health worldwide. It causes a substantial economic burden, mental and physical disabilities, poor quality of life, and high mortality. Limonite is formed when iron-rich materials from the ... ...

Abstract	Introduction: Diabetes mellitus is a serious threat to public health worldwide. It causes a substantial economic burden, mental and physical disabilities, poor quality of life, and high mortality. Limonite is formed when iron-rich materials from the underground emerge and oxidized on the ground surface. It is currently used to purify contaminated water, absorption of irritant gases, and improve livestock breeding. Limonite can change the composition of environmental microbial communities. In the present study, we evaluated whether limonite can ameliorate glucose metabolism abnormalities by remodeling the gut microbiome. Methods: The investigation was performed using mouse models of streptozotocin-induced diabetes mellitus and high-calorie diet-induced metabolic syndrome. Results: Oral limonite supplement was associated with significant body weight recovery, reduced glycemia with improved insulin secretion, increased number of regulatory T cells, and abundant beneficial gut microbial populations in mice with diabetes mellitus compared to control. Similarly, mice with obesity fed with limonite supplements had significantly reduced body weight, insulin resistance, steatohepatitis, and systemic inflammatory response with significant gut microbiome remodeling. Conclusion: This study demonstrates that limonite supplement ameliorates abnormal glucose metabolism in diabetes mellitus and obesity. Gut microbiome remodeling, inhibition of inflammatory cytokines, and the host immune response regulation may explain the limonite's beneficial activity under pathological conditions in vivo.
Language	English
Publishing date	2021-07-09
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2494878-0
ISSN	1178-7031
ISSN	1178-7031
DOI	10.2147/JIR.S320451
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Article ; Online: Corrigendum for: "Protein S protects against allergic bronchial asthma by modulating Th1/Th2 balance. Allergy 2020 Sept; 75 (9) 2267-2278".

Asayama, Kentaro / Kobayashi, Tetsu / D'Alessandro-Gabazza, Corina N / Toda, Masaaki / Yasuma, Taro / Fujimoto, Hajime / Okano, Tomohito / Saiki, Haruko / Takeshita, Atsuro / Fujiwara, Kentaro / Fridman D'Alessandro, Valeria / Nishihama, Kota / Totoki, Toshiaki / Inoue, Ryo / Takei, Yoshiyuki / Gabazza, Esteban C

Allergy

2021 Volume 76, Issue 6, Page(s) 1946–1947

Language	English
Publishing date	2021-06-15
Publishing country	Denmark
Document type	Published Erratum
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.14696
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Article: Low-Dose of Intrapulmonary Pirfenidone Improves Human Transforming Growth Factorβ1-Driven Lung Fibrosis.

Okano, Tomohito / Kobayashi, Tetsu / Yasuma, Taro / D'Alessandro-Gabazza, Corina N / Toda, Masaaki / Fujimoto, Hajime / Nakahara, Hiroki / Okano, Yuko / Takeshita, Atsuro / Nishihama, Kota / Saiki, Haruko / Tomaru, Atsushi / Fridman D'Alessandro, Valeria / Ishida, Satoru / Sugimoto, Hiromi / Takei, Yoshiyuki / Gabazza, Esteban C

Frontiers in pharmacology

2020 Volume 11, Page(s) 593620

Abstract: Idiopathic pulmonary fibrosis is a chronic, progressive, and lethal lung disease of unknown etiology. Antifibrotic drugs, including pirfenidone, are currently used for the treatment of the disease. The oral administration of pirfenidone is an effective ... ...

Abstract	Idiopathic pulmonary fibrosis is a chronic, progressive, and lethal lung disease of unknown etiology. Antifibrotic drugs, including pirfenidone, are currently used for the treatment of the disease. The oral administration of pirfenidone is an effective therapy, as demonstrated by several clinical trials, although it causes severe adverse events in some patients. We hypothesized that low-dose intrapulmonary delivery of pirfenidone is effective in human transforming growth factorβ1-driven pulmonary fibrosis. To demonstrate our hypothesis, we compared the therapeutic efficacy of varying doses of pirfenidone administered by oral and intranasal routes in a human transforming growth factor-β1 transgenic mouse with established pulmonary fibrosis. We found similar amelioration of lung cell infiltration, inflammatory and fibrotic cytokines, lung fibrosis score, and hydroxyproline content in mice with human transforming growth factor-β1-mediated pulmonary fibrosis treated with low-dose intranasal pirfenidone and high-dose oral pirfenidone. This study showed that pirfenidone is a potent inhibitor of human transforming growth factor-β1-driven lung fibrosis and that intrapulmonary delivery of low-dose pirfenidone produces therapeutic responses equivalent to high-dose of oral pirfenidone.
Language	English
Publishing date	2020-11-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.593620
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Article ; Online: Protein S protects against allergic bronchial asthma by modulating Th1/Th2 balance.

Allergy

2020 Volume 75, Issue 9, Page(s) 2267–2278

Abstract: Background: Bronchial asthma is a chronic disease characterized by inflammation, obstruction, and hyperresponsiveness of the airways. There is currently no curative therapy for asthma. Type 2 helper T cell response plays a critical role in the ... ...

Abstract	Background: Bronchial asthma is a chronic disease characterized by inflammation, obstruction, and hyperresponsiveness of the airways. There is currently no curative therapy for asthma. Type 2 helper T cell response plays a critical role in the pathogenesis of the disease. Protein S is a glycoprotein endowed with anticoagulant, anti-inflammatory, and anti-apoptotic properties. Whether protein S can suppress bronchial asthma and be useful for its therapy is unknown. Methods: To address this question here we compared the development of allergen-associated bronchial asthma between wild type and protein S-overexpressing transgenic mice. Mice were sensitized and challenged with ovalbumin. We also evaluated the circulating levels of total and active protein S in patients with bronchial asthma and healthy controls. Results: The circulating level of total protein S and of its active form was significantly decreased in patients with bronchial asthma compared to controls. Allergic protein S transgenic mice showed a significant reduction of airway hyperresponsiveness, lung tissue inflammatory cell infiltration, lung levels of Th2 cytokines and IgE compared to their wild-type counterparts. Administration of exogenous human protein S also decreased airway hyperresponsiveness and Th2-mediated lung inflammation in allergic wild-type mice compared with their untreated mouse counterparts. Human protein S significantly shifted the Th1/Th2 balance to Th1 and promoted the secretion of Th1 cytokines (IL-12, tumor necrosis factor-α) from dendritic cells. Conclusions: These observations suggest the strong protective activity of protein S against the development of allergic bronchial asthma implicating its potential usefulness for the disease treatment.
MeSH term(s)	Animals ; Asthma/prevention & control ; Bronchial Hyperreactivity ; Cytokines ; Disease Models, Animal ; Humans ; Immunoglobulin E ; Lung ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; Protein S ; Th2 Cells
Chemical Substances	Cytokines ; Protein S ; Immunoglobulin E (37341-29-0) ; Ovalbumin (9006-59-1)
Language	English
Publishing date	2020-03-23
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391933-x
ISSN	1398-9995 ; 0105-4538
ISSN (online)	1398-9995
ISSN	0105-4538
DOI	10.1111/all.14261
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