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Article ; Online: Pax6 isoforms shape eye development: Insights from developmental stages and organoid models.

Hung, Shih-Shun / Tsai, Po-Sung / Po, Ching-Wen / Hou, Pei-Shan

Differentiation; research in biological diversity

2024 Volume 137, Page(s) 100781

Abstract: Pax6 is a critical transcription factor involved in the development of the central nervous system. However, in humans, mutations in Pax6 predominantly result in iris deficiency rather than neurological phenotypes. This may be attributed to the distinct ... ...

Abstract	Pax6 is a critical transcription factor involved in the development of the central nervous system. However, in humans, mutations in Pax6 predominantly result in iris deficiency rather than neurological phenotypes. This may be attributed to the distinct functions of Pax6 isoforms, Pax6a and Pax6b. In this study, we investigated the spatial and temporal expression patterns of Pax6 isoforms during different stages of mouse eye development. We observed a strong correlation between Pax6a expression and the neuroretina gene Sox2, while Pax6b showed a high correlation with iris-component genes, including the mesenchymal gene Foxc1. During early patterning from E10.5, Pax6b was expressed in the hinge of the optic cup and neighboring mesenchymal cells, whereas Pax6a was absent in these regions. At E14.5, both Pax6a and Pax6b were expressed in the future iris and ciliary body, coinciding with the integration of mesenchymal cells and Mitf-positive cells in the outer region. From E18.5, Pax6 isoforms exhibited distinct expression patterns as lineage genes became more restricted. To further validate these findings, we utilized ESC-derived eye organoids, which recapitulated the temporal and spatial expression patterns of lineage genes and Pax6 isoforms. Additionally, we found that the spatial expression patterns of Foxc1 and Mitf were impaired in Pax6b-mutant ESC-derived eye organoids. This in vitro eye organoids model suggested the involvement of Pax6b-positive local mesodermal cells in iris development. These results provide valuable insights into the regulatory roles of Pax6 isoforms during iris and neuroretina development and highlight the potential of ESC-derived eye organoids as a tool for studying normal and pathological eye development.
Language	English
Publishing date	2024-04-10
Publishing country	England
Document type	Journal Article
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2024.100781
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Article ; Online: C-type lectins and extracellular vesicles in virus-induced NETosis.

Sung, Pei-Shan / Hsieh, Shie-Liang

Journal of biomedical science

2021 Volume 28, Issue 1, Page(s) 46

Abstract: Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory ... ...

Abstract	Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Furthermore, excessive NET formation (NETosis) is associated with disease severity in patients suffering from SARS-CoV-2-induced multiple organ injuries. Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and other members of C-type lectin family (L-SIGN, LSECtin, CLEC10A) have been reported to interact with viral glycans to facilitate virus spreading and exacerbates inflammatory reactions. Moreover, spleen tyrosine kinase (Syk)-coupled C-type lectin member 5A (CLEC5A) has been shown as the pattern recognition receptor for members of flaviviruses, and is responsible for DV-induced cytokine storm and Japanese encephalomyelitis virus (JEV)-induced neuronal inflammation. Moreover, DV activates platelets via CLEC2 to release extracellular vesicles (EVs), including microvesicles (MVs) and exosomes (EXOs). The DV-activated EXOs (DV-EXOs) and MVs (DV-MVs) stimulate CLEC5A and Toll-like receptor 2 (TLR2), respectively, to enhance NET formation and inflammatory reactions. Thus, EVs from virus-activated platelets (PLT-EVs) are potent endogenous danger signals, and blockade of C-type lectins is a promising strategy to attenuate virus-induced NETosis and intravascular coagulopathy.
MeSH term(s)	Blood Platelets/immunology ; Blood Platelets/pathology ; COVID-19/immunology ; COVID-19/pathology ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/pathology ; Encephalitis Virus, Japanese/immunology ; Encephalitis, Japanese/immunology ; Encephalitis, Japanese/pathology ; Extracellular Traps/immunology ; Humans ; Lectins, C-Type/immunology ; Platelet Activation/immunology ; SARS-CoV-2/immunology ; Signal Transduction/immunology
Chemical Substances	Lectins, C-Type
Language	English
Publishing date	2021-06-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-021-00741-7
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Article ; Online: Inhibition of SARS-CoV-2-mediated thromboinflammation by CLEC2.Fc.

Sung, Pei-Shan / Sun, Cheng-Pu / Tao, Mi-Hua / Hsieh, Shie-Liang

EMBO molecular medicine

2023 Volume 15, Issue 7, Page(s) e16351

Abstract: Thromboinflammation is the major cause of morbidity and mortality in COVID-19 patients, and post-mortem examination demonstrates the presence of platelet-rich thrombi and microangiopathy in visceral organs. Moreover, persistent microclots were detected ... ...

Abstract	Thromboinflammation is the major cause of morbidity and mortality in COVID-19 patients, and post-mortem examination demonstrates the presence of platelet-rich thrombi and microangiopathy in visceral organs. Moreover, persistent microclots were detected in both acute COVID-19 and long COVID plasma samples. However, the molecular mechanism of SARS-CoV-2-induced thromboinflammation is still unclear. We found that the spleen tyrosine kinase (Syk)-coupled C-type lectin member 2 (CLEC2), which was highly expressed in platelets and alveolar macrophages, interacted with the receptor-binding domain (RBD) of SARS-CoV-2 spike protein (SARS-CoV-2 RBD) directly. Unlike the thread-like NETs, SARS-CoV-2-induced aggregated NET formation in the presence of wild-type (WT), but not CLEC2-deficient platelets. Furthermore, SARS-CoV-2 spike pseudotyped lentivirus was able to induce NET formation via CLEC2, indicating SARS-CoV-2 RBD engaged CLEC2 to activate platelets to enhance NET formation. Administration of CLEC2.Fc inhibited SARS-CoV-2-induced NET formation and thromboinflammation in AAV-ACE2-infected mice. Thus, CLEC2 is a novel pattern recognition receptor for SARS-CoV-2, and CLEC2.Fc and may become a promising therapeutic agent to inhibit SARS-CoV-2-induced thromboinflammation and reduced the risk of post-acute sequelae of COVID-19 (PASC) in the future.
MeSH term(s)	Humans ; Mice ; Animals ; SARS-CoV-2 ; COVID-19 ; Inflammation ; Thromboinflammation ; Post-Acute COVID-19 Syndrome ; Thrombosis ; Protein Binding
Chemical Substances	spike protein, SARS-CoV-2
Language	English
Publishing date	2023-05-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202216351
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Zs.A 6784: Show issues

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Article ; Online: Quantification Quality Control Emerges as A Crucial Factor to Enhance Single Cell Proteomics Data Analysis.

Yu, Sung-Huan / Chen, Shiau-Ching / Wu, Pei-Shan / Kuo, Pei-I / Chen, Ting-An / Lee, Hsiang-Ying / Lin, Miao-Hsia

Molecular & cellular proteomics : MCP

2024 , Page(s) 100768

Abstract: Mass spectrometry (MS)-based single-cell proteomics (SCP) provides us the opportunity to unbiasedly explore biological variability within cells without the limitation of antibody availability. This field is rapidly developed with the main focuses on ... ...

Abstract	Mass spectrometry (MS)-based single-cell proteomics (SCP) provides us the opportunity to unbiasedly explore biological variability within cells without the limitation of antibody availability. This field is rapidly developed with the main focuses on instrument advancement, sample preparation refinement, and signal boosting methods; however, the optimal data processing and analysis are rarely investigated which holds an arduous challenge because of the high proportion of missing values and batch effect. Here, we introduced a quantification quality control to intensify the identification of differentially expressed proteins (DEPs) by considering both within and across SCP data. Combining quantification quality control with isobaric matching between runs (IMBR) and PSM-level normalization, an additional 12% and 19% of proteins and peptides, with more than 90% of proteins/peptides containing valid values, were quantified. Clearly, quantification quality control was able to reduce quantification variations and q-values with the more apparent cell type separations. In addition, we found that PSM-level normalization performed similarly to other protein-level normalizations but kept the original data profiles without the additional requirement of data manipulation. In proof of concept of our refined pipeline, six uniquely identified DEPs exhibiting varied fold-changes and playing critical roles for melanoma and monocyte functionalities were selected for validation using immunoblotting. Five out of six validated DEPs showed an identical trend with the SCP dataset, emphasizing the feasibility of combining the IMBR, cell quality control, and PSM-level normalization in SCP analysis, which is beneficial for future SCP studies.
Language	English
Publishing date	2024-04-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2075924-1
ISSN	1535-9484 ; 1535-9476
ISSN (online)	1535-9484
ISSN	1535-9476
DOI	10.1016/j.mcpro.2024.100768
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Zs.A 5599: Show issues

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Article ; Online: Inhibition of SARS‐CoV‐2‐mediated thromboinflammation by CLEC2.Fc

Pei‐Shan Sung / Cheng‐Pu Sun / Mi‐Hua Tao / Shie‐Liang Hsieh

EMBO Molecular Medicine, Vol 15, Iss 7, Pp n/a-n/a (2023)

2023

Abstract: Abstract Thromboinflammation is the major cause of morbidity and mortality in COVID‐19 patients, and post‐mortem examination demonstrates the presence of platelet‐rich thrombi and microangiopathy in visceral organs. Moreover, persistent microclots were ... ...

Abstract	Abstract Thromboinflammation is the major cause of morbidity and mortality in COVID‐19 patients, and post‐mortem examination demonstrates the presence of platelet‐rich thrombi and microangiopathy in visceral organs. Moreover, persistent microclots were detected in both acute COVID‐19 and long COVID plasma samples. However, the molecular mechanism of SARS‐CoV‐2‐induced thromboinflammation is still unclear. We found that the spleen tyrosine kinase (Syk)‐coupled C‐type lectin member 2 (CLEC2), which was highly expressed in platelets and alveolar macrophages, interacted with the receptor‐binding domain (RBD) of SARS‐CoV‐2 spike protein (SARS‐CoV‐2 RBD) directly. Unlike the thread‐like NETs, SARS‐CoV‐2‐induced aggregated NET formation in the presence of wild‐type (WT), but not CLEC2‐deficient platelets. Furthermore, SARS‐CoV‐2 spike pseudotyped lentivirus was able to induce NET formation via CLEC2, indicating SARS‐CoV‐2 RBD engaged CLEC2 to activate platelets to enhance NET formation. Administration of CLEC2.Fc inhibited SARS‐CoV‐2‐induced NET formation and thromboinflammation in AAV‐ACE2‐infected mice. Thus, CLEC2 is a novel pattern recognition receptor for SARS‐CoV‐2, and CLEC2.Fc and may become a promising therapeutic agent to inhibit SARS‐CoV‐2‐induced thromboinflammation and reduced the risk of post‐acute sequelae of COVID‐19 (PASC) in the future.
Keywords	CLEC2 ; NET ; platelet ; SARS‐CoV‐2 ; thromboinflammation ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
Language	English
Publishing date	2023-07-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
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Article ; Online: C-type lectins and extracellular vesicles in virus-induced NETosis

Pei-Shan Sung / Shie-Liang Hsieh

Journal of Biomedical Science, Vol 28, Iss 1, Pp 1-

2021 Volume 12

Abstract: Abstract Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute ... ...

Abstract	Abstract Dysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Furthermore, excessive NET formation (NETosis) is associated with disease severity in patients suffering from SARS-CoV-2-induced multiple organ injuries. Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and other members of C-type lectin family (L-SIGN, LSECtin, CLEC10A) have been reported to interact with viral glycans to facilitate virus spreading and exacerbates inflammatory reactions. Moreover, spleen tyrosine kinase (Syk)-coupled C-type lectin member 5A (CLEC5A) has been shown as the pattern recognition receptor for members of flaviviruses, and is responsible for DV-induced cytokine storm and Japanese encephalomyelitis virus (JEV)-induced neuronal inflammation. Moreover, DV activates platelets via CLEC2 to release extracellular vesicles (EVs), including microvesicles (MVs) and exosomes (EXOs). The DV-activated EXOs (DV-EXOs) and MVs (DV-MVs) stimulate CLEC5A and Toll-like receptor 2 (TLR2), respectively, to enhance NET formation and inflammatory reactions. Thus, EVs from virus-activated platelets (PLT-EVs) are potent endogenous danger signals, and blockade of C-type lectins is a promising strategy to attenuate virus-induced NETosis and intravascular coagulopathy.
Keywords	COVID-19 ; SARS-CoV-2 ; Dengue virus (DV) ; Platelet ; C-type lectin receptor (CLR) ; CLEC2 ; Medicine ; R
Subject code	616
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Early double-balloon enteroscopy was not related to better clinical outcomes in patients with suspected overt small bowel bleeding.

Ye, Yong-Cheng / Sung, Kuan-Yi / Chang, Tien-En / Wu, Pei-Shan / Wang, Yen-Po / Luo, Jiing-Chyuan / Hou, Ming-Chih / Lu, Ching-Liang

Journal of the Chinese Medical Association : JCMA

2024 Volume 87, Issue 4, Page(s) 377–383

Abstract: Background: Device-assisted enteroscopy has been used for over 20 years for the management of patients with suspected small bowel bleeding. Unlike esophagogastroduodenoscopy and colonoscopy, the appropriate timing of enteroscopy is still unknown. In ... ...

Abstract	Background: Device-assisted enteroscopy has been used for over 20 years for the management of patients with suspected small bowel bleeding. Unlike esophagogastroduodenoscopy and colonoscopy, the appropriate timing of enteroscopy is still unknown. In recent guidelines, early enteroscopy is suggested to maximize diagnostic yield and therapeutic yield in patients with suspected small bowel bleeding. However, few studies have identified its influence on clinical outcomes, including mortality or rebleeding rate. We conducted this study to evaluate the influence of the timing of double-balloon enteroscopy on clinical outcomes in patients with suspected small bowel bleeding. Methods: Patients with overt small bowel bleeding who underwent double-balloon enteroscopy from January 2013 to February 2021 were retrospectively reviewed. Patients were categorized into an early enteroscopy group (≤14 days) and a nonearly enteroscopy group (>14 days). Clinical outcomes, including short-term mortality and rebleeding rate, long-term mortality and rebleeding rate, diagnostic yield, and therapeutic yield, were analyzed. Results: A total of 100 patients (mean age, 66.2 years; 53% male) were included, and 44 patients were stratified into the early enteroscopy group. The diagnostic yield, therapeutic yield, mortality, and rebleeding rate were similar between two groups. In multivariate conditional logistic regression analysis, there were no significant differences between two groups regarding the 30-day rebleeding rate (adjusted odds ratio [aOR], 1.43; 95% CI, 0.47-4.33), 90-day rebleeding rate (aOR, 1.18; 95% CI, 0.47-2.94), 30-day mortality rate (aOR, 1.29; 95% CI, 0.21-8.13), 90-day mortality rate (aOR, 1.94; 95% CI, 0.48-7.87), and 90-day bleeding-related mortality (aOR, 2.18; 95% CI, 0.24-19.52). The Kaplan-Meier survival curve analysis showed that the timing of DBE was not associated with the long-term rebleeding rate or mortality rate ( p = 0.57 and 0.83, respectively). Conclusion: The timing of enteroscopy did not influence the clinical outcomes, including the short-term mortality rate, short-term rebleeding rate, long-term mortality rate, and rebleeding rate, in patients with suspected overt small bowel bleeding.
MeSH term(s)	Humans ; Male ; Aged ; Female ; Double-Balloon Enteroscopy ; Intestine, Small ; Retrospective Studies ; Gastrointestinal Hemorrhage/diagnosis ; Gastrointestinal Hemorrhage/therapy ; Colonoscopy
Language	English
Publishing date	2024-02-09
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2107283-8
ISSN	1728-7731 ; 1726-4901
ISSN (online)	1728-7731
ISSN	1726-4901
DOI	10.1097/JCMA.0000000000001067
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Zs.A 2699: Show issues

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Article ; Online: CLEC2 and CLEC5A: Pathogenic Host Factors in Acute Viral Infections.

Sung, Pei-Shan / Hsieh, Shie-Liang

Frontiers in immunology

2019 Volume 10, Page(s) 2867

Abstract: The protective roles of endosomal toll-like receptors (TLRs) and cytosolic nucleic acid sensors are well elucidated, but the pathogenic host factors during viral infections remain unclear. Spleen tyrosine kinase (Syk)-coupled C-type lectins (CLECs) CLEC2 ...

Abstract	The protective roles of endosomal toll-like receptors (TLRs) and cytosolic nucleic acid sensors are well elucidated, but the pathogenic host factors during viral infections remain unclear. Spleen tyrosine kinase (Syk)-coupled C-type lectins (CLECs) CLEC2 and CLEC5A are highly expressed on platelets and myeloid cells, respectively. CLEC2 has been shown to recognize snake venom aggretin and the endogenous ligand podoplanin and acts as a critical regulator in the development and immunothrombosis. Although CLEC2 has been reported to interact with type I immunodeficiency virus (HIV-1), its role in viral infections is still unclear. CLEC5A binds to fucose and mannose moieties of dengue virus membrane glycans, as well as to N-acetylglucosamine (GlcNAc)/N-acetylmuramic acid (MurNAc) disaccharides that form the backbone of
MeSH term(s)	Acute Disease ; Dengue/immunology ; Dengue/pathology ; Dengue Virus/immunology ; Extracellular Traps/immunology ; Humans ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza, Human/immunology ; Influenza, Human/pathology ; Lectins, C-Type/immunology ; Receptors, Cell Surface/immunology ; Toll-Like Receptor 2/immunology
Chemical Substances	CLEC2A protein, human ; CLEC5A protein, human ; Lectins, C-Type ; Receptors, Cell Surface ; TLR2 protein, human ; Toll-Like Receptor 2
Keywords	covid19
Language	English
Publishing date	2019-12-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.02867
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Article: CLEC5A: A Promiscuous Pattern Recognition Receptor to Microbes and Beyond.

Sung, Pei-Shan / Chang, Wei-Chiao / Hsieh, Shie-Liang

Advances in experimental medicine and biology

2020 Volume 1204, Page(s) 57–73

Abstract: CLEC5A is a spleen tyrosine kinase (Syk)-coupled C-type lectin that is highly expressed by monocytes, macrophages, neutrophils, and dendritic cells and interacts with virions directly, via terminal fucose and mannose moieties of viral glycans. CLEC5A ... ...

Abstract	CLEC5A is a spleen tyrosine kinase (Syk)-coupled C-type lectin that is highly expressed by monocytes, macrophages, neutrophils, and dendritic cells and interacts with virions directly, via terminal fucose and mannose moieties of viral glycans. CLEC5A also binds to N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc) disaccharides of bacterial cell walls. Compared to other C-type lectins (DC-SIGN and DC-SIGNR) and TLRs, CLEC5A binds its ligands with relatively low affinities. However, CLEC5A forms a multivalent hetero-complex with DC-SIGN and other C-type lectins upon engagement with ligands, and thereby mediates microbe-induced inflammatory responses via activation of Syk. For example, in vivo studies in mouse models have demonstrated that CLEC5A is responsible for flaviviruses-induced hemorrhagic shock and neuroinflammation, and a CLEC5A polymorphism in humans is associated with disease severity following infection with dengue virus. In addition, CLEC5A is co-activated with TLR2 by Listeria and Staphylococcus. Furthermore, CLEC5A-postive myeloid cells are responsible for Concanavilin A-induced aseptic inflammatory reactions. Thus, CLEC5A is a promiscuous pattern recognition receptor in myeloid cells and is a potential therapeutic target for attenuation of both septic and aseptic inflammatory reactions.
MeSH term(s)	Animals ; Dengue Virus/immunology ; Flavivirus/immunology ; Humans ; Inflammation/immunology ; Lectins, C-Type/immunology ; Macrophages/immunology ; Monocytes/immunology ; Neutrophils/immunology ; Receptors, Cell Surface/immunology ; Receptors, Pattern Recognition/immunology
Chemical Substances	CLEC5A protein, human ; Lectins, C-Type ; Receptors, Cell Surface ; Receptors, Pattern Recognition
Keywords	covid19
Language	English
Publishing date	2020-03-09
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-15-1580-4_3
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Article ; Online: CLEC5A is critical in Pseudomonas aeruginosa-induced NET formation and acute lung injury.

Sung, Pei-Shan / Peng, Yu-Chun / Yang, Shao-Ping / Chiu, Cheng-Hsun / Hsieh, Shie-Liang

JCI insight

2022 Volume 7, Issue 18

Abstract: Pseudomonas aeruginosa is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, ...

Abstract	Pseudomonas aeruginosa is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, thereby aggravating ventilator-induced lung damage. While pattern recognition receptors (PRRs) TLR4 and TLR5 are required for host defense against P. aeruginosa invasion, the PRR responsible for P. aeruginosa-induced NET formation, proinflammatory cytokine release, and acute lung injury remains unclear. We found that myeloid C-type lectin domain family 5 member A (CLEC5A) interacts with LPS of P. aeruginosa and is responsible for P. aeruginosa-induced NET formation and lung inflammation. P. aeruginosa activates CLEC5A to induce caspase-1-dependent NET formation, but it neither causes gasdermin D (GSDMD) cleavage nor contributes to P. aeruginosa-induced neutrophil death. Blockade of CLEC5A attenuates P. aeruginosa-induced NETosis and lung injury, and simultaneous administration of anti-CLEC5A mAb with ciprofloxacin increases survival rate and decreases collagen deposition in the lungs of mice challenged with a lethal dose of P. aeruginosa. Thus, CLEC5A is a promising therapeutic target to reduce ventilator-associated lung injury and fibrosis in P. aeruginosa-induced pneumonia.
MeSH term(s)	Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Animals ; Caspases ; Ciprofloxacin ; Cytokines ; Lectins, C-Type/metabolism ; Lipopolysaccharides/toxicity ; Mice ; Pneumonia/metabolism ; Pneumonia/pathology ; Pseudomonas aeruginosa ; Receptors, Cell Surface ; Toll-Like Receptor 4 ; Toll-Like Receptor 5
Chemical Substances	Clec5a protein, mouse ; Cytokines ; Lectins, C-Type ; Lipopolysaccharides ; Receptors, Cell Surface ; Toll-Like Receptor 4 ; Toll-Like Receptor 5 ; Ciprofloxacin (5E8K9I0O4U) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2022-09-01
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.156613
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