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Article ; Online: Extracellular CIRP induces CD4CD8αα intraepithelial lymphocyte cytotoxicity in sepsis.

Akama, Yuichi / Murao, Atsushi / Aziz, Monowar / Wang, Ping

2024 Volume 30, Issue 1, Page(s) 17

Abstract: Background: In sepsis, intestinal barrier dysfunction is often caused by the uncontrolled death of intestinal epithelial cells (IECs). CD4CD8αα intraepithelial lymphocytes (IELs), a subtype of CD4: Methods: We subjected wild-type (WT) and CIRP: ... ...

Abstract	Background: In sepsis, intestinal barrier dysfunction is often caused by the uncontrolled death of intestinal epithelial cells (IECs). CD4CD8αα intraepithelial lymphocytes (IELs), a subtype of CD4 Methods: We subjected wild-type (WT) and CIRP Results: We found a significant increase in the expression of GrB and Prf in CD4CD8αα IELs of septic mice compared to sham mice. We found that GrB and Prf levels in CD4CD8αα IELs were increased in the small intestines of WT septic mice, while CD4CD8αα IELs of CIRP Conclusion: In sepsis, the cytotoxicity initiated by the eCIRP/TLR4 axis in CD4CD8αα IELs is associated with intestinal epithelial cell (IEC) death, which could lead to gut injury.
MeSH term(s)	Animals ; Mice ; Intestinal Mucosa/metabolism ; Intestines ; Intraepithelial Lymphocytes ; Mice, Inbred C57BL ; Sepsis/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
Chemical Substances	Toll-Like Receptor 4 ; Cirbp protein, mouse
Language	English
Publishing date	2024-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-024-00790-2
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Article ; Online: Harnessing Extracellular microRNAs for Diagnostics and Therapeutics in Acute Systemic Inflammation.

Hollis, Russell / Aziz, Monowar / Jacob, Asha / Wang, Ping

Cells

2024 Volume 13, Issue 6

Abstract: Micro-ribonucleic acids (miRNAs) are small sequences of genetic materials that are primarily transcribed from the intronic regions of deoxyribonucleic acid (DNAs), and they are pivotal in regulating messenger RNA (mRNA) expression. miRNAs were first ... ...

Abstract	Micro-ribonucleic acids (miRNAs) are small sequences of genetic materials that are primarily transcribed from the intronic regions of deoxyribonucleic acid (DNAs), and they are pivotal in regulating messenger RNA (mRNA) expression. miRNAs were first discovered to regulate mRNAs of the same cell in which they were transcribed. Recent studies have unveiled their ability to traverse cells, either encapsulated in vesicles or freely bound to proteins, influencing distant recipient cells. Activities of extracellular miRNAs have been observed during acute inflammation in clinically relevant pathologies, such as sepsis, shock, trauma, and ischemia/reperfusion (I/R) injuries. This review comprehensively explores the activity of miRNAs during acute inflammation as well as the mechanisms of their extracellular transport and activity. Evaluating the potential of extracellular miRNAs as diagnostic biomarkers and therapeutic targets in acute inflammation represents a critical aspect of this review. Finally, this review concludes with novel concepts of miRNA activity in the context of alleviating inflammation, delivering potential future directions to advance the field of miRNA therapeutics.
MeSH term(s)	Humans ; MicroRNAs/genetics ; Sepsis ; RNA, Messenger/genetics
Chemical Substances	MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2024-03-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13060545
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Article ; Online: An engineered poly(A) tail attenuates gut ischemia/reperfusion-induced acute lung injury.

Murao, Atsushi / Jha, Alok / Aziz, Monowar / Wang, Ping

Surgery

2024 Volume 175, Issue 5, Page(s) 1346–1351

Abstract: Background: Gut ischemia/reperfusion causes the release of damage-associated molecular patterns, leading to acute lung injury and high mortality. Cold-inducible ribonucleic acid-binding protein is a ribonucleic acid chaperon that binds the ... ...

Abstract	Background: Gut ischemia/reperfusion causes the release of damage-associated molecular patterns, leading to acute lung injury and high mortality. Cold-inducible ribonucleic acid-binding protein is a ribonucleic acid chaperon that binds the polyadenylation tail of messenger ribonucleic acid intracellularly. Upon cell stress, cold-inducible ribonucleic acid-binding protein is released, and extracellular cold-inducible ribonucleic acid-binding protein acts as a damage-associated molecular pattern, worsening inflammation. To inhibit extracellular cold-inducible ribonucleic acid-binding protein, we have recently developed an engineered polyadenylation tail named A Methods: Male C57BL6/J mice underwent superior mesenteric artery occlusion and were treated with intraperitoneal A Results: Gut ischemia/reperfusion significantly increased the serum extracellular cold-inducible ribonucleic acid-binding protein levels. A Conclusion: A
MeSH term(s)	Mice ; Male ; Animals ; Interleukin-6/metabolism ; Reperfusion Injury/etiology ; Reperfusion Injury/prevention & control ; Lung/metabolism ; Ischemia/metabolism ; Reperfusion/adverse effects ; Acute Lung Injury/etiology ; Acute Lung Injury/prevention & control ; Acute Lung Injury/drug therapy ; Cytokines/metabolism ; RNA, Messenger/metabolism ; RNA/metabolism ; RNA/therapeutic use ; Mice, Inbred C57BL ; Inflammation/metabolism ; Peroxidase/metabolism ; Lactate Dehydrogenases/metabolism
Chemical Substances	Interleukin-6 ; Cytokines ; RNA, Messenger ; RNA (63231-63-0) ; Peroxidase (EC 1.11.1.7) ; Lactate Dehydrogenases (EC 1.1.-)
Language	English
Publishing date	2024-02-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	202467-6
ISSN	1532-7361 ; 0039-6060
ISSN (online)	1532-7361
ISSN	0039-6060
DOI	10.1016/j.surg.2024.01.002
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Article ; Online: Transcriptomic profiling of immune cells in murine polymicrobial sepsis.

Murao, Atsushi / Jha, Alok / Aziz, Monowar / Wang, Ping

Frontiers in immunology

2024 Volume 15, Page(s) 1347453

Abstract: Introduction: Various immune cell types play critical roles in sepsis with numerous distinct subsets exhibiting unique phenotypes even within the same cell population. Single-cell RNA sequencing (scRNA-seq) enables comprehensive transcriptome profiling ... ...

Abstract	Introduction: Various immune cell types play critical roles in sepsis with numerous distinct subsets exhibiting unique phenotypes even within the same cell population. Single-cell RNA sequencing (scRNA-seq) enables comprehensive transcriptome profiling and unbiased cell classification. In this study, we have unveiled the transcriptomic landscape of immune cells in sepsis through scRNA-seq analysis. Methods: We induced sepsis in mice by cecal ligation and puncture. 20 h after the surgery, the spleen and peritoneal lavage were collected. Single-cell suspensions were processed using a 10× Genomics pipeline and sequenced on an Illumina platform. Count matrices were generated using the Cell Ranger pipeline, which maps reads to the mouse reference transcriptome, GRCm38/mm10. Subsequent scRNA-seq analysis was performed using the R package Seurat. Results: After quality control, we subjected the entire data set to unsupervised classification. Four major clusters were identified as neutrophils, macrophages, B cells, and T cells according to their putative markers. Based on the differentially expressed genes, we identified activated pathways in sepsis for each cell type. In neutrophils, pathways related to inflammatory signaling, such as NF-κB and responses to pathogen-associated molecular patterns (PAMPs), cytokines, and hypoxia were activated. In macrophages, activated pathways were the ones related to cell aging, inflammatory signaling, and responses to PAMPs. In B cells, pathways related to endoplasmic reticulum stress were activated. In T cells, activated pathways were the ones related to inflammatory signaling, responses to PAMPs, and acute lung injury. Next, we further classified each cell type into subsets. Neutrophils consisted of four clusters. Some subsets were activated in inflammatory signaling or cell metabolism, whereas others possessed immunoregulatory or aging properties. Macrophages consisted of four clusters, namely, the ones with enhanced aging, lymphocyte activation, extracellular matrix organization, or cytokine activity. B cells consisted of four clusters, including the ones possessing the phenotype of cell maturation or aging. T cells consisted of six clusters, whose phenotypes include molecular translocation or cell activation. Conclusions: Transcriptomic analysis by scRNA-seq has unveiled a comprehensive spectrum of immune cell responses and distinct subsets in the context of sepsis. These findings are poised to enhance our understanding of sepsis pathophysiology, offering avenues for targeting novel molecules, cells, and pathways to combat infectious diseases.
MeSH term(s)	Mice ; Animals ; Pathogen-Associated Molecular Pattern Molecules ; Gene Expression Profiling ; Transcriptome ; Cytokines/metabolism ; Sepsis
Chemical Substances	Pathogen-Associated Molecular Pattern Molecules ; Cytokines
Language	English
Publishing date	2024-01-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1347453
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Article ; Online: The Novel MFG-E8-derived Oligopeptide, MOP3, Improves Outcomes in a Preclinical Murine Model of Neonatal Sepsis.

Nofi, Colleen P / Prince, Jose M / Aziz, Monowar / Wang, Ping

Journal of pediatric surgery

2024

Abstract: Introduction: Neonatal sepsis is a devastating inflammatory condition that remains a leading cause of morbidity and mortality. Milk fat globule-EGF-factor VIII (MFG-E8) is a glycoprotein that reduces inflammation, whereas extracellular cold-inducible ... ...

Abstract	Introduction: Neonatal sepsis is a devastating inflammatory condition that remains a leading cause of morbidity and mortality. Milk fat globule-EGF-factor VIII (MFG-E8) is a glycoprotein that reduces inflammation, whereas extracellular cold-inducible RNA binding protein (eCIRP) worsens inflammation. This study aimed to determine the therapeutic potential of a novel MFG-E8-derived oligopeptide 3 (MOP3) designed to clear eCIRP and protect against inflammation, organ injury, and mortality in neonatal sepsis. Methods: C57BL6 mouse pups were injected intraperitoneally with cecal slurry (CS) and treated with MOP3 (20 μg/g) or vehicle. 10 h after injection, blood, lungs, and intestines were collected for analyses, and in a 7-day experiment, pups were monitored for differences in mortality. Results: MOP3 treatment protected septic pups from inflammation by reducing eCIRP, IL-6, TNFα, and LDH. MOP3 reduced lung and intestinal inflammation and injury as assessed by reductions in tissue mRNA levels of inflammatory markers, histopathologic injury, and apoptosis in lung and intestines. MOP3 also significantly improved 7-day overall survival for CS-septic mouse pups compared to vehicle (75% vs. 46%, respectively). Conclusion: Deriving from MFG-E8 and designed to clear eCIRP, MOP3 protects against sepsis-induced inflammation, organ injury, and mortality in a preclinical model of neonatal sepsis, implicating it as an exciting potential new therapeutic. Level of evidence: Level 1.
Language	English
Publishing date	2024-03-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	80165-3
ISSN	1531-5037 ; 0022-3468
ISSN (online)	1531-5037
ISSN	0022-3468
DOI	10.1016/j.jpedsurg.2024.03.025
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Article ; Online: DAMPs and radiation injury.

Yamaga, Satoshi / Aziz, Monowar / Murao, Atsushi / Brenner, Max / Wang, Ping

Frontiers in immunology

2024 Volume 15, Page(s) 1353990

Abstract: The heightened risk of ionizing radiation exposure, stemming from radiation accidents and potential acts of terrorism, has spurred growing interests in devising effective countermeasures against radiation injury. High-dose ionizing radiation exposure ... ...

Abstract	The heightened risk of ionizing radiation exposure, stemming from radiation accidents and potential acts of terrorism, has spurred growing interests in devising effective countermeasures against radiation injury. High-dose ionizing radiation exposure triggers acute radiation syndrome (ARS), manifesting as hematopoietic, gastrointestinal, and neurovascular ARS. Hematopoietic ARS typically presents with neutropenia and thrombocytopenia, while gastrointestinal ARS results in intestinal mucosal injury, often culminating in lethal sepsis and gastrointestinal bleeding. This deleterious impact can be attributed to radiation-induced DNA damage and oxidative stress, leading to various forms of cell death, such as apoptosis, necrosis and ferroptosis. Damage-associated molecular patterns (DAMPs) are intrinsic molecules released by cells undergoing injury or in the process of dying, either through passive or active pathways. These molecules then interact with pattern recognition receptors, triggering inflammatory responses. Such a cascade of events ultimately results in further tissue and organ damage, contributing to the elevated mortality rate. Notably, infection and sepsis often develop in ARS cases, further increasing the release of DAMPs. Given that lethal sepsis stands as a major contributor to the mortality in ARS, DAMPs hold the potential to function as mediators, exacerbating radiation-induced organ injury and consequently worsening overall survival. This review describes the intricate mechanisms underlying radiation-induced release of DAMPs. Furthermore, it discusses the detrimental effects of DAMPs on the immune system and explores potential DAMP-targeting therapeutic strategies to alleviate radiation-induced injury.
MeSH term(s)	Humans ; Receptors, Pattern Recognition/metabolism ; Acute Radiation Syndrome/etiology ; Cell Death ; Sepsis/metabolism
Chemical Substances	Receptors, Pattern Recognition
Language	English
Publishing date	2024-01-25
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1353990
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Article ; Online: B-1a Cells Scavenge NETs to Attenuate Sepsis.

Murata, Kensuke / Murao, Atsushi / Tan, Chuyi / Wang, Ping / Aziz, Monowar

Journal of leukocyte biology

2024

Abstract: B-1a cells, a regulatory subset of B lymphocytes, produce natural IgM and IL-10. Neutrophil extracellular traps (NETs) play a crucial role in pathogen defense, but their excessive formation during sepsis can cause further inflammation and tissue damage. ... ...

Abstract	B-1a cells, a regulatory subset of B lymphocytes, produce natural IgM and IL-10. Neutrophil extracellular traps (NETs) play a crucial role in pathogen defense, but their excessive formation during sepsis can cause further inflammation and tissue damage. In sepsis, extracellular cold-inducible RNA-binding protein (eCIRP), a damage-associated molecular pattern, is released to induce NET formation. We hypothesize that B-1a cells clear NETs to prevent sepsis-induced injury. Sepsis in mice was induced by injecting 1 × 107 and 5 × 107 CFU E. coli intraperitoneally (i.p.). After 4 and 20 hours, we assessed the number of B-1a cells in the peritoneal cavity using flow cytometry. Our results showed that the number of peritoneal B-1a cells was significantly decreased in E. coli-sepsis mice. Importantly, replenishing B-1a cells via i.p. injection in sepsis mice significantly decreased NETs in peritoneal neutrophils. We also observed a decrease in serum inflammation and injury markers and a significant increase in overall survival rate in B-1a cell-treated septic mice. To understand the mechanism, we co-cultured bone marrow-derived neutrophils (BMDNs) with peritoneal B-1a cells in a contact or non-contact condition using an insert and stimulated them with eCIRP. After 4 hours, we found that eCIRP significantly increased NET formation in BMDNs. Interestingly, we observed that B-1a cells inhibited NETs by 67% in a contact-dependent manner. Surprisingly, when B-1a cells were cultured in inserts, there was no significant decrease in NET formation, suggesting that direct cell-to-cell contact is crucial for this inhibitory effect. We further determined that B-1a cells promoted NET phagocytosis and this was mediated through natural IgM, as blocking IgM receptor attenuated the engulfment of NETs by B-1a cells. Finally, we identified that following their engulfment, NETs were localized into the lysosomal compartment for lysis. Thus, our study suggests that B-1a cells decrease NET content in eCIRP-treated neutrophils and E. coli-sepsis mice.
Language	English
Publishing date	2024-03-14
Publishing country	England
Document type	Journal Article
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1093/jleuko/qiae066
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Article ; Online: Glucocorticoid resistance and hyperlactatemia: A tag team to worsen sepsis.

Aziz, Monowar / Wang, Ping

Cell metabolism

2021 Volume 33, Issue 9, Page(s) 1717–1718

Abstract: Glucocorticoid resistance often dims glucocorticoid's therapeutic efficacy in sepsis. However, the mechanism is incompletely understood. In this issue, Vandewalle et al. (2021) demonstrate that glucocorticoid resistance leads to hyperlactatemia and that ... ...

Abstract	Glucocorticoid resistance often dims glucocorticoid's therapeutic efficacy in sepsis. However, the mechanism is incompletely understood. In this issue, Vandewalle et al. (2021) demonstrate that glucocorticoid resistance leads to hyperlactatemia and that this combination facilitates lethal sepsis. This insight gives important clarity to the pathophysiology of sepsis, while further suggesting therapeutic avenues for its treatment.
MeSH term(s)	Glucocorticoids ; Humans ; Hyperlactatemia ; Metabolism, Inborn Errors ; Receptors, Glucocorticoid ; Sepsis/drug therapy
Chemical Substances	Glucocorticoids ; Receptors, Glucocorticoid
Language	English
Publishing date	2021-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.08.007
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Article ; Online: EXTRACELLULAR CIRP INHIBITS NEUTROPHIL APOPTOSIS TO PROMOTE ITS AGING BY UPREGULATING SERPINB2 IN SEPSIS.

Shimizu, Junji / Murao, Atsushi / Aziz, Monowar / Wang, Ping

Shock (Augusta, Ga.)

2023 Volume 60, Issue 3, Page(s) 450–460

Abstract: Abstract: Background: Sepsis reduces neutrophil apoptosis. As the result, neutrophils may become aged, exacerbating inflammation and tissue injury. Extracellular cold-inducible RNA-binding protein (eCIRP) acts as a damage-associated molecular pattern to ...

Abstract	Abstract: Background: Sepsis reduces neutrophil apoptosis. As the result, neutrophils may become aged, exacerbating inflammation and tissue injury. Extracellular cold-inducible RNA-binding protein (eCIRP) acts as a damage-associated molecular pattern to promote inflammation and tissue injury in sepsis. SerpinB2, a serine protease inhibitor, has been shown to inhibit apoptosis. We hypothesize that eCIRP upregulates SerpinB2 to promote aged neutrophil subset by inhibiting apoptosis in sepsis. Methods: We stimulated bone marrow-derived neutrophils (BMDNs) of wild-type (WT) mice with 1 μg/mL of recombinant mouse CIRP (i.e., eCIRP) and assessed cleaved caspase-3 and SerpinB2 by western blotting. Apoptotic neutrophils were assessed by Annexin V/PI. Bone marrow-derived neutrophils were stimulated with 1 μg/mL eCIRP and treated with or without PAC-1 (caspase-3 activator) and aged neutrophils (CXCR4 hi CD62L lo ) were assessed by flow cytometry. To induce sepsis, we performed cecal ligation and puncture in WT or CIRP -/- mice. We determined the percentage of aged neutrophils and SerpinB2 + neutrophils in blood and spleen by flow cytometry. Results: We found that cleaved caspase-3 levels were increased at 4 h of PBS treatment compared with 0 h but decreased by eCIRP treatment. Extracellular cold-inducible RNA-binding protein reduced apoptotic cells after 20 h of treatment. Extracellular cold-inducible RNA-binding protein also increased the frequencies of aged neutrophils compared with PBS after 20 h, while PAC-1 treatment reduced aging in eCIRP-treated BMDNs. Extracellular cold-inducible RNA-binding protein significantly increased the expression of SerpinB2 at protein levels in BMDNs at 20 h. In WT mice, the frequencies of aged and SerpinB2 + neutrophils in blood and spleen were increased after 20 h of cecal ligation and puncture, while in CIRP -/- mice, aged and SerpinB2 + neutrophils were significantly decreased compared with WT mice. We also found that aged neutrophils expressed significantly higher levels of SerpinB2 compared with non-aged neutrophils. Conclusions: eCIRP inhibits neutrophil apoptosis to increase aged phenotype by increasing SerpinB2 expression in sepsis. Thus, targeting eCIRP could be a new therapeutic strategy to ameliorate inflammation caused by neutrophil aging in sepsis.
MeSH term(s)	Mice ; Animals ; Neutrophils/metabolism ; Lung/metabolism ; Caspase 3/metabolism ; Inflammation/metabolism ; Sepsis/metabolism ; Apoptosis ; RNA-Binding Proteins/metabolism ; Mice, Inbred C57BL
Chemical Substances	Caspase 3 (EC 3.4.22.-) ; RNA-Binding Proteins
Language	English
Publishing date	2023-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000002187
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Article ; Online: Damage-Associated Molecular Patterns As Double-Edged Swords in Sepsis.

Zhou, Mian / Aziz, Monowar / Wang, Ping

Antioxidants & redox signaling

2021 Volume 35, Issue 15, Page(s) 1308–1323

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Animals ; Humans ; Inflammation/immunology ; Sepsis/immunology
Language	English
Publishing date	2021-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2021.0008
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