Influenza B virus infection alters the regenerative potential of murine alveolar type 2 pneumocytes DOI Creative Commons
Satoko Nakano, Cait E. Hamele, Aleksandra Tata

et al.

mBio, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 31, 2024

Respiratory epithelial cells can survive direct infection by influenza viruses, and the long-term consequences of that have been characterized in a subset proximal airway cell types. The impact on viral distal lung epithelia, however, is much less well-characterized. Utilizing Cre-expressing B virus (IBV) lox-stop-lox tdTomato reporter mouse model, we identified alveolar type 2 (AT2) pneumocytes, progenitor lung, infection. We show survival associated with transcriptional dysregulation compared to bystander AT2 pneumocytes from same lung. Furthermore,

Language: Английский

The role of trained immunity in sepsis DOI Creative Commons
Wenjuan Wang,

Lisi Ma,

Bin Liu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Aug. 15, 2024

Sepsis is defined as a life-threatening organ dysfunction syndrome caused by dysregulated host response to infection, characterized systemic inflammatory infection. The use of antibiotics, fluid resuscitation, and support therapy has limited prognostic benefit in patients with sepsis, its incidence not diminishing, which attracting increased attention medicine. remains one the most debilitating expensive illnesses. One main reasons septic mortality now understood be disruption immune homeostasis. Immunotherapy revolutionizing treatment illnesses responses play significant role. This “trained immunity”, potent defense against infection regardless type bacteria, fungus, or virus, attributed discovery that innate cells possess memory via metabolic epigenetic reprogramming. Here we reviewed immunotherapy features trained immunity, relationship between immunity sepsis.

Language: Английский

Citations

5
From genome to epigenome: Who is a predominant player in the molecular hallmarks determining epigenetic mechanisms underlying ontogenesis? DOI Creative Commons
M. Samiec, Monika Trzcińska

Reproductive Biology, Journal Year: 2024, Volume and Issue: 24(4), P. 100965 - 100965

Published: Oct. 30, 2024

Language: Английский

Citations

4
Aurora kinase A promotes trained immunity via regulation of endogenous S-adenosylmethionine metabolism DOI Open Access
Mengyun Li,

Huan Jin,

Yongxiang Liu

et al.

Published: Jan. 8, 2025

Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying regulation of immunity remains largely elusive. Here, we demonstrate that inhibition Aurora kinase A (AurA) dampens induced by β-glucan. ATAC-seq and RNA-seq analysis reveals AurA restricts chromatin accessibility genes associated with inflammatory pathways such as JAK-STAT, TNF NF-κB pathways. Specifically, promotes nuclear localization FOXO3 expression glycine N-methyltransferase (GNMT), key enzyme responsible for adenosylmethionine (SAM) consumption. Metabolomic confirms reduction in SAM level upon inhibition. As result deficiency, mouse macrophages exhibit decreased H3K4me3 H3K36me3 enrichment on gene regions Il6 Tnfα . Additionally, tumor effect β-glucan is notably abolished Together, our findings identify an essential role regulating via methylation-dependent manner maintaining endogenous through mTOR-FOXO3-GNMT axis.

Language: Английский

Citations

0
Aurora kinase A promotes trained immunity via regulation of endogenous S-adenosylmethionine metabolism DOI Open Access
Mengyun Li,

Huan Jin,

Yongxiang Liu

et al.

Published: Jan. 8, 2025

Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying regulation of immunity remains largely elusive. Here, we demonstrate that inhibition Aurora kinase A (AurA) dampens induced by β-glucan. ATAC-seq and RNA-seq analysis reveals AurA restricts chromatin accessibility genes associated with inflammatory pathways such as JAK-STAT, TNF NF-κB pathways. Specifically, promotes nuclear localization FOXO3 expression glycine N-methyltransferase (GNMT), key enzyme responsible for adenosylmethionine (SAM) consumption. Metabolomic confirms reduction in SAM level upon inhibition. As result deficiency, mouse macrophages exhibit decreased H3K4me3 H3K36me3 enrichment on gene regions Il6 Tnfα . Additionally, tumor effect β-glucan is notably abolished Together, our findings identify an essential role regulating via methylation-dependent manner maintaining endogenous through mTOR-FOXO3-GNMT axis.

Language: Английский

Citations

0
Reanalysis of two metritis studies demonstrates different patterns of postpartum uterine infection for primiparous versus multiparous cows DOI Creative Commons
J.C.C. Silva, M.C. Lucy

JDS Communications, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
The Role of Sustained Type I Interferon Secretion in Chronic HIV Pathogenicity: Implications for Viral Persistence, Immune Activation, and Immunometabolism DOI Creative Commons
Eman Teer, Nyasha C. Mukonowenzou, M. Faadiel Essop

et al.

Viruses, Journal Year: 2025, Volume and Issue: 17(2), P. 139 - 139

Published: Jan. 22, 2025

Human immunodeficiency virus (HIV) infection induces chronic immune activation by stimulating both the innate and adaptive systems, resulting in persistent inflammation cell exhaustion. Of note, modulation of cytokine production its release can significantly influence response. Type I interferons (IFN-Is) are cytokines that play a crucial role immunity due to their potent antiviral effects, regulation IFN-stimulated genes essential for viral clearance, initiation responses. Thus, an understanding dual IFN-I (protective versus harmful) during HIV-1 infections elucidating contributions HIV pathogenesis is advancing therapeutic interventions. This review therefore delves into intricate involvement acute phases emphasizes impact on persistence, activation, immunometabolism treated HIV-infected individuals.

Language: Английский

Citations

0
Protocol for CHIEF (cochlear implants and inner ear inflammation) study; an observational, cross-sectional study of children and young people undergoing cochlear implantation. DOI Creative Commons
Kate Hough, Jaya Nichani, C. Findlay

et al.

NIHR Open Research, Journal Year: 2025, Volume and Issue: 5, P. 18 - 18

Published: March 4, 2025

Introduction Cochlear implantation is a surgical intervention for people with severe-to-profound hearing loss. Electrodes in the cochlea generate electrical currents that stimulate auditory nerve to elicit hearing. Despite success of cochlear implants, some do not receive expected benefits. One reason this tissues vary their response electrode array. Many have healthy wound-healing results mature scar tissue (fibrosis). However, individuals heightened inflammatory associated excessive fibrosis. This leads greater resistance current flow (impedance) and reduces quality stimulation, both which can lead poorer outcomes implant. Excessive inflammation damage structures result loss residual study will increase our understanding why We propose there are detectable individual differences between when they implanted, may variable following implantation. If we could understand identify these differences, detect who be at risk less favorable use therapies modulate improve outcomes. Methods analysis A cross-sectional children young undergoing On day surgery, middle ear mucosa sample, swabs nasopharynx ear, fluid, blood samples collected. Samples analyzed using molecular techniques determine status person time Clinical data collected up five years after explore relationship long-term outcomes.

Language: Английский

Citations

0
Innate immune training in the neonatal response to sepsis DOI Creative Commons
Jaimar C. Rincon,

Dayuan Wang,

Valerie E. Polcz

et al.

Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)

Published: April 30, 2025

Neonates, especially those born prematurely, are highly vulnerable to infection-induced mortality. Numerous observational and immunological studies in newborns have shown that live attenuated vaccines beneficial, non-specific effects (NSEs) against secondary infections unrelated pathogens. These beneficial been attributed trained immunity, emergency granulopoiesis plays an essential role. However, immunity has affect multiple myeloid subsets how influences the host protective response is still undefined. Here we show Bacillus-Calmette-Guérin (BCG) vaccination improves survival polymicrobial sepsis by simultaneously reprogramming broad aspects of myelopoiesis. Specifically, BCG expands subsets, including lineage (Lin)-Sca- 1+c-kit+ (LSK) granulocytic-macrophage progenitors (GMPs), increases CD11b+Gr1+ cell number, as well their oxidative metabolism capacity stimulate T-cell proliferation sepsis. Single-cell RNA sequencing neonatal splenocytes suggests BCG-vaccination changes transcriptional landscape subsets. The result maturation various neutrophil monocyte stimulation antimicrobial processes, suppression inflammatory pathways myeloid-derived suppressor transcription. findings reveal administration early after birth fundamentally reorganizes benefit subsequent infection.

Language: Английский

Citations

0
Aurora kinase A promotes trained immunity via regulation of endogenous S-adenosylmethionine metabolism DOI Creative Commons
Mengyun Li, Xin Jin, Yongxiang Liu

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 11, 2024

Abstract Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying regulation of immunity remains largely elusive. Here, we demonstrate that inhibition Aurora kinase A (AurA) dampens induced by β-glucan. ATAC-seq and RNA-seq analysis reveals AurA restricts chromatin accessibility genes associated with inflammatory pathways such as JAK-STAT, TNF NF-κB pathways. Specifically, promotes nuclear localization FOXO3 expression glycine N-methyltransferase (GNMT), key enzyme responsible for adenosylmethionine (SAM) consumption. Metabolomic confirms reduction in SAM level upon inhibition. As result deficiency, mouse macrophages exhibit decreased H3K4me3 H3K36me3 enrichment on gene regions Il6 Tnfα . Additionally, tumor effect β-glucan is notably abolished Together, our findings identify an essential role regulating via methylation-dependent manner maintaining endogenous through mTOR-FOXO3-GNMT axis.

Language: Английский

Citations

0
The Cellular and Transcriptomic Early Innate Immune Response to BCG Vaccination in Mice DOI Creative Commons
L. G. Kondratyeva, Olga Rakitina, В. В. Плешкан

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(24), P. 2043 - 2043

Published: Dec. 11, 2024

It is established that BCG vaccination results in the development of both a specific immune response to mycobacterial infections and nonspecific (heterologous) response, designated as trained immunity (TRIM), other pathogens. We hypothesized local immunization may induce an early bone marrow spleen innate cells. The transcriptomic various populations cells, including monocytes, neutrophils, natural killer (NK) was examined. To this end, C57Bl/6J mice were subcutaneously immunized with 106 CFU BCG. Three days following administration, three cell collected from control BCG-vaccinated groups using FACS. All obtained utilized for preparation sequencing RNA-seq libraries. analysis FACS data revealed increase proportion splenic NK cells monocytes 3 post-vaccination. Transcriptomic deregulation genes associated regulation (according Gene Ontology terms) unsorted Two cell-specific ligands (Tnfsf14 S100a8) two marrow-specific receptors (C5ar1 Csf2rb) identified among differentially expressed genes. No alterations neutrophils either their percentage or at level. Thus, study, we demonstrated provides murine populations, well non-sorted This be beneficial enhancing TRIM.

Language: Английский

Citations

0