bims-traimu Biomed News
on Trained immunity
Issue of 2025–06–01
thirteen papers selected by
Yantong Wan, Southern Medical University
  1. Lactate trains immunity.
  2. Trained immunity in diabetes: emerging targets for cardiovascular complications.
  3. Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity.
  4. β-Glucan modulates trained immunity to inhibit osteoclast differentiation via NOD2/RIPK2 signaling pathway.
  5. Redox-signaling in innate immune memory: Similar mechanisms in animals/humans and plants.
  6. The promoting effect of high-fat diet-induced trained immunity on ulcerative colitis and the mechanism of the therapeutic effect of Dahuang Mudan Decoction.
  7. Enteral immunization with live bacteria reprograms innate immune cells and protects neonatal foals from pneumonia.
  8. Dad's legacy: Epigenetic reprogramming and paternal inflammatory memory in offspring health.
  9. Time Course of Plasma Proteomic and Oxylipin Changes Induced by LPS Challenge and Modulated by Antioxidant Supplementation in a Randomized Controlled Trial.
  10. Phage-induced protection against lethal bacterial reinfection.
  11. Identification of a multiple DAMP scavenger mimicking the DAMP-binding site of TLR4 to ameliorate lethal sepsis.
  12. Multi-Omics and -Organ Insights into Energy Metabolic Adaptations in Early Sepsis Onset.
  13. Impact of thermoneutral acclimation on a murine model of polymicrobial peritonitis.
  1. Trends Immunol. 2025 May 26. pii: S1471-4906(25)00123-1. [Epub ahead of print]
    Lactate trains immunity.
    Alba Llibre, Claudio Mauro.
      Understanding the mechanisms implicated in the establishment of trained immunity could aid the design of novel therapeutic approaches. By studying Bacille Calmette-Guerin (BCG) vaccination in a human cohort, Ziogas and colleagues demonstrate the role of lactate generation and its use for histone lactylation as a key mechanism for establishing innate immune memory.
    DOI:  https://doi.org/10.1016/j.it.2025.05.002
  2. Front Endocrinol (Lausanne). 2025 ;16 1533620
    Trained immunity in diabetes: emerging targets for cardiovascular complications.
    Yanan Bai, Jianglan Wu, Weixiong Jian.
      Diabetes is a metabolic disorder primarily characterized by persistent hyperglycemia. Diabetes-induced inflammation significantly compromises cardiovascular health, greatly increasing the risk of atherosclerosis. The increasing prevalence of harmful lifestyle habits and overconsumption has contributed substantially to the global rise in diabetes-related cardiovascular diseases, creating a significant economic and healthcare burden. Although current therapeutic strategies focus on blood glucose control and metabolic regulation, clinical observations show that diabetic patients still face persistent residual risk of AS even after achieving metabolic stability. Recent studies suggest that this phenomenon is linked to diabetes-induced trained immunity. Diabetes can induce trained immunity in bone marrow progenitor cells and myeloid cells, thus promoting the long-term development of AS. This article first introduces the concept and molecular mechanisms of trained immunity, with particular emphasis on metabolic and epigenetic reprogramming, which plays a crucial role in sustaining chronic inflammation during trained immunity. Next, it summarizes the involvement of trained immunity in diabetes and its contribution to AS, outlining the cell types that can be trained in AS. Finally, it discusses the connection between diabetes-induced trained immunity and AS, as well as the potential of targeting trained immunity as an intervention strategy. Understanding the molecular mechanisms of trained immunity and their impact on disease progression may provide innovative strategies to address the persistent clinical challenges in managing diabetes and its complications.
    Keywords:  atherosclerosis; diabetes; epigenetics; inflammation; metabolism; trained immunity
    DOI:  https://doi.org/10.3389/fendo.2025.1533620
  3. Cancer Cell. 2025 May 28. pii: S1535-6108(25)00211-9. [Epub ahead of print]
    Microbial cancer immunotherapy reprograms hematopoiesis to enhance myeloid-driven anti-tumor immunity.
    Andrew W Daman, Anthony C Antonelli, Gil Redelman-Sidi, Lucinda Paddock, Shireen Khayat, Mythili Ketavarapu, Jin Gyu Cheong, Leonardo F Jurado, Anna Benjamin, Song Jiang, Dughan Ahimovic, Victoria R Lawless, Michael J Bale, Oleg Loutochin, Victor A McPherson, Maziar Divangahi, Rachel E Niec, Dana Pe'er, Eugene Pietzak, Steven Z Josefowicz, Michael S Glickman.
      Mycobacterium bovis Bacillus Calmette-Guérin (BCG) is the vaccine against tuberculosis and an immunotherapy for bladder cancer. When administered intravenously, BCG reprograms bone marrow hematopoietic stem and progenitor cells (HSPCs), leading to heterologous protection against infections. Whether HSPC reprogramming contributes to the anti-tumor effects of BCG administered into the bladder is unknown. We demonstrate that BCG administered in the bladder colonizes the bone marrow and, in both mice and humans, reprograms HSPCs to alter and amplify myelopoiesis. BCG-reprogrammed HSPCs are sufficient to confer augmented anti-tumor immunity through production of neutrophils, monocytes, and dendritic cells that broadly remodel the tumor microenvironment, drive T cell-dependent anti-tumor responses, and synergize with checkpoint blockade. We conclude that bladder BCG acts systemically through hematopoiesis, highlighting the broad potential of HSPC reprogramming to enhance the innate drivers of T cell-dependent tumor immunity.
    Keywords:  BCG; bladder cancer; epigenetics; hematopoiesis; immunotherapy; innate immune memory; trained immunity; tumor immunity
    DOI:  https://doi.org/10.1016/j.ccell.2025.05.002
  4. Int Immunopharmacol. 2025 May 26. pii: S1567-5769(25)00876-8. [Epub ahead of print]159 114886
    β-Glucan modulates trained immunity to inhibit osteoclast differentiation via NOD2/RIPK2 signaling pathway.
    Yanjie Li, Mingzhu Chen, Zhenjin Yang, Junxiong Li, Liya Ma, Guangyu Bao, Yanxia Chen, Jiangtian Hu.
       OBJECTIVE: This study investigated how β-glucan (BG)-induced trained immunity (TI) regulates osteoclast-driven bone resorption, with emphasis on the pivotal signaling axis governing this anti-resorptive memory.
    METHODS: Bone marrow-derived macrophages (BMMs) were primed with BG for 24 h and subsequently challenged with LPS to establish a TI model, validated by cytokine secretion profiling (IL-1β, IL-6, TNF-α). Osteoclastogenesis was induced by M-CSF/RANKL and assessed via TRAP staining, F-actin ring formation, immunofluorescence for CTSK/MMP-9, and bone resorption assays. Histological evaluation (H&E and TRAP staining) and micro-CT analysis were performed to assess alveolar bone remodeling in a murine periodontitis model. Transcriptomic profiling and functional validation using genetic/pharmacological perturbations identified critical signaling pathways.
    RESULTS: BG induced robust TI in macrophages under osteoclastogenic stimuli. Trained BMMs maintained long-term suppression of LPS-driven osteoclast reactivation. Systemic BG preconditioning preserved alveolar bone architecture in vivo. Complete abolition of BG's anti-osteoclastic effects by NOD2/RIPK2 blockade validated the mechanism.
    CONCLUSION: BG establishes innate immune memory through NOD2/RIPK2 signaling to counter pathological osteoclast activation, positioning TI modulation as a translational strategy against inflammatory bone loss.
    Keywords:  Bone marrow-derived macrophages (BMMs); Nucleotide-binding oligomerization domain-containing protein 2 (NOD2); Osteoclastogenesis; Receptor interacting protein kinase 2 (RIPK2); Trained immunity (TI); β-Glucan (BG)
    DOI:  https://doi.org/10.1016/j.intimp.2025.114886
  5. Redox Biol. 2025 May 27. pii: S2213-2317(25)00215-0. [Epub ahead of print]84 103702
    Redox-signaling in innate immune memory: Similar mechanisms in animals/humans and plants.
    Christian Lindermayr, Ali Önder Yildirim.
      Plants and animals/humans have evolved sophisticated innate immune systems to cope with microbial attack. Innate immunity implies the presence of membrane-located and intracellular receptors to recognize compounds released by damage or by invading pathogens. After detection the receptor molecules initiate intracellular defense signaling, resulting in cell death and/or production of defense molecules. Interestingly, the defense response includes also memory mechanisms, which allow the organisms to better cope with future microbial attacks. Redox mechanisms play an important role in defense signaling. In this review article, we compare the innate immune memory of animals/humans and plants and describe how reversible nitric oxide- and reactive oxygen species-dependent protein modifications enable the activation of defense signaling proteins and transcription factors and regulate the activity of chromatin modifying enzymes to establish innate immune memory. We hope to encourage efforts to characterize further molecular redox mechanisms of the innate immune memory, which might enable the development of new immunotherapies.
    Keywords:  Chromatin modulation; Innate immunity; Nitric oxide; Reactive oxygen species; Redox-signaling; Trained immunity
    DOI:  https://doi.org/10.1016/j.redox.2025.103702
  6. Phytomedicine. 2025 May 21. pii: S0944-7113(25)00531-8. [Epub ahead of print]143 156893
    The promoting effect of high-fat diet-induced trained immunity on ulcerative colitis and the mechanism of the therapeutic effect of Dahuang Mudan Decoction.
    Pengcheng Li, Rui Xu, Hongxu Chen, Shuiling Cao, Xueqian Xie, Bo Xu, Yunliang Chen, Xuting Xie, Caiyi Yang, Qing Wang, Xia Luo, Lian Zhou.
       BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory disease driven by intestinal immune imbalance. In addition, its pathogenesis includes environment, genetics, microbiota, genes, and diet. Epidemiological and related studies have shown that a high-fat diet habit can promote the progression of UC. The trained immunity induced by a high-fat diet is a key factor in the occurrence and development of chronic inflammatory diseases. As a chronic inflammatory disease, the research on how the trained immunity induced by a high-fat diet promotes the progression of UC is still unclear. Previous studies have shown that Dahuang Mudan Decoction can effectively alleviate the progression of UC, but whether its mechanism of action can also inhibit trained immunity is not clear.
    METHODS: To explore the promoting effect of trained immunity induced by a high-fat diet on UC, in this study, mice were fed a high-fat diet for 4 weeks and then modeled with 2 % DSS. Subsequently, by transplanting the bone marrow of a high-fat diet, it was repeatedly verified that a high-fat diet can promote the progression of UC through trained immunity. Then, to explore the therapeutic effect of Dahuang Mudan Decoction (DMD) and its mechanism, the above-mentioned model was intervened with DMD (125, 250, 500mg/kg). By transplanting the bone marrow of a high-fat diet and intervening with DMD, it was repeatedly verified that DMD can alleviate UC promoted by a high-fat diet by inhibiting trained immunity.
    RESULTS: The results of this study showed that the intervention of a high-fat diet promoted the progression of UC, aggravated the disease-related indicators of UC, promoted the damage of the colonic mucosal structure, reduced the expression of colonic mucin tight junction proteins, increased the number of bone marrow hematopoietic stem and progenitor cells (HSPCs), granulocyte-monocyte progenitor cells (GMPs), splenic monocytes, and colonic macrophages; promoted the expression of colonic inflammatory factors (IL-6, TNF-α). After transplanting the bone marrow intervention with a high-fat diet can promote the progression of UC, which is consistent with the trend of the above indicators. After the intervention of DMD, the above indicators were alleviated, and the subsequent transplantation of the bone marrow from a high-fat diet intervened with DMD can effectively alleviate the UC-related symptoms.
    CONCLUSION: A high-fat diet promotes the progression of UC disease by promoting trained immunity and increasing the proportion of bone marrow HSPCs and GMPs, thereby increasing the proportion of splenic monocytes, the number of colonic tissue macrophages, and the level of inflammatory factors. DMD can alleviate the inflammatory response of UC mice intervened with a high-fat diet by inhibiting bone marrow trained immunity.
    Keywords:  Bone marrow transplantation; Dahuang mudan decoction; High-fat diet; Trained immunity; Ulcerative colitis
    DOI:  https://doi.org/10.1016/j.phymed.2025.156893
  7. Sci Rep. 2025 May 25. 15(1): 18156
    Enteral immunization with live bacteria reprograms innate immune cells and protects neonatal foals from pneumonia.
    Bibiana Petri da Silveira, Susanne K Kahn, Rebecca M Legere, Jocelyne M Bray, Hannah M Cole-Pfeiffer, Michael C Golding, Noah D Cohen, Angela I Bordin.
      Using a horse foal model, we show that enteral immunization of newborn foals with Rhodococcus equi overcomes neonatal vaccination challenges by reprogramming innate immune responses, inducing R. equi-specific adaptive humoral and cell-mediated immune responses and protecting foals against experimental pneumonia challenge. Foals were immunized twice via gavage of R. equi (immunized group) or saline (control group) at ages 1 and 3 days. At age 28 days, all foals were challenged intrabronchially with R. equi. Post-challenge, all 5 immunized foals remained healthy, whereas 67% (4/6) of control foals developed clinical pneumonia. Immunized foals exhibit changes in the epigenetic profile of blood monocytes, > 1,000 differentially-expressed genes in neutrophils, higher concentrations of R. equi-specific IgG1 and IgG4/7, and a higher number of IFN-γ producing lymphocytes in response to R. equi stimulation indicating T helper type 1 response compared to control foals. Together, our data indicate that early life exposure to R. equi in the gastrointestinal tract can modulate innate immune responses, generate specific antibodies and cell-mediated immunity, and protect against pneumonia.
    Keywords:   Rhodococcus equi ; Horse; Infection; Trained Immunity; Vaccine
    DOI:  https://doi.org/10.1038/s41598-025-02060-5
  8. J Intern Med. 2025 May 29.
    Dad's legacy: Epigenetic reprogramming and paternal inflammatory memory in offspring health.
    Shamila D Alipoor, Parisa Norouzitallab, Anita Öst, Maria Lerm.
      Over the past decade, numerous reports have highlighted intergenerational and even transgenerational epigenetic effects resulting from parental exposure to diets, toxins, and stress. In many cases, these parentally induced phenotypes do not seem to confer an obvious benefit, making it challenging to understand the evolutionary drivers behind them. In this perspective, we discuss recent observations in humans and rodents indicating that a parental infection or vaccination can enhance the offspring's ability to cope with infections. Such parental priming of their offspring's immune system and cellular defense would provide immediate protection to the newborn, offering a clear evolutionary advantage. Here, focusing mainly on paternal effects, we propose that a parentally induced inflammatory memory in the offspring could be the underlying mechanism for many of the reported inter- and transgenerational effects. Sperm-borne RNA could be a triggering signal to initiate inflammatory pathways in early embryogenesis. This gene-regulatory state would then be maintained via epigenetic mechanisms throughout each mitosis and last for the individual's lifetime. The accumulating understanding that diet, stress, toxins, and infections affect offspring health raises important questions about public health policies. There is an urgent need to understand what consequences different exposures during sensitive time windows have on future generations.
    Keywords:  epigenetic; immunity; intergenerational; molecular genetics; sncRNA
    DOI:  https://doi.org/10.1111/joim.20094
  9. Antioxidants (Basel). 2025 Apr 29. pii: 536. [Epub ahead of print]14(5):
    Time Course of Plasma Proteomic and Oxylipin Changes Induced by LPS Challenge and Modulated by Antioxidant Supplementation in a Randomized Controlled Trial.
    Gerhard Hagn, Andrea Bileck, Thomas Mohr, Doreen Schmidl, David M Baron, Bernd Jilma, Leopold Schmetterer, Gerhard Garhöfer, Christopher Gerner.
      Systemic molecular responses to pathogen-associated molecular patterns and their modulation by antioxidants are poorly understood in humans. Here, we present a two-stage clinical interventional study in healthy humans challenged with lipopolysaccharide. In the first step, the kinetics of inflammatory modulators within 8 h were investigated by plasma proteomics and lipidomics. In a second step, the effects of a placebo-controlled antioxidant intervention on the individual responses prior to another lipopolysaccharide challenge were determined. Plasma proteomics revealed an early involvement of the endothelium and platelets, followed by the induction of liver-derived acute phase proteins and an innate immune cell response. Untargeted lipidomics revealed an early release of fatty acids and taurocholic acid, followed by complex regulatory events exerted by oxylipins. The consistent lipopolysaccharide-induced downregulation of lysophospholipids suggested the involvement of the Lands cycle, and the downregulation of deoxycholic acid reinforced emerging links between the inflammasome and bile acids. Groups of molecules with similar kinetics to lipopolysaccharide challenge were observed to share precursors, synthesizing enzymes or cellular origin. Dietary antioxidant supplementation prior to lipopolysaccharide challenge had no detectable effect on protein kinetics but significantly downregulated pro-inflammatory sphingosine-1-phosphate and increased levels of oxylipins, 20-HEPE, and 22-HDoHE, which have been described to facilitate the resolution of inflammation. The present study identified a complex network of lipid mediators deregulated in plasma upon lipopolysaccharide challenge and highlighted the role of platelets, endothelial cells, and erythrocytes as potential inflammatory modulators. While dietary antioxidant supplementation hardly affected the initiation of inflammation, it may exert its effects supporting the resolution of inflammation.
    Keywords:  Lands cycle; antioxidant supplementation; inflammation; lipids; lipopolysaccharide; oxylipins; proteomics; resolution of inflammation
    DOI:  https://doi.org/10.3390/antiox14050536
  10. Proc Natl Acad Sci U S A. 2025 Jun 03. 122(22): e2423286122
    Phage-induced protection against lethal bacterial reinfection.
    Yikun Xing, Haroldo J Hernandez Santos, Ling Qiu, Samantha R Ritter, Jacob J Zulk, Rachel Lahowetz, Kathryn A Patras, Austen L Terwilliger, Anthony W Maresso.
      Bacteriophages, or phages, are viruses that target and infect bacteria. Due to a worldwide rise in antimicrobial resistance (AMR), phages have been proposed as a promising alternative to antibiotics for the treatment of resistant bacterial infections. Up to this point in history, phage use in preclinical animal studies, clinical trials, and emergency-use compassionate care cases has centered around the original observation from 1915 showing phage as lytic agent, and thus a treatment that kills bacteria. Here, we describe an activity associated with phage therapy that extends beyond lytic activity that results in long-term protection against reinfection. This activity is potent, providing almost complete protection against a second lethal infection for animals treated with phage therapy. The activity also reduced infection burden an astounding billion-fold over the control. Reinfection protection requires phage lytic killing of its target bacterium but is independent of additional phage therapy. The effect is not driven by phage alone, lingering phage resistors, or a sublethal inoculum. In vitro phage-lysed bacteria provide partial protection, suggesting a combination of phage-induced lytic activity and immune stimulation by phage treatment is responsible for the effect. These observations imply certain phages may induce host adaptive responses following the lysis of the infecting bacteria. This work suggests phage therapy may contain a dual-action effect, an initial treatment efficacy followed by a long-term protection against reoccurring infection, a therapeutic-vaccination mechanism of action.
    Keywords:  ExPEC; immunity; phage therapy; sepsis
    DOI:  https://doi.org/10.1073/pnas.2423286122
  11. Front Immunol. 2025 ;16 1540908
    Identification of a multiple DAMP scavenger mimicking the DAMP-binding site of TLR4 to ameliorate lethal sepsis.
    Takuya Murao, Gaifeng Ma, Atsushi Murao, Alok Jha, Jingsong Li, Yongchan Lee, Mian Zhou, Ping Wang, Monowar Aziz.
      Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Current treatments are limited to source control and supportive care, underscoring the urgent need for novel therapeutic interventions. Endogenous molecules released from stressed or damaged cells, known as damage-associated molecular patterns (DAMPs), exacerbate inflammation, organ injury, and mortality in sepsis. In this study, we discovered a novel therapeutic compound, opsonic peptide 18 (OP18), designed to scavenge multiple DAMPs, including extracellular cold-inducible RNA-binding protein (eCIRP), high mobility group box 1 (HMGB1) and histone H3, by facilitating their clearance via macrophages. OP18 was developed by identifying a 15-amino acid (aa) binding site within the extracellular domain of Toll-like receptor 4 (TLR4) shared by eCIRP, HMGB1, and histone H3, then extending it with an αvβ3-integrin binding RGD (Arg-Gly-Asp) motif, resulting in an 18-aa peptide. Our data show that OP18 binds strongly to the above DAMPs and interacts with αvβ3-integrin on macrophages, promoting phagocytosis of DAMPs and facilitating their lysosomal degradation. In vitro, OP18 reduced the production of the inflammatory cytokine TNF-α in DAMP-activated macrophages and restored mitochondrial function, as evidenced by improved oxygen consumption rate (OCR) and ATP production. In a lethal sepsis model induced by cecal ligation and puncture (CLP), DAMP levels were significantly elevated, while OP18 treatment markedly reduced the serum DAMP levels. Additionally, OP18-treated septic mice demonstrated reduced blood organ injury markers, decreased proinflammatory cytokine levels, attenuated ALI, and improved survival. These findings establish OP18 as a promising therapeutic molecule that reduces DAMP-induced inflammation, offering a potential strategy to improve outcomes in lethal sepsis.
    Keywords:  DAMPs; H3; HMGB1; eCIRP; macrophage; phagocytosis; sepsis
    DOI:  https://doi.org/10.3389/fimmu.2025.1540908
  12. Adv Sci (Weinh). 2025 May 24. e04418
    Multi-Omics and -Organ Insights into Energy Metabolic Adaptations in Early Sepsis Onset.
    Lin-Lin Xu, Zhengyuan Zhou, Sascha Schäuble, Wolfgang Vivas, Karen Dlubatz, Michael Bauer, Sebastian Weis, Mervyn Singer, Roman Lukaszewski, Gianni Panagiotou.
      Systemic metabolic dysregulation in sepsis critically impacts patient survival. To better understand its onset, untargeted serum metabolomics and lipidomics are analyzed from 152 presymptomatic patients undergoing major elective surgery, and identified key metabolites, including serine and aminoadipic acid, that differentiate postoperative uncomplicated infection from sepsis. Using single-nucleus RNA sequencing data from an in vivo mouse model of sepsis, tissue-independent down-regulation and tissue-specific differences of serine and energy-related genes including key module roles for the mitochondria-linked genes, Cox4i1, Cox8a, and Ndufa4 are identified. Finally, serine-dependent metabolic shifts, especially in the liver, are revealed by using 12C/13C murine data with labeled serine, and link altered activity of the serine hydroxymethyltransferase (SHMT) cycle with perturbed purine metabolism during sepsis. This study demonstrates the close interrelationship between early metabolite changes and mitochondrial dysfunction in sepsis, improves the understanding of the underlying pathophysiology, and highlights metabolic targets to prospectively treat presymptomatic, but at-risk, patients.
    Keywords:  cell–cell communication; energy imbalance; lipid metabolism; metabolic modeling; sepsis biomarkers; single‐nucleus RNA sequencing (snRNA‐Seq)
    DOI:  https://doi.org/10.1002/advs.202504418
  13. PLoS One. 2025 ;20(5): e0322855
    Impact of thermoneutral acclimation on a murine model of polymicrobial peritonitis.
    Goldia Chan, Christopher Fry, Jean Nemzek.
      To examine the effects of ambient temperature on the reproducibility and translation of a murine sepsis model, we hypothesized that acclimation of mice in temperatures within their thermoneutral zone would alter immune responses and outcomes compared to standard housing temperatures. Mice housed for one week in thermoneutral (30°C) as compared to standard (22°C) conditions displayed lower counts of circulating neutrophils (0.52 ± 0.20 vs. 1.10 ± 0.54 x103/μL; p = 0.011) and peritoneal macrophages (0.80 ± 0.57 vs. 1.62 ± 0.62 x 105/μL; p = 0.002) as well as reduced in vitro production of IFN-γ by stimulated splenocytes (0.38 ± 0.68 vs 2.55 ± 0.76 x104 pg/mL, respectively, p = 0.004). After one week of temperature acclimation followed by CLP, the 7-day mortality was significantly lower under thermoneutral as compared to standard temperatures (80% vs 30%, respectively; p = 0.012), although core body temperature was preserved (average for 24 hours: 36.4 ± 1.3°C vs 31.7 ± 4.7°C; p < 0.0001). The lower survival was accompanied by increased systemic IL-6 levels (3.8 ± 3.3 vs 1.9 ± 1.3 x103 pg/mL; p = 0.04) and less robust influx of neutrophils into the peritoneum (1.68 ± 1.07 vs. 4.20 ± 2.46 x105/μL, respectively; p = 0.0003). Overall, thermoneutral temperatures impacted innate immune parameters before and after CLP, producing distinctly different outcomes. Therefore, ambient temperature is an important variable that could impact model reproducibility and should be reported for the acclimation period and experimentation phases of murine sepsis studies.
    DOI:  https://doi.org/10.1371/journal.pone.0322855
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