bims-traimu Biomed News
on Trained immunity
Issue of 2025–03–23
eight papers selected by
Yantong Wan, Southern Medical University
  1. Immune Memory: A New Frontier in Treating Recurrent Inflammatory Skin Diseases.
  2. Trained Immunity: Can We Get One Transplanted Kidney to Last a Lifetime?
  3. Trained immunity-based mucosal immunotherapies for the prevention of respiratory infections.
  4. Immunometabolic effects of β-glucan-trained immunity in newborn goats.
  5. Weight loss-induced adipose macrophage memory corresponds with lower adipose bacterial burden in murine systemic Staphylococcus aureus infection.
  6. Recycling dead bacteria to fuel macrophage immunometabolism.
  7. Adiponectin pathway activation dampens inflammation and enhances alveolar macrophage fungal killing via LC3-associated phagocytosis.
  8. Neutrophil extracellular trap-derived double-stranded RNA aggravates PANoptosis in renal ischemia reperfusion injury.
  1. Clin Rev Allergy Immunol. 2025 Mar 18. 68(1): 31
    Immune Memory: A New Frontier in Treating Recurrent Inflammatory Skin Diseases.
    Hang Yin, Jianru Chen, Chunying Li.
      The recurrence of inflammatory skin diseases represents a significant challenge in clinical practice, primarily mediated by immune memory. In inflammatory skin diseases, immune memory encompasses adaptive immune memory, trained immunity, and inflammatory memory, which are conducted by adaptive immune cells, innate immune cells, and structural cells, respectively. Adaptive immune memory is established through gene rearrangement, leading to antigen-specific immune memory. In contrast, trained immunity and inflammatory memory are formed through epigenetic and metabolic reprogramming, resulting in non-specific immune memory. Different types of immune memory work synergistically to aggravate localized inflammation in recurrent inflammatory skin diseases. However, immune memory in specific cells, such as macrophages, may also play an immunoregulatory role under certain conditions. We reviewed the immune memory mechanisms in different inflammatory skin diseases and discussed future strategies for targeted regulation of the molecular mechanisms underlying immune memory, such as targeted biological agents and epigenetic modifications. Additionally, we explored the potential for precise regulation of immune memory and its application in personalized treatment for recurrent inflammatory skin diseases.
    Keywords:  Immune memory; Inflammatory memory; Inflammatory skin diseases; Trained immunity
    DOI:  https://doi.org/10.1007/s12016-025-09039-0
  2. Am J Transplant. 2025 Mar 17. pii: S1600-6135(25)00144-3. [Epub ahead of print]
    Trained Immunity: Can We Get One Transplanted Kidney to Last a Lifetime?
    Lara C Pullen.
      
    DOI:  https://doi.org/10.1016/j.ajt.2025.03.015
  3. Trends Immunol. 2025 Mar 19. pii: S1471-4906(25)00055-9. [Epub ahead of print]
    Trained immunity-based mucosal immunotherapies for the prevention of respiratory infections.
    Luna Minute, Karla Montalbán-Hernández, Laura Bravo-Robles, Laura Conejero, Salvador Iborra, Carlos Del Fresno.
      The devastating impact of respiratory infections demonstrates the critical need for novel prophylactic vaccines. In this opinion article, we advocate for bacterial immunotherapies as a complementary tool in our fight against respiratory infections. These immunotherapies can activate a wide spectrum of immunological mechanisms, with trained immunity (TI) being particularly significant. This phenomenon has led to the concept of trained immunity-based vaccines (TIbVs), which represent a novel approach in vaccinology. We discuss examples of TIbVs, including the tuberculosis vaccine Bacille Calmette-Guérin (BCG) and the polybacterial immunotherapy MV130. From our viewpoint, illustrating the mode of action and clinical evidence supports the proposal that TIbVs should be considered as next-generation vaccines to confer protection against a wide range of respiratory infections.
    Keywords:  BCG; MV130; TIbVs; innate immune memory; mucosal immunotherapy; trained immunity
    DOI:  https://doi.org/10.1016/j.it.2025.02.012
  4. Res Vet Sci. 2025 Mar 16. pii: S0034-5288(25)00086-4. [Epub ahead of print]187 105612
    Immunometabolic effects of β-glucan-trained immunity in newborn goats.
    Miriam Angulo, Carlos Angulo.
      Debaryomyces hansenii CBS 8339 β-glucans induced trained immunity in newborn goats. However, the metabolic shifts and potential signaling pathways have not been described yet. Thus, the present study aims to prove, firstly, modifications in cell metabolism related to trained immunity induction (β-glucans) and inhibition (MCC950) in an in vitro model upon lipopolysaccharide (LPS) re-stimulation; secondly, metabolic changes and possible signaling pathways are related to immune memory induced by β-glucan per os in newborns after ex vivo re-stimulation with a bacterial pathogen. Immune training leads to augmenting glycolysis (glucose and lactate) metabolites. Nevertheless, these changes were unaffected by a NOD-like receptor (NLRP3) inhibitor. In vivo training with oral β-glucan doses also evidenced an increase in glycolysis metabolites mediated by up-regulating AKT/MTOR/HIF1Α genes signaling pathway in monocytes; β-glucan in vivo training up-regulated Dectin1, TLR4, TLR6 RAF1, IL1Β and IL6 gene expressions in monocytes, while TNFΑ gene down-regulated. In conclusion, the results demonstrated that D. hansenii β-glucan induced trained immunity in newborn goat monocytes after LPS re-stimulation through glycolysis shifts, which were not reverted by the MCC950 inhibitor.
    Keywords:  Animal health; Functional carbohydrates; Memory in innate leukocytes; Metabolic shift
    DOI:  https://doi.org/10.1016/j.rvsc.2025.105612
  5. Shock. 2025 Mar 03.
    Weight loss-induced adipose macrophage memory corresponds with lower adipose bacterial burden in murine systemic Staphylococcus aureus infection.
    McArthur Bolden, Xenia D Davis, Munira Kapadia, Emily Nguyen, Edward R Sherwood, Julia K Bohannon, Heather L Caslin.
       ABSTRACT: Different stimuli can induce innate immune memory to improve pathogen defense or worsen cardiometabolic disease. However, it is less clear if the same stimuli can induce both the protective and detrimental effects of innate immune memory. Weight loss following high fat diet feeding induces innate immune memory in adipose macrophages that correlates with worsened diabetes risk after weight regain. Here, we investigated the effect of weight gain and loss on adipose macrophage memory and infection outcomes in systemic Staphylococcus aureus infection in C57Bl/6 J male mice. Lean controls remained on low-fat diet, weight gain mice started on low-fat diet and were moved to high-fat for 9 weeks, and weight loss mice began on high-fat diet for 9 weeks before moving to low-fat diet for 9 weeks. At 18 weeks, functional analyses were performed on adipose macrophages from each group of mice. Weight loss increased cytokine production and reactive oxygen species compared to lean controls. The remaining mice were infected intravenously with 2.5x10^8 colony forming units S.aureus. There was no effect of weight change on survival, however, weight gain reduced body temperature and increased sepsis scoring, blood neutrophils, and bacterial burden in the kidney. Weight loss increased plasma tumor necrosis factor (TNF-α) and adipose macrophage cytokine production that correlated with reduced bacterial burden in the adipose tissue. Thus, weight loss restores systemic infection defenses that are impaired with weight gain, and weight loss-induced adipose macrophage memory may further reduce local S. aureus growth. Collectively, innate immune memory to weight loss may be protective in local anti-microbial defense.
    DOI:  https://doi.org/10.1097/SHK.0000000000002575
  6. Nat Immunol. 2025 Mar 19.
    Recycling dead bacteria to fuel macrophage immunometabolism.
    Shane M O'Carroll, Luke A J O'Neill.
      
    DOI:  https://doi.org/10.1038/s41590-025-02117-7
  7. PLoS Pathog. 2025 Mar 17. 21(3): e1012363
    Adiponectin pathway activation dampens inflammation and enhances alveolar macrophage fungal killing via LC3-associated phagocytosis.
    Sri Harshini Goli, Joo-Yeon Lim, Nese Basaran-Akgul, Steven P Templeton.
      Although innate immunity is critical for antifungal host defense against the human opportunistic fungal pathogen Aspergillus fumigatus, potentially damaging inflammation must be controlled. Adiponectin (APN) is an adipokine produced mainly in adipose tissue that exerts anti-inflammatory effects in adipose-distal tissues such as the lung. We observed increased mortality and increased fungal burden and inflammation in neutropenic mice with invasive aspergillosis (IA) that lack APN or the APN receptors AdipoR1 or AdipoR2. Alveolar macrophages (AMs), early immune sentinels that detect and respond to lung infection, express both receptors, and APN-deficient AMs exhibited an inflammatory phenotype that was associated with decreased fungal killing. Pharmacological stimulation of AMs with AdipoR agonist AdipoRon rescued deficient killing in APN-/- AMs and was dependent on the presence of either receptor. Finally, APN-enhanced fungal killing was associated with increased activation of the non-canonical LC3 pathway of autophagy. Thus, our study identifies a novel role for APN in LC3-mediated killing of A.fumigatus.
    DOI:  https://doi.org/10.1371/journal.ppat.1012363
  8. Cell Commun Signal. 2025 Mar 17. 23(1): 140
    Neutrophil extracellular trap-derived double-stranded RNA aggravates PANoptosis in renal ischemia reperfusion injury.
    Shaoyong Zhuang, Fangzhou Li, Liya Wang, Zilong Lai, Dawei Li, Haoyu Wu, Jiajin Wu, Junwen Qu, Xianyun Zhang, Ming Zhang, Ruoyang Chen, Xiaodong Yuan.
      A dysregulated inflammatory response and inflammation-associated cell death are central features of renal ischemia-reperfusion injury (IRI). PANoptosis, is a recently recognized form of inflammatory programmed cell death characterized by key features of pyroptosis, apoptosis and necroptosis; however, the specific involvement of PANoptosis in renal IRI remains unknown. By using neutrophil extracellular trap (NETs)-depleted Pad4-/- mice, we found that NETs are essential for exacerbating tissue injury in renal IRI. Single-cell RNA sequencing (scRNA-seq) revealed that IRI promoted PANoptosis signalling in proximal tubular epithelial cells (PTs), whereas PAD4 knockout inhibited PANoptosis signalling. PTs expressed mainly RIPK1-PANoptosomes, which executed NET-induced PANoptosis in PTs in renal IRI model mice. Mechanistically, NET-derived double-stranded RNA (dsRNA) promoted PANoptosis in PTs, and PT-expressed TLR3 was responsible for the sensing the extracellular dsRNA. Treating mice with chemical inhibitors of the dsRNA/TLR3 complex suppressed PANoptosis and alleviated tissue injury in renal IRI. Together, the results of this study reveal a mechanism by which the NET-dsRNA-TLR3 axis aggravates PT cell PANoptosis in renal IRI.
    DOI:  https://doi.org/10.1186/s12964-025-02145-8
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