bims-bac4me Biomed News
on Microbiome and trained immunity
Issue of 2025–07–13
seventeen papers selected by
Chun-Chi Chang, Lunds universitet
  1. β-Glucan reprograms alveolar macrophages via neutrophil/IFNγ axis in a murine model of lung injury.
  2. Long-term DNA methylation changes mediate heterologous cytokine responses after BCG vaccination.
  3. Trained Innate Immunity.
  4. Upper vs. lower airways: Microbes shape the local milieu.
  5. Waste as an antibacterial weapon.
  6. Succinate Dehydrogenase Regulates Homeostasis and Metabolic Integrity of Alveolar Macrophages.
  7. Microbial-induced trained immunity for cancer immunotherapy.
  8. Trained immunity of osteoclasts controls inflammatory arthritis.
  9. How hosts accurately command bacteria for gut health.
  10. BCG plus β-glucan trains neutrophils to beat bladder cancer.
  11. Pattern recognition receptors: function, regulation and therapeutic potential.
  12. Quantifying the intra- and inter-species community interactions in microbiomes by dynamic covariance mapping.
  13. The host response to influenza infections in human lung and macrophages cell lines.
  14. Transcriptional programs underlying human monocyte differentiation and diversity.
  15. Lacticaseibacillus paracasei strain Shirota suppresses upper respiratory tract infections and activates mononuclear phagocytic cells in healthy Japanese office workers: a randomized, double-blind, controlled trial.
  16. Theory of host-microbe symbioses: Challenges and opportunities.
  17. Native Lactobacillus and Bifidobacterium probiotics modulate autophagy genes and exert anti-inflammatory effect.
  1. Elife. 2025 Jul 08. pii: RP102068. [Epub ahead of print]13
    β-Glucan reprograms alveolar macrophages via neutrophil/IFNγ axis in a murine model of lung injury.
    Renaud Prevel, Erwan Pernet, Kim A Tran, Abderrahmane Sadek, Mina Sadeghi, Elizabeth Lapshina, Leonardo F Jurado, Arnold S Kristof, Mohieddine Moumni, Jeremie Poschmann, Maziar Divangahi.
      Alveolar macrophages (AMs) reside in the lower airways and play a crucial role in lung health and response to sterile inflammation and infections. AMs possess remarkable adaptability to different environmental challenges that can persist through their memory capacity (trained immunity). β-Glucan has been characterized as a potent inducer of central trained immunity by reprogramming haematopoietic stem cells in the bone marrow. In the present study, we show that systemic administration of β-glucan in mice induces peripheral trained immunity by reprogramming AMs in the lungs, in a Dectin1-independent manner. We furthermore demonstrate that AM reprogramming at both the transcriptional and metabolic levels exacerbate lung injury following bacterial (lipopolysaccharide) or viral (polyI:C) challenges via a neutrophil/IFN-γ-dependent manner. These findings identify an additional facet of β-glucan in trained immunity involving AM reprogramming and shed light on the potential detrimental effects of trained immunity.
    Keywords:  acute lung injury; immunology; inflammation; mouse; trained immunity; β-glucan
    DOI:  https://doi.org/10.7554/eLife.102068
  2. Genome Biol. 2025 Jul 09. 26(1): 180
    Long-term DNA methylation changes mediate heterologous cytokine responses after BCG vaccination.
    Cancan Qi, Zhaoli Liu, Gizem Kilic, Andrei S Sarlea, Priya A Debisarun, Xuan Liu, Yonatan Ayalew Mekonnen, Wenchao Li, Martin Grasshoff, Ahmed Alaswad, Apostolos Petkoglou, Valerie A C M Koeken, Simone J C F M Moorlag, L Charlotte J de Bree, Vera P Mourits, Leo A B Joosten, Yang Li, Mihai G Netea, Cheng-Jian Xu.
       BACKGROUND: Epigenetic reprogramming shapes immune memory in both innate (trained immunity) and adaptive immune cells following Bacillus Calmette-Guérin (BCG) vaccination. However, the role of dynamic DNA methylation changes in post-vaccination immune responses remains unclear.
    RESULTS: We established a cohort of 284 healthy Dutch individuals, profiling genome-wide DNA methylation and cytokine responses to ex vivo stimulation at baseline, 14 days, and 90 days post-BCG vaccination. We identified distinct patterns of DNA methylation alternations in the short- and long-term following BCG vaccination. Moreover, we established that baseline DNA methylation profiles exert influence on the change in interferon-γ (IFN-γ) production upon heterologous (Staphylococcus aureus) stimulation before and after BCG vaccination. Specifically, we identified the regulation of kisspeptin as a novel pathway implicated in the modulation of IFN-γ production, and this finding has been substantiated through experimental validation. We also observed associations between BCG-induced DNA methylation changes and increased IFN-γ and interleukin-1 β (IL-1β) production upon S. aureus stimulation. Interestingly, by integrating with genetic, epigenetic, and cytokine response data from the same individuals, mediation analysis demonstrated that most of the identified DNA methylation changes played a mediating role between genetic variants and cytokine responses; for example, the changes of cg21375332 near SLC12 A3 gene mediated the regulation of genetic variants on IFN-γ changes after BCG vaccination. Sex-specific effects were observed in DNA methylation and cytokine responses, highlighting the importance of considering sex in immune studies.
    CONCLUSIONS: These findings provide deeper insights into immune response mechanisms, crucial for developing effective epigenetic-based medical interventions for personalized medicine.
    Keywords:  BCG vaccination; Cytokines response; DNA methylation; Systems biology; Trained immunity
    DOI:  https://doi.org/10.1186/s13059-025-03611-9
  3. Adv Exp Med Biol. 2025 ;1476 275-296
    Trained Innate Immunity.
    Sayanti Pal, Zaina Rafiq, Rekha Kumari, Ahmad Al Aiyan, Basel Al-Ramadi, Uday Kishore, Pretty Ponnachan.
      Recent research has increasingly highlighted the adaptive characteristics of the innate immune system, revealing its capacity for a heterologous memory of previous infections. Allergen-specific immunotherapy (AIT) has demonstrated that innate immune cells, such as monocytes, macrophages, and natural killer (NK) cells, can provide protection against specific diseases even in the absence of lymphocyte support. The mechanisms underlying innate host defense and the immunological memory of adaptive immunity differ significantly in terms of cellular populations and molecular pathways. Prototypical innate immune cells, including NK cells and monocytes/macrophages, contribute to the sustained heightened state of innate immunity known as "trained immunity," which enhances resistance to secondary infections. Trained immunity is typically initiated through the engagement of pattern recognition receptors (PRRs) by microbial structures, suggesting that vaccines designed to induce trained immunity should incorporate appropriate PRR ligands. This approach not only offers protection against reinfection in a manner independent of T and B cells but also promotes nonspecific epigenetic reprogramming that enhances immune responses. For instance, Bacillus Calmette-Guérin (BCG) vaccination has been linked to long-lasting immune modifications associated with a non-specific immune response to various infections, characterized by heterologous T helper 1 (Th1) and Th17 responses. Emerging evidence indicates that heat-killed Mycobacterium manresensis can induce trained immunity in vitro, although its effectiveness in vivo remains to be fully established. This highlights the potential of novel strategies in vaccine development, particularly through the lens of trained immunity. The concept of trained immunity-based vaccines (TIbV) presents a paradigm shift in immunization strategies, as these vaccines can elicit broad-spectrum protection against a variety of pathogens. By leveraging the principles of trained immunity, TIbV can enhance both innate and adaptive immune responses, potentially improving the efficacy of conventional vaccines and offering new avenues for immunotherapy.The integration of trained innate immunity into vaccine development holds significant promise for enhancing immune protection against infectious diseases. By harnessing the principles of trained immunity, these innovative vaccines can enhance innate immune responses, potentially improving protection against a wide range of infectious diseases and contributing to better public health outcomes.
    DOI:  https://doi.org/10.1007/978-3-031-85340-1_11
  4. Cell Host Microbe. 2025 Jul 09. pii: S1931-3128(25)00236-7. [Epub ahead of print]33(7): 1043-1045
    Upper vs. lower airways: Microbes shape the local milieu.
    Shifen Xu, Zhang Wang.
      In this issue of Cell Host & Microbe, Wong et al. investigate the contribution of the microbiome to airway metabolism, revealing differential microbial pathways and metabolites between the upper and lower airways. Oral commensals contribute to the metabolic milieu with Prevotella melaninogenica synthesizing inosine and glutamate in the lower airways.
    DOI:  https://doi.org/10.1016/j.chom.2025.06.007
  5. Cell Host Microbe. 2025 Jul 09. pii: S1931-3128(25)00240-9. [Epub ahead of print]33(7): 1045-1047
    Waste as an antibacterial weapon.
    M Maria Elgrail, Michael S Glickman.
      Intracellular pathogens neutralize and evade macrophage-intrinsic host defenses. In this issue of Cell Host & Microbe, Anaya-Sanchez et al. show that methylglyoxal, a metabolic byproduct of glycolysis, is part of the macrophage arsenal limiting L. monocytogenes and M. tuberculosis infections but is countered by pathogen expression of methylglyoxal detoxification enzymes.
    DOI:  https://doi.org/10.1016/j.chom.2025.06.011
  6. Immune Netw. 2025 Jun;25(3): e16
    Succinate Dehydrogenase Regulates Homeostasis and Metabolic Integrity of Alveolar Macrophages.
    Seung Geun Song, Ein Lee, Jaemoon Koh, Doo Hyun Chung.
      Lung tissue-resident macrophages, including alveolar macrophages (AMs) and interstitial macrophages (IMs), are pivotal in maintaining both immune defense and tissue homeostasis. Although the distinct functional roles of these macrophage populations are well recognized, the specific metabolic pathways that support their functions are not fully understood. Comparative RNA sequencing analysis identified Sdha, a key enzyme in mitochondrial metabolism, as one of the most highly expressed and differentially regulated genes involved in metabolic pathways in AMs relative to IMs. This finding led us to investigate the role of succinate dehydrogenase complex subunit A (SDHA) in regulating AM metabolism and function. Here, we demonstrated that SDHA is crucial for maintaining AM homeostasis. Deletion of SDHA resulted in a significant reduction in AM populations without affecting IMs, highlighting an AM-specific requirement for SDHA. In the absence of SDHA, AMs underwent metabolic reprogramming towards glycolysis compared with IMs, along with significant transcriptional changes and cell death. Furthermore, SDHA-deficient AMs showed lipid accumulation and increased endoplasmic reticulum stress. These findings establish SDHA as a crucial regulator of AM metabolism and underscore the importance of maintaining metabolic integrity for AM function and survival within the lung microenvironment.
    Keywords:  Alveolar macrophages; Homeostasis; Metabolic reprogramming; Mitochondria; Succinate dehydrogenase
    DOI:  https://doi.org/10.4110/in.2025.25.e16
  7. Pharmacol Rev. 2025 Jun 12. pii: S0031-6997(25)07482-4. [Epub ahead of print]77(5): 100074
    Microbial-induced trained immunity for cancer immunotherapy.
    Patricia Vuscan, Brenda Kischkel, Leo A B Joosten, Mihai G Netea.
      Myeloid innate immune cells, including macrophages, neutrophils, myeloid-derived suppressor cells, and dendritic cells, represent major components of the tumor microenvironment (TME), exhibiting remarkable plasticity and dual roles in cancer progression and immune regulation. In recent years, microbial-induced innate immune memory, also termed "trained immunity" (TRIM), has emerged as a novel strategy to reprogram myeloid cells into an immunostimulatory, antitumor state. In this review, we explore the intricate landscape of myeloid cells in cancer and examine how microbial ligands, such as the Bacillus Calmette-Guérin vaccine and β-glucan, reprogram both bone marrow progenitors and tissue-resident myeloid cells to enhance inflammatory and antitumor responses. Notable findings include the hematopoietic stem and progenitor cell reprogramming by Bacillus Calmette-Guérin for sustained anticancer immunity, and the enhanced granulopoiesis and neutrophil-mediated tumor killing mediated by β-glucan-induced TRIM. These mechanisms synergize with immunotherapies, such as immune checkpoint inhibitors, by reshaping the immunosuppressive TME and enhancing adaptive immunity. However, challenges remain, including the structural complexity of microbial products, the lack of predictive biomarkers, and the need for optimized dosing and delivery strategies. Addressing these gaps by introducing precise characterization of microbial-derived ligands, biomarker-driven patient selection through large-scale clinical trials, as well as the development of novel approaches for targeted therapy will be essential to harness the full potential of microbial-induced TRIM, ultimately paving the way for more effective and durable cancer immunotherapies. SIGNIFICANCE STATEMENT: Tumor-promoting myeloid cells within the tumor microenvironment remain a major barrier to effective cancer immunotherapy. Microbial-induced trained immunity offers a novel strategy to reprogram myeloid cells into an antitumor state. This review provides a comprehensive overview of myeloid cell populations in cancer and the mechanisms underlying microbial-induced trained immunity. It also highlights preclinical and clinical evidence demonstrating the efficacy of microbial-based strategies in overcoming immunosuppression and synergizing with existing immunotherapies, offering a promising approach to improve cancer treatment outcomes.
    DOI:  https://doi.org/10.1016/j.pharmr.2025.100074
  8. Dev Cell. 2025 Jul 07. pii: S1534-5807(25)00259-X. [Epub ahead of print]60(13): 1813-1815
    Trained immunity of osteoclasts controls inflammatory arthritis.
    I E Adamopoulos.
      In this issue of Developmental Cell, Haacke et al. demonstrate that osteoclasts undergo innate immune training, resulting in increased bone resorption and exacerbation of arthritis. These data highlight the complexity of inflammatory osteoclast precursors and costimulatory pathways in arthritis and open new research avenues in the ever-growing field of osteoimmunology.
    DOI:  https://doi.org/10.1016/j.devcel.2025.04.021
  9. Cell Host Microbe. 2025 Jul 09. pii: S1931-3128(25)00237-9. [Epub ahead of print]33(7): 1033-1035
    How hosts accurately command bacteria for gut health.
    Jianglin Zhang, Xianda Ma, Zheng Kuang.
      Amid the vast "ocean" of gut microbes, how hosts distinguish and respond to specific symbionts remains elusive. In a recent issue of Nature, Yang et al. show that host APOL proteins selectively engage Bacteroidales to trigger outer membrane vesicle release, illuminating a host-microbe mutualism that sustains gut immune homeostasis.
    DOI:  https://doi.org/10.1016/j.chom.2025.06.008
  10. Nat Rev Immunol. 2025 Jul 07.
    BCG plus β-glucan trains neutrophils to beat bladder cancer.
    Lucy Bird.
      
    DOI:  https://doi.org/10.1038/s41577-025-01209-7
  11. Signal Transduct Target Ther. 2025 Jul 11. 10(1): 216
    Pattern recognition receptors: function, regulation and therapeutic potential.
    Ruochan Chen, Ju Zou, Jiawang Chen, Xiao Zhong, Rui Kang, Daolin Tang.
      Pattern recognition receptors (PRRs) are sensors in the immune system, detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). They serve as essential links between the innate and adaptive immune responses, initiating defense mechanisms against pathogens and maintaining immune homeostasis. This review examines the classification, structure, and signaling cascades of key PRR families, including toll-like receptors (TLRs), C-type lectin receptors (CLRs), nucleotide-binding oligomerization domain-like receptors (NLRs), AIM2-like receptors (ALRs), and others. It explores the dual roles of PRRs in immune defense and regulation, particularly through inhibitory PRRs (iPRRs), which prevent immune overactivation. The review also investigates the ligand recognition mechanisms and signaling pathways, highlighting the involvement of PRRs in disease progression and immune modulation. Notable signaling pathways, including NF-κB, MAPK, cGAS-STING, and MYD88-mediated and non-MYD88-mediated cascades, are discussed in the context of immune responses. Mechanisms that fine-tune PRR-mediated responses include transcriptional and fpost-transcriptional regulation, protein degradation, subcellular localization, and the recruitment of amplifiers and inhibitors, along with metabolic and microbial factors. These regulatory strategies ensure immune signaling remains adaptable and precise, preventing excessive inflammation. The review also explores the therapeutic potential of targeting PRRs in treating infectious, inflammatory, autoimmune, and malignant diseases, underscoring their importance in advancing immunological research and precision medicine.
    DOI:  https://doi.org/10.1038/s41392-025-02264-1
  12. Nat Commun. 2025 Jul 09. 16(1): 6314
    Quantifying the intra- and inter-species community interactions in microbiomes by dynamic covariance mapping.
    Melis Gencel, Gisela Marrero Cofino, Cang Hui, Zahra Sahaf, Louis Gauthier, Chloé Matta, David Gagné-Leroux, Derek K L Tsang, Dana P Philpott, Sheela Ramathan, Alfredo Menendez, Shimon Bershtein, Adrian W R Serohijos.
      A microbiome's composition, stability, and response to perturbations are governed by its community interaction matrix, typically quantified through pairwise competition. However, in natural environments, microbes encounter multispecies interactions, complex conditions, and unculturable members. Moreover, evolutionary and ecological processes occur on overlapping timescales, making intra-species clonal diversity a critical but poorly understood factor influencing community interactions. Here, we present Dynamic Covariance Mapping (DCM), a general approach to infer microbiome interaction matrices from abundance time-series data. By combining DCM with high-resolution chromosomal barcoding, we quantify inter- and intra-species interactions during E. coli colonization in the mouse gut under three contexts: germ-free, antibiotic-perturbed, and innate microbiota. We identify distinct temporal phases in susceptible communities: (1) destabilization upon E. coli invasion, (2) partial recolonization of native bacteria, and (3) a quasi-steady state where E. coli sub-lineages coexist with resident microbes. These phases are shaped by specific interactions between E. coli clones and community members, emphasizing the dynamic and lineage-specific nature of microbial networks. Our results reveal how ecological and evolutionary dynamics jointly shape microbiome structure over time. The DCM framework provides a scalable method to dissect complex community interactions and is broadly applicable to bacterial ecosystems both in vitro and in situ.
    DOI:  https://doi.org/10.1038/s41467-025-61368-y
  13. BMC Genom Data. 2025 Jul 08. 26(1): 46
    The host response to influenza infections in human lung and macrophages cell lines.
    Carmen Aguilar, Ruth Lydia Olga Lambertz, Mark Heise, Ana Eulalio, Klaus Schughart.
       OBJECTIVE: The innate immune response of an infected host is an essential defense mechanism to fight influenza virus infections in the respiratory tract. This response is essential to limit virus replication and spread. However, an exacerbated response may cause severe immune-pathologies. Therefore, it is very important to better understand innate immune responses at the level of its molecular networks in the context of viral infections.
    DATA: We infected human lung adenocarcinoma (A549) and human monocytic (THP-1) cells with H3N2 influenza virus A virus and performed transcriptome analysis using next generation RNA sequencing at various times post infection. We report raw sequence data and normalized log2 transformed gene expression values. This data will allow researchers in the field to identify differentially expressed genes and pathways between the two cell types and over times post infection. Furthermore, our data enables comparisons to molecular studies performed in humans and animal models in the context of respiratory viral infections.
    Keywords:  Human; Influenza; Lung cells; Macrophage; Transcriptome
    DOI:  https://doi.org/10.1186/s12863-025-01341-2
  14. J Leukoc Biol. 2025 Jul 09. pii: qiaf058. [Epub ahead of print]117(7):
    Transcriptional programs underlying human monocyte differentiation and diversity.
    Ravi K Komaravolu, Daniel J Araujo, Catherine C Hedrick, Ahmad Alimadadi.
      Classical monocytes (CD14hiCD16-) differentiate into intermediate monocytes (CD14+CD16+), which in turn yield nonclassical monocytes (CD14-CD16hi). To investigate the transcriptional regulation underlying this differentiation or conversion, we analyzed 3 single-cell RNA-sequencing datasets of peripheral mononuclear blood cells from healthy individuals using the single-cell regulatory network inference and clustering package. Cells were re-annotated into classical monocytes, intermediate monocytes, nonclassical monocytes, classical dendritic cells (cDCs), and plasmacytoid dendritic cells (pDCs) based on gene signatures. Regulon activity was analyzed, revealing 220 shared regulons across datasets. Distinct regulons characterized most myeloid subsets except intermediate monocytes, which appeared as a transitional state, sharing regulons with both classical and nonclassical monocytes. Regulons such as HMGB2, CREB5, and FOSB were enriched in classical monocytes, while TCF7L2 and POU2F2 were specific to nonclassical monocytes. Plasmacytoid DCs showed the greatest divergence, possessing many unique regulons, including AR and RUNX2, whereas cDCs shared more regulons with monocytes than pDCs, with RUNX1 specific to cDCs. All mononuclear phagocytes shared a common core of active regulons, including RELB, ID1, CLOCK, BACH1, and FLI1. Notably, FLI1 was expressed across all myeloid subclasses but emerged as a key regulator influencing monocyte gene regulatory networks. Pseudotime modeling using regulon activity demonstrated that monocyte conversion is a continuous process. Differential regulon analysis identified distinct biological processes that were enriched in monocyte subsets, highlighting that regulon activity analysis provides novel insights into myeloid cell biology. Our findings underscore the key role of transcriptional regulatory programs in defining mononuclear phagocyte identity and reveal novel signatures associated with monocyte diversity and differentiation.
    Keywords:  immune cell classification; monocyte; pseudotime; regulon activity; transcription factors
    DOI:  https://doi.org/10.1093/jleuko/qiaf058
  15. Biosci Microbiota Food Health. 2025 ;44(3): 215-226
    Lacticaseibacillus paracasei strain Shirota suppresses upper respiratory tract infections and activates mononuclear phagocytic cells in healthy Japanese office workers: a randomized, double-blind, controlled trial.
    Tomoaki Naito, Masatoshi Morikawa, Ayaka Maki, Noriko Kato-Nagaoka, Yuya Hagihira, Akira Iwata, Osamu Watanabe, Kan Shida, Satoshi Matsumoto, Tetsuji Hori.
      Certain probiotics prevent upper respiratory tract infections (URTIs) by activating immune cells, particularly mononuclear phagocytic cells (MPCs). However, the influence of Lacticaseibacillus paracasei strain Shirota (LcS), a representative probiotic strain, remains underexplored. This study aimed to investigate the effects of LcS ingestion on URTIs and MPC activation. Two hundred healthy workers aged 23-59 consumed a fermented milk drink containing 4.0 × 1010 CFU of LcS (LcS-FM) or a control unfermented milk drink (CM) daily for 28 days during winter. The incidence and severity of URTIs were surveyed using a questionnaire. Peripheral blood mononuclear cells (PBMCs) and serum samples were analyzed for immune cell subsets, cell surface molecules, and cytokines. The LcS-FM group showed a significantly lower incidence and severity of URTIs than the CM group. Notably, the incidence, cumulative incidence, and severity of URTI symptoms were markedly suppressed after 14 days of consumption. LcS-FM also affected MPC activation during this period. The expression of HLA-DR on conventional dendritic cells (cDCs) and monocytes (Mos) was significantly higher in the LcS-FM group on days 14 and 28, along with the expression of CD86 on cDCs on day 14. Among the study participants positive for serum interferon (IFN), the IFNα2 concentration in the LcS-FM group was higher than that in the CM group on day 28. These findings suggest that LcS suppresses the incidence and severity of URTIs in healthy adults, which is associated with the activation of cDCs and Mos.
    Keywords:  HLA-DR; Lacticaseibacillus paracasei strain Shirota (LcS); dendritic cell; monocyte; upper respiratory tract infections (URTIs)
    DOI:  https://doi.org/10.12938/bmfh.2025-004
  16. Cell Host Microbe. 2025 Jul 09. pii: S1931-3128(25)00156-8. [Epub ahead of print]33(7): 1052-1056
    Theory of host-microbe symbioses: Challenges and opportunities.
    Pamela Ferretti, Maria M Martignoni, Lisa C McManus, Taom Sakal, Armun Liaghat, Bethany Stevens, Kyle J-M Dahlin, Lucas S Souza, Zoe G Cardon, Cynthia B Silveira, Seth R Bordenstein, Joan Roughgarden.
      Growing insight into microbial symbioses highlights the need to model these systems mathematically. We discuss three areas requiring theoretical advancement: nested ecology within a host or holobiont, holobiont population dynamics, and symbiont-mediated speciation. Developing the proposed frameworks will bridge theory and empirical findings, accelerating our understanding of host-microbe symbioses.
    DOI:  https://doi.org/10.1016/j.chom.2025.05.001
  17. Sci Rep. 2025 Jul 11. 15(1): 25006
    Native Lactobacillus and Bifidobacterium probiotics modulate autophagy genes and exert anti-inflammatory effect.
    Fatemeh Haririzadeh Jouriani, Mahdi Torkamaneh, Mahnaz Torfeh, Fatemeh Ashrafian, Shadi Aghamohammad, Mahdi Rohani.
      Probiotics are beneficial microorganisms that modulate various signaling pathways to improve human health status. In this study we aimed to evaluate the precise molecular effects of Lactobacillus spp., Bifidobacterium spp., and a mixture of our native potential probiotics on the autophagy signaling pathway during the presence of inflammation. The evaluation of autophagy gene expression was performed after exposing the HT -29 cell line with the sonicated pathogens and probiotics, before and simultaneously with inflammation induction by quantitative real-time polymerase chain reaction (qPCR) and cytokine assays. The results of the current study showed that our native potential probiotic cocktails could upregulate the expression level of the autophagy genes including pik3c3, atg14, beclin, pik3r4, atg5, atg16, atg7, and atg3 compared with sonicated pathogen treatments, and also these native potential probiotic strains could exert anti-inflammatory effects, especially before inflammation induction. In conclusion, our native potential probiotic cocktail indicated the preventive and therapeutic effect on inflammation, but our selected probiotics could affect autophagy genes stronger before inflammation compared to expose simultaneously with inflammation. Therefore, the administration of probiotics as a prophylactic agent with the least side effects could be considered a suitable treatment for patients with inflammatory-related disease, even before or at the beginning of inflammation.
    Keywords:   Bifidobacterium ; Lactobacillus ; Autophagy; Gut-inflammation
    DOI:  https://doi.org/10.1038/s41598-025-09596-6
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