bims-bac4me Biomed News
on Microbiome and trained immunity
Issue of 2023–01–29
twelve papers selected by
Chun-Chi Chang, University Hospital Zurich
  1. Epigenetic regulation of macrophage polarization in wound healing.
  2. Obesity induces epigenetic memory in innate immune cells.
  3. Modulating the Microbiome for Disease Treatment.
  4. Toxin expression during Staphylococcus aureus infection imprints host immunity to inhibit vaccine efficacy.
  5. Inflammatory cell death: how macrophages sense neighbouring cell infection and damage.
  6. Staphylococcus aureus host interactions and adaptation.
  7. The role of the microbiota in myelopoiesis during homeostasis and inflammation.
  8. Treatment of Bacterial Infections with β-Lactams: Cooperation with Innate Immunity.
  9. How antidepressants help bacteria resist antibiotics.
  10. Role of Microbiota in the Skin Colonization of Candida auris.
  11. NET formation is independent of gasdermin D and pyroptotic cell death.
  12. The roles of long noncoding RNA-mediated macrophage polarization in respiratory diseases.
  1. Burns Trauma. 2023 ;11 tkac057
    Epigenetic regulation of macrophage polarization in wound healing.
    Cheng Chen, Tengfei Liu, Yuanyang Tang, Gaoxing Luo, Guangping Liang, Weifeng He.
      The immune microenvironment plays a critical role in regulating skin wound healing. Macrophages, the main component of infiltrating inflammatory cells, play a pivotal role in shaping the immune microenvironment in the process of skin wound healing. Macrophages comprise the classic proinflammatory M1 subtype and anti-inflammatory M2 population. In the early inflammatory phase of skin wound closure, M1-like macrophages initiate and amplify the local inflammatory response to disinfect the injured tissue. In the late tissue-repairing phase, M2 macrophages are predominant in wound tissue and limit local inflammation to promote tissue repair. The biological function of macrophages is tightly linked with epigenomic organization. Transcription factors are essential for macrophage polarization. Epigenetic modification of transcription factors determines the heterogeneity of macrophages. In contrast, transcription factors also regulate the expression of epigenetic enzymes. Both transcription factors and epigenetic enzymes form a complex network that regulates the plasticity of macrophages. Here, we describe the latest knowledge concerning the potential epigenetic mechanisms that precisely regulate the biological function of macrophages and their effects on skin wound healing.
    Keywords:  Epigenetics; Immune microenvironment; Macrophage polarization; Signaling pathways; Wound healing
    DOI:  https://doi.org/10.1093/burnst/tkac057
  2. Nat Rev Endocrinol. 2023 Jan 23.
    Obesity induces epigenetic memory in innate immune cells.
    Olivia Tysoe.
      
    DOI:  https://doi.org/10.1038/s41574-023-00806-7
  3. Gastroenterology. 2023 Jan 23. pii: S0016-5085(23)00049-5. [Epub ahead of print]
    Modulating the Microbiome for Disease Treatment.
    Rachael Gowan, Ahmed Gamal, Luca Di Martino, Thomas S McCormick, Mahmoud A Ghannoum.
      The central role of gut microbiota in the regulation of health and disease has been convincingly demonstrated. Polymicrobial inter-kingdom interactions between bacteria (the bacteriome) and fungal (the mycobiome) communities of the gut have become a prominent focus for development of potential therapeutic approaches. In addition to polymicrobial interactions, the complex gut ecosystem also mediates interactions between host and the microbiota. These interactions are complex and bidirectional, microbiota composition can be influenced by host immune response, disease-specific therapeutics, antimicrobial drugs, and overall ecosystems. However, the gut microbiota also influences host immune response to a drug or therapy by potentially transforming the drug's structure and altering bioavailability, activity or toxicity, this is especially true in cases where the gut microbiota has produced a biofilm. The negative ramifications of biofilm formation include alteration of gut permeability, enhanced antimicrobial resistance, and alteration of host immune response effectiveness. Natural modulation of the gut microbiota, using pro- and pre-biotic approaches may also be used to affect the host microbiome, a type of "natural" modulation of the host microbiota composition. In this review we discuss potential bidirectional interactions between microbes and host, describe the changes in gut microbiota induced by probiotic and prebiotic approaches, and their potential clinical consequences and summarize how to develop a systematic approach to designing probiotics capable of altering the host microbiota in disease states, using Crohn's Disease (CD) as a model chronic disease. Understanding how the effective changes in the microbiome may enhance treatment efficacy may unlock the possibility of modulating the gut microbiome to improve treatment using a natural approach.
    Keywords:  Crohn’s disease; biotherapeutics; microbiome; nutritional supplements; targeting the microbiome
    DOI:  https://doi.org/10.1053/j.gastro.2023.01.017
  4. NPJ Vaccines. 2023 Jan 24. 8(1): 3
    Toxin expression during Staphylococcus aureus infection imprints host immunity to inhibit vaccine efficacy.
    Omid Teymournejad, Zhaotao Li, Pavani Beesetty, Ching Yang, Christopher P Montgomery.
      Staphylococcus aureus infections are a major public health issue, and a vaccine is urgently needed. Despite a considerable promise in preclinical models, all vaccines tested thus far have failed to protect humans against S. aureus. Unlike laboratory mice, humans are exposed to S. aureus throughout life. In the current study, we hypothesized that prior exposure to S. aureus "imprints" the immune response to inhibit vaccine-mediated protection. We established a mouse model in which S. aureus skin and soft tissue infection (SSTI) is followed by vaccination and secondary SSTI. Unlike naïve mice, S. aureus-sensitized mice were incompletely protected against secondary SSTI by vaccination with the inactivated α-hemolysin (Hla) mutant HlaH35L. Inhibition of protection was specific for the HlaH35L vaccine and required hla expression during primary SSTI. Surprisingly, inhibition occurred at the level of vaccine-elicited effector T cells; hla expression during primary infection limited the expansion of T cells and dendritic cells and impaired vaccine-specific T cell responses. Importantly, the T cell-stimulating adjuvant CAF01 rescued inhibition and restored vaccine-mediated protection. Together, these findings identify a potential mechanism for the failure of translation of promising S. aureus vaccines from mouse models to clinical practice and suggest a path forward to prevent these devastating infections.
    DOI:  https://doi.org/10.1038/s41541-022-00598-3
  5. Biochem Soc Trans. 2023 Jan 25. pii: BST20220807. [Epub ahead of print]
    Inflammatory cell death: how macrophages sense neighbouring cell infection and damage.
    Xiaohui Wang, Larisa I Labzin.
      Programmed cell death is a critical host defence strategy during viral infection. Neighbouring cells deal with this death in distinct ways depending on how the infected cell dies. While apoptosis is considered immunologically silent, the lytic pathways of necroptosis and pyroptosis trigger inflammatory responses by releasing inflammatory host molecules. All these pathways have been implicated in influenza A virus infection. Here, we review how cells sense neighbouring infection and death and how sensing shapes ensuing inflammatory responses.
    Keywords:  apoptosis; inflammation; influenza; macrophage; necroptosis; pyroptosis
    DOI:  https://doi.org/10.1042/BST20220807
  6. Nat Rev Microbiol. 2023 Jan 27.
    Staphylococcus aureus host interactions and adaptation.
    Benjamin P Howden, Stefano G Giulieri, Tania Wong Fok Lung, Sarah L Baines, Liam K Sharkey, Jean Y H Lee, Abderrahman Hachani, Ian R Monk, Timothy P Stinear.
      Invasive Staphylococcus aureus infections are common, causing high mortality, compounded by the propensity of the bacterium to develop drug resistance. S. aureus is an excellent case study of the potential for a bacterium to be commensal, colonizing, latent or disease-causing; these states defined by the interplay between S. aureus and host. This interplay is multidimensional and evolving, exemplified by the spread of S. aureus between humans and other animal reservoirs and the lack of success in vaccine development. In this Review, we examine recent advances in understanding the S. aureus-host interactions that lead to infections. We revisit the primary role of neutrophils in controlling infection, summarizing the discovery of new immune evasion molecules and the discovery of new functions ascribed to well-known virulence factors. We explore the intriguing intersection of bacterial and host metabolism, where crosstalk in both directions can influence immune responses and infection outcomes. This Review also assesses the surprising genomic plasticity of S. aureus, its dualism as a multi-mammalian species commensal and opportunistic pathogen and our developing understanding of the roles of other bacteria in shaping S. aureus colonization.
    DOI:  https://doi.org/10.1038/s41579-023-00852-y
  7. Int Immunol. 2023 Jan 24. pii: dxad002. [Epub ahead of print]
    The role of the microbiota in myelopoiesis during homeostasis and inflammation.
    Yeji Kim, Nobuhiko Kamada.
      The microbiota engages in the development and maintenance of the host immune system. The microbiota affects not only mucosal tissues where it localizes but also the distal organs. Myeloid cells are essential for host defense as first responders of the host immune system. Their generation, called myelopoiesis, is regulated by environmental signals, including commensal microbiota. Hematopoietic stem and progenitor cells in bone marrow can directly or indirectly sense microbiota-derived signals, thereby giving rise to myeloid cell lineages at steady-state and during inflammation. In this review, we discuss the role of commensal microorganisms in the homeostatic regulation of myelopoiesis in the bone marrow. We also outline the effects of microbial signals on myelopoiesis during inflammation and infection, with a particular focus on the development of innate immune memory. Studying the relationship between the microbiota and myelopoiesis will help us understand how the microbiota regulates immune responses at a systemic level beyond the local mucosa.
    Keywords:  Commensal microorganisms; hematopoietic stem and progenitor cells; trained immunity
    DOI:  https://doi.org/10.1093/intimm/dxad002
  8. Infect Immun. 2023 Jan 25. e0050322
    Treatment of Bacterial Infections with β-Lactams: Cooperation with Innate Immunity.
    Mélanie Mondemé, Christophe Carnoy, Jean-Claude Sirard, Christelle Faveeuw.
      β-Lactams are the most widely prescribed antibiotics used for the control and treatment of bacterial infections. The direct effect of β-lactams on bacteria is well studied worldwide. In the context of infections and as a consequence of their direct activity against the pathogen, β-lactams also regulate antibacterial immune responses. This knowledge has led to the theorem that the effectiveness of β-lactam treatment results from the synergy between the drug and the immune response. Key players in this immune response, with an essential role in the clearance of live and dead bacteria, are the myeloid cells. In this review, we summarize the data that shed light on how β-lactams interact with myeloid cells during bacterial infection treatment.
    Keywords:  bacterial infections; monocytes; neutrophils; pathogen-associated molecular patterns; phagocytosis; proinflammatory responses; β-lactams
    DOI:  https://doi.org/10.1128/iai.00503-22
  9. Nature. 2023 Jan 24.
    How antidepressants help bacteria resist antibiotics.
    Liam Drew.
      
    Keywords:  Antibiotics; Infection; Microbiome
    DOI:  https://doi.org/10.1038/d41586-023-00186-y
  10. mSphere. 2023 Jan 25. e0062322
    Role of Microbiota in the Skin Colonization of Candida auris.
    Brooke Tharp, Rachel Zheng, Garrett Bryak, Anastasia P Litvintseva, Mary K Hayden, Anuradha Chowdhary, Shankar Thangamani.
      Candida auris is an emerging multidrug-resistant fungal pathogen that can cause life-threatening infections in humans. Unlike other Candida species that colonize the gut, C. auris efficiently colonizes the skin and contaminates the patient's environment, resulting in rapid nosocomial transmission and outbreaks of systemic infections. As the largest organ of the body, the skin harbors beneficial microbiota that play a critical role to protect from invading pathogens. However, the role of skin microbiota in the colonization and pathogenesis of C. auris remains to be explored. With this perspective, we review and discuss recent insights into skin microbiota and their potential interactions with the immune system in the context of C. auris skin colonization. Understanding microbiota, C. auris, and host interactions in the skin is important to develop microbiome-based therapeutic approaches to prevent and treat this emerging fungal pathogen in humans.
    Keywords:  C. auris; horizontal transmission; host defense; microbiome-based therapeutics; skin microbiota
    DOI:  https://doi.org/10.1128/msphere.00623-22
  11. Sci Signal. 2023 Jan 24. 16(769): eabm0517
    NET formation is independent of gasdermin D and pyroptotic cell death.
    Darko Stojkov, Meike J Claus, Evelyne Kozlowski, Kevin Oberson, Olivier P Schären, Charaf Benarafa, Shida Yousefi, Hans-Uwe Simon.
      Neutrophil extracellular traps (NETs) are DNA scaffolds coated with granule proteins that are released by neutrophils to ensnare and kill bacteria. NET formation occurs in response to many stimuli through independent molecular pathways. Although NET release has been equated to a form of lytic cell death, live neutrophils can rapidly release antimicrobial NETs. Gasdermin D (GSDMD), which causes pyroptotic death in macrophages, is thought to be required for NET formation by neutrophils. Through experiments with known physiological activators of NET formation and ligands that activate canonical and noncanonical inflammasome signaling pathways, we demonstrated that Gsdmd-deficient mouse neutrophils were as competent as wild-type mouse neutrophils in producing NETs. Furthermore, GSDMD was not cleaved in wild-type neutrophils during NET release in response to inflammatory mediators. We found that activation of both canonical and noncanonical inflammasome signaling pathways resulted in GSDMD cleavage in wild-type neutrophils but was not associated with cell death. Moreover, NET formation as a result of either pathway of inflammasome activation did not require GSDMD. Together, these data suggest that NETs can be formed by viable neutrophils after inflammasome activation and that this function does not require GSDMD.
    DOI:  https://doi.org/10.1126/scisignal.abm0517
  12. Front Immunol. 2022 ;13 1110774
    The roles of long noncoding RNA-mediated macrophage polarization in respiratory diseases.
    Xin Qiao, Yuxiao Ding, Dasen Wu, Anle Zhang, Yan Yin, Qiuyue Wang, Wei Wang, Jian Kang.
      Macrophages play an essential role in maintaining the normal function of the innate and adaptive immune responses during host defence. Macrophages acquire diverse functional phenotypes in response to various microenvironmental stimuli, and are mainly classified into classically activated macrophages (M1) and alternatively activated macrophages (M2). Macrophage polarization participates in the inflammatory, fibrotic, and oncogenic processes of diverse respiratory diseases by changing phenotype and function. In recent decades, with the advent of broad-range profiling methods such as microarrays and next-generation sequencing, the discovery of RNA transcripts that do not encode proteins termed "noncoding RNAs (ncRNAs)" has become more easily accessible. As one major member of the regulatory ncRNA family, long noncoding RNAs (lncRNAs, transcripts >200 nucleotides) participate in multiple pathophysiological processes, including cell proliferation, differentiation, and apoptosis, and vary with different stimulants and cell types. Emerging evidence suggests that lncRNAs account for the regulation of macrophage polarization and subsequent effects on respiratory diseases. In this review, we summarize the current published literature from the PubMed database concerning lncRNAs relevant to macrophage polarization and the underlying molecular mechanisms during the occurrence and development of respiratory diseases. These differentially expressed lncRNAs are expected to be biomarkers and targets for the therapeutic regulation of macrophage polarization during disease development.
    Keywords:  M1/M2 polarization; long noncoding RNAs; lung cancer; macrophages; respiratory diseases
    DOI:  https://doi.org/10.3389/fimmu.2022.1110774
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