Pub Date : 2025-04-02DOI: 10.1016/j.mib.2025.102608
Gaurav Kumar Lohia, Sebastián A Riquelme
Opportunistic pathogens like Pseudomonas aeruginosa and Staphylococcus aureus rapidly adapt to the dynamic metabolic landscape of the respiratory mucosa during infection. Host phagocytes recognize these pathogens and trigger metabolic reprogramming, releasing immunometabolites such as succinate and itaconate. P. aeruginosa preferentially consumes succinate as a carbon source to enhance planktonic growth. In response to itaconate-induced membrane stress, it forms protective biofilms, allowing bacterial survival despite host defenses. Additionally, host ketone bodies support microbial communities that are less immunostimulatory and better tolerated by the lung. Similarly, S. aureus responds to itaconate by forming biofilms, aiding colonization in glucose-limited airways. In this milieu, S. aureus consumes proline, linking its survival with the metabolic activity of proline-producing fibroblasts. Here, we will review the competence of both P. aeruginosa and S. aureus to hijack host metabolic pathways, underscoring pathogen metabolic plasticity as an essential strategy to thrive in the human lung.
{"title":"Pathogen adaptation to lung metabolites","authors":"Gaurav Kumar Lohia, Sebastián A Riquelme","doi":"10.1016/j.mib.2025.102608","DOIUrl":"10.1016/j.mib.2025.102608","url":null,"abstract":"<div><div>Opportunistic pathogens like <em>Pseudomonas aeruginosa</em> and <em>Staphylococcus aureus</em> rapidly adapt to the dynamic metabolic landscape of the respiratory mucosa during infection. Host phagocytes recognize these pathogens and trigger metabolic reprogramming, releasing immunometabolites such as succinate and itaconate. <em>P. aeruginosa</em> preferentially consumes succinate as a carbon source to enhance planktonic growth. In response to itaconate-induced membrane stress, it forms protective biofilms, allowing bacterial survival despite host defenses. Additionally, host ketone bodies support microbial communities that are less immunostimulatory and better tolerated by the lung. Similarly, <em>S. aureus</em> responds to itaconate by forming biofilms, aiding colonization in glucose-limited airways. In this milieu, <em>S. aureus</em> consumes proline, linking its survival with the metabolic activity of proline-producing fibroblasts. Here, we will review the competence of both <em>P. aeruginosa</em> and <em>S. aureus</em> to hijack host metabolic pathways, underscoring pathogen metabolic plasticity as an essential strategy to thrive in the human lung.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102608"},"PeriodicalIF":5.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143758968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inflammatory bowel disease (IBD) is a chronic immune-mediated condition linked to gut microbiota dysbiosis and altered production of bacterial metabolites, including succinate, which is also a key intermediate in human mitochondrial energy metabolism in human cells. Succinate levels in the gut are influenced by microbial community dynamics and cross-feeding interactions, highlighting its dual metabolic and ecological importance. Extracellular succinate acts as a key signaling metabolite linking microbial metabolism to host physiology, with transient rises supporting metabolic regulation but chronic elevations contributing to metabolic disorders and disease progression. Succinate signals through its cognate receptor SUCNR1, which mediates adaptive metabolic responses under normal conditions but drives inflammation and fibrosis when dysregulated.
IBD patients display a dysbiotic gut microbiota characterized by an increased prevalence of succinate-producing bacteria, contributing to elevated succinate levels in the gut and circulation. This imbalance drives inflammation, worsens IBD severity, and contributes to complications like Clostridioides difficile infection and fibrosis. Emerging evidence highlights the potential of intestinal and systemic succinate levels as indicators of microbial dysbiosis, with a bidirectional relationship between microbial composition and succinate metabolism. Understanding the factors influencing succinate levels and their interaction with dysbiosis shows promise in the development of therapeutic strategies to restore microbial balance. Approaches such as dietary fiber enrichment, prebiotics, and probiotics to enhance succinate-consuming bacteria, combined with targeted modulation of succinate pathways (e.g. SDH inhibitors, SUCNR1 antagonists), hold promise for mitigating inflammation and improving gut health in IBD.
{"title":"The role of microbial succinate in the pathophysiology of inflammatory bowel disease: mechanisms and therapeutic potential","authors":"Sonia Fernández-Veledo , Carme Grau-Bové , Sara Notararigo , Isabel Huber-Ruano","doi":"10.1016/j.mib.2025.102599","DOIUrl":"10.1016/j.mib.2025.102599","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) is a chronic immune-mediated condition linked to gut microbiota dysbiosis and altered production of bacterial metabolites, including succinate, which is also a key intermediate in human mitochondrial energy metabolism in human cells. Succinate levels in the gut are influenced by microbial community dynamics and cross-feeding interactions, highlighting its dual metabolic and ecological importance. Extracellular succinate acts as a key signaling metabolite linking microbial metabolism to host physiology, with transient rises supporting metabolic regulation but chronic elevations contributing to metabolic disorders and disease progression. Succinate signals through its cognate receptor SUCNR1, which mediates adaptive metabolic responses under normal conditions but drives inflammation and fibrosis when dysregulated.</div><div>IBD patients display a dysbiotic gut microbiota characterized by an increased prevalence of succinate-producing bacteria, contributing to elevated succinate levels in the gut and circulation. This imbalance drives inflammation, worsens IBD severity, and contributes to complications like <em>Clostridioides difficile</em> infection and fibrosis. Emerging evidence highlights the potential of intestinal and systemic succinate levels as indicators of microbial dysbiosis, with a bidirectional relationship between microbial composition and succinate metabolism. Understanding the factors influencing succinate levels and their interaction with dysbiosis shows promise in the development of therapeutic strategies to restore microbial balance. Approaches such as dietary fiber enrichment, prebiotics, and probiotics to enhance succinate-consuming bacteria, combined with targeted modulation of succinate pathways (e.g. SDH inhibitors, SUCNR1 antagonists), hold promise for mitigating inflammation and improving gut health in IBD.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102599"},"PeriodicalIF":5.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143685137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-19DOI: 10.1016/j.mib.2025.102598
Samuel G Chamberlain , Shiroh Iwanaga , Matthew K Higgins
Two protein families are found on the surfaces of erythrocytes infected with Plasmodium falciparum, a causative agent of deadly malaria. PfEMP1 are tethers binding endothelial receptors and holding infected erythrocytes to tissue and blood vessel surfaces, away from splenic clearance. RIFINs interact with immune receptors on natural killer cells, suppressing infected erythrocyte destruction. Both have expanded into families of diverse members to allow antigenic variation but retain surfaces of conserved chemistry and shape to bind human receptors. Recently discovered broadly inhibitory antibodies target one such surface on many EPCR-binding PfEMP1. Remarkable antibodies take this one step further, directly incorporating ectodomains of immune receptors into their loops, allowing RIFIN recognition. Finally, some RIFINs are targets of activating killer immune receptors, helping natural killer cells destroy infected erythrocytes. Studies of these two families therefore reveal a snapshot of the battle between this ancient parasite and the immune system of its human host.
{"title":"Immune evasion runs in the family: two surface protein families of Plasmodium falciparum–infected erythrocytes","authors":"Samuel G Chamberlain , Shiroh Iwanaga , Matthew K Higgins","doi":"10.1016/j.mib.2025.102598","DOIUrl":"10.1016/j.mib.2025.102598","url":null,"abstract":"<div><div>Two protein families are found on the surfaces of erythrocytes infected with <em>Plasmodium falciparum</em>, a causative agent of deadly malaria. PfEMP1 are tethers binding endothelial receptors and holding infected erythrocytes to tissue and blood vessel surfaces, away from splenic clearance. RIFINs interact with immune receptors on natural killer cells, suppressing infected erythrocyte destruction. Both have expanded into families of diverse members to allow antigenic variation but retain surfaces of conserved chemistry and shape to bind human receptors. Recently discovered broadly inhibitory antibodies target one such surface on many EPCR-binding PfEMP1. Remarkable antibodies take this one step further, directly incorporating ectodomains of immune receptors into their loops, allowing RIFIN recognition. Finally, some RIFINs are targets of activating killer immune receptors, helping natural killer cells destroy infected erythrocytes. Studies of these two families therefore reveal a snapshot of the battle between this ancient parasite and the immune system of its human host.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102598"},"PeriodicalIF":5.9,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-12DOI: 10.1016/j.mib.2025.102597
Abdulbasit Amin , David V Ferreira , Luisa M Figueiredo
Weight loss is a hallmark of many infections, including those caused by bacteria, fungi and parasites. This loss is often attributed to infection-induced anorexia and the need to mobilise energy from internal sources to cope with the pathogens. Weight loss during infection results from a significant reduction of muscle and fat mass, two organs that together account for approximately 60% of body mass in the healthy state. While muscle wasting is a well-documented aspect of infection-related weight loss, adipose tissue loss via lipolysis also plays a critical role and can determine disease outcomes. This review explores the regulators of adipose tissue depletion via excessive lipolysis during infection, the probable mechanisms, and the potential consequences for host survival and pathogen fitness.
{"title":"How pathogens drive adipose tissue loss in the host","authors":"Abdulbasit Amin , David V Ferreira , Luisa M Figueiredo","doi":"10.1016/j.mib.2025.102597","DOIUrl":"10.1016/j.mib.2025.102597","url":null,"abstract":"<div><div>Weight loss is a hallmark of many infections, including those caused by bacteria, fungi and parasites. This loss is often attributed to infection-induced anorexia and the need to mobilise energy from internal sources to cope with the pathogens. Weight loss during infection results from a significant reduction of muscle and fat mass, two organs that together account for approximately 60% of body mass in the healthy state. While muscle wasting is a well-documented aspect of infection-related weight loss, adipose tissue loss via lipolysis also plays a critical role and can determine disease outcomes. This review explores the regulators of adipose tissue depletion via excessive lipolysis during infection, the probable mechanisms, and the potential consequences for host survival and pathogen fitness.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102597"},"PeriodicalIF":5.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143600668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-25DOI: 10.1016/j.mib.2025.102585
François Korbmacher , Maria Bernabeu
Most in vitro studies on parasite development and pathogenesis in the human host have been conducted using traditional primary or immortalized cells, despite their inherent limitations. Breakthroughs in the field of induced pluripotent stem cells (iPSCs) are revolutionizing disease modeling, offering alternatives to traditional in vivo and in vitro infection models. Human iPSCs differentiate into all cell types, proliferate indefinitely, and offer experimental advantages, like genome editing and donor control. iPSCs can be engineered into complex 3D tissue models that closely mimic morphology and function of their in vivo counterparts and allow for precise experimental manipulation.
The physiological complexity of iPSC-based tissue models has improved rapidly. Given Plasmodium's systemic impact across multiple organs, these models provide an invaluable resource for studying parasite–tissue interactions. This opinion article focuses on recent developments of iPSC-based models for Plasmodium research. We describe the main highlights and potential use of these systems while acknowledging current limitations.
{"title":"Induced pluripotent stem cell–based tissue models to study malaria: a new player in the research game","authors":"François Korbmacher , Maria Bernabeu","doi":"10.1016/j.mib.2025.102585","DOIUrl":"10.1016/j.mib.2025.102585","url":null,"abstract":"<div><div>Most <em>in vitro</em> studies on parasite development and pathogenesis in the human host have been conducted using traditional primary or immortalized cells, despite their inherent limitations. Breakthroughs in the field of induced pluripotent stem cells (iPSCs) are revolutionizing disease modeling, offering alternatives to traditional <em>in vivo</em> and <em>in vitro</em> infection models. Human iPSCs differentiate into all cell types, proliferate indefinitely, and offer experimental advantages, like genome editing and donor control. iPSCs can be engineered into complex 3D tissue models that closely mimic morphology and function of their <em>in vivo</em> counterparts and allow for precise experimental manipulation.</div><div>The physiological complexity of iPSC-based tissue models has improved rapidly. Given <em>Plasmodium</em>'s systemic impact across multiple organs, these models provide an invaluable resource for studying parasite–tissue interactions. This opinion article focuses on recent developments of iPSC-based models for <em>Plasmodium</em> research. We describe the main highlights and potential use of these systems while acknowledging current limitations.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"84 ","pages":"Article 102585"},"PeriodicalIF":5.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143488213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-20DOI: 10.1016/j.mib.2025.102596
Afra Salazar , Sara Mitri
Microbial communities provide crucial services for human well-being, driving an interest in designing and controlling them towards optimised or novel functions. Unfortunately, promising strategies such as community breeding — sometimes referred to as ‘directed evolution’ or ‘artificial community selection’ — have shown limited success. A key issue is that microbial communities do not reliably exhibit heritable variation, limiting their capacity for adaptive evolution. In other words, microbial communities are not evolutionary individuals. Here, we provide an overview of the literature on evolutionary transitions in individuality and, with insights from paradigmatic organisms, build a multidimensional space in which the individuality of a multispecies community is characterised by three ecological traits: positive interactions, functional integration, and entrenchment. We then place microbial communities within this individuality space, explore how they can be directed toward increased individuality, and discuss how this perspective can help improve our approach to community breeding.
{"title":"Can a microbial community become an evolutionary individual?","authors":"Afra Salazar , Sara Mitri","doi":"10.1016/j.mib.2025.102596","DOIUrl":"10.1016/j.mib.2025.102596","url":null,"abstract":"<div><div>Microbial communities provide crucial services for human well-being, driving an interest in designing and controlling them towards optimised or novel functions. Unfortunately, promising strategies such as community breeding — sometimes referred to as ‘directed evolution’ or ‘artificial community selection’ — have shown limited success. A key issue is that microbial communities do not reliably exhibit heritable variation, limiting their capacity for adaptive evolution. In other words, microbial communities are not evolutionary individuals. Here, we provide an overview of the literature on evolutionary transitions in individuality and, with insights from paradigmatic organisms, build a multidimensional space in which the individuality of a multispecies community is characterised by three ecological traits: positive interactions, functional integration, and entrenchment. We then place microbial communities within this individuality space, explore how they can be directed toward increased individuality, and discuss how this perspective can help improve our approach to community breeding.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"84 ","pages":"Article 102596"},"PeriodicalIF":5.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143444717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-16DOI: 10.1016/j.mib.2025.102584
Mostafa Hagar , Sangwook Kang , Raymond J Andersen , Dong-Chan Oh , Katherine S Ryan
Piperazic acid (Piz) is an intriguing hydrazine-containing amino acid found in a diverse variety of natural products, the majority of which are bioactive. Recently, several approaches have been reported for targeted isolation of Piz-containing molecules, combining spectroscopic techniques for screening Piz moieties with recent advances in Piz biosynthesis. Here, we highlight bioactive natural products recently isolated using these methods and bring into focus structural elucidation challenges impeding the discovery of more Piz-containing molecules.
{"title":"Targeted isolation of piperazate-containing molecules: bioinformatics and spectroscopy","authors":"Mostafa Hagar , Sangwook Kang , Raymond J Andersen , Dong-Chan Oh , Katherine S Ryan","doi":"10.1016/j.mib.2025.102584","DOIUrl":"10.1016/j.mib.2025.102584","url":null,"abstract":"<div><div>Piperazic acid (Piz) is an intriguing hydrazine-containing amino acid found in a diverse variety of natural products, the majority of which are bioactive. Recently, several approaches have been reported for targeted isolation of Piz-containing molecules, combining spectroscopic techniques for screening Piz moieties with recent advances in Piz biosynthesis. Here, we highlight bioactive natural products recently isolated using these methods and bring into focus structural elucidation challenges impeding the discovery of more Piz-containing molecules.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"84 ","pages":"Article 102584"},"PeriodicalIF":5.9,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-15DOI: 10.1016/j.mib.2025.102582
Florent Colomb, Henry J McSorley
Parasitic nematodes release a wide variety of immunomodulatory proteins, which allow them to escape the host’s immune-mediated killing or ejection mechanisms. This immunomodulation is mediated by nematode excretory/secretory (E/S) products, which contain multiple families of immunomodulatory proteins. Many of these families are conserved across different parasitic nematodes, while others are apparently unique to specific species. While some E/S products interact with host proteins, others have evolved to target host lipids, glycans, and metabolites. In this review, we will focus on three families of immunomodulatory proteins, which are particularly expanded in intestinal nematodes: the venom allergen-like proteins, the apyrases, and the complement control protein domain-containing proteins. These families of proteins suppress host immune responses, and evidence is gathering that these could be effective vaccine antigens against these intractable parasites.
{"title":"Protein families secreted by nematodes to modulate host immunity","authors":"Florent Colomb, Henry J McSorley","doi":"10.1016/j.mib.2025.102582","DOIUrl":"10.1016/j.mib.2025.102582","url":null,"abstract":"<div><div>Parasitic nematodes release a wide variety of immunomodulatory proteins, which allow them to escape the host’s immune-mediated killing or ejection mechanisms. This immunomodulation is mediated by nematode excretory/secretory (E/S) products, which contain multiple families of immunomodulatory proteins. Many of these families are conserved across different parasitic nematodes, while others are apparently unique to specific species. While some E/S products interact with host proteins, others have evolved to target host lipids, glycans, and metabolites. In this review, we will focus on three families of immunomodulatory proteins, which are particularly expanded in intestinal nematodes: the venom allergen-like proteins, the apyrases, and the complement control protein domain-containing proteins. These families of proteins suppress host immune responses, and evidence is gathering that these could be effective vaccine antigens against these intractable parasites.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"84 ","pages":"Article 102582"},"PeriodicalIF":5.9,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.mib.2024.102577
Franziska Hildebrandt , Ana N. Matias , Moritz Treeck
Genome editing technologies, such as CRISPR-Cas9, have revolutionised the study of genes in a variety of organisms, including unicellular parasites. Today, the CRISPR-Cas9 technology is vastly applied in high-throughput screens to investigate interactions between the Apicomplexan parasite Toxoplasma gondii and its hosts. In vitro and in vivo T. gondii screens performed in naive and restrictive conditions have led to the discovery of essential and fitness-conferring T. gondii genes, as well as factors important for virulence and dissemination. Recent studies have adapted the CRISPR-Cas9 screening technology to study T. gondii genes based on phenotypes unrelated to parasite survival. These advances were achieved by using conditional systems coupled with imaging, as well as single-cell RNA sequencing and phenotypic selection. Here, we review the state-of-the-art of CRISPR-Cas9 screening technologies with a focus on T. gondii, highlighting strengths, current limitations and future avenues for its development, including its application to other Apicomplexan species.
{"title":"A CRISPR view on genetic screens in Toxoplasma gondii","authors":"Franziska Hildebrandt , Ana N. Matias , Moritz Treeck","doi":"10.1016/j.mib.2024.102577","DOIUrl":"10.1016/j.mib.2024.102577","url":null,"abstract":"<div><div>Genome editing technologies, such as CRISPR-Cas9, have revolutionised the study of genes in a variety of organisms, including unicellular parasites. Today, the CRISPR-Cas9 technology is vastly applied in high-throughput screens to investigate interactions between the Apicomplexan parasite <em>Toxoplasma gondii</em> and its hosts. <em>In vitro</em> and <em>in vivo T. gondii</em> screens performed in naive and restrictive conditions have led to the discovery of essential and fitness-conferring <em>T. gondii</em> genes, as well as factors important for virulence and dissemination. Recent studies have adapted the CRISPR-Cas9 screening technology to study <em>T. gondii</em> genes based on phenotypes unrelated to parasite survival. These advances were achieved by using conditional systems coupled with imaging, as well as single-cell RNA sequencing and phenotypic selection. Here, we review the state-of-the-art of CRISPR-Cas9 screening technologies with a focus on <em>T. gondii</em>, highlighting strengths, current limitations and future avenues for its development, including its application to other Apicomplexan species.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"83 ","pages":"Article 102577"},"PeriodicalIF":5.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.mib.2025.102581
Reginald A Woods , Sarai Guzman Vela , Francis Alonzo III
The host lipid environment is a barrier to bacterial infection that comprises antimicrobial fatty acids and impermeable lipids that keep infectious agents from penetrating tissues. Bacterial and host lipids also signal to the immune system to regulate inflammation. Notably, bacterial lipids activate Toll-like receptors to initiate cytokine production, immune cell recruitment, and oxidative burst to control infection. Bacterial pathogens must adapt to the lipid environment, including bactericidal host fatty acids and inflammatory lipids, in ways that promote persistence in diverse tissues. Here, we discuss current advances in the understanding of Staphylococcus aureus lipid interactions that contribute to inflammation and innate immunity and consider the complex roles of host inflammatory lipids in driving immune defenses and antibacterial activity. In addition, we endeavor to introduce similar processes in other Gram-positive pathogens. These recent studies highlight the growing body of knowledge on the effects of lipid metabolism on host immunity and pathogenesis.
{"title":"Gram-positive pathogens, inflammation, and the host lipid environment","authors":"Reginald A Woods , Sarai Guzman Vela , Francis Alonzo III","doi":"10.1016/j.mib.2025.102581","DOIUrl":"10.1016/j.mib.2025.102581","url":null,"abstract":"<div><div>The host lipid environment is a barrier to bacterial infection that comprises antimicrobial fatty acids and impermeable lipids that keep infectious agents from penetrating tissues. Bacterial and host lipids also signal to the immune system to regulate inflammation. Notably, bacterial lipids activate Toll-like receptors to initiate cytokine production, immune cell recruitment, and oxidative burst to control infection. Bacterial pathogens must adapt to the lipid environment, including bactericidal host fatty acids and inflammatory lipids, in ways that promote persistence in diverse tissues. Here, we discuss current advances in the understanding of <em>Staphylococcus aureus</em> lipid interactions that contribute to inflammation and innate immunity and consider the complex roles of host inflammatory lipids in driving immune defenses and antibacterial activity. In addition, we endeavor to introduce similar processes in other Gram-positive pathogens. These recent studies highlight the growing body of knowledge on the effects of lipid metabolism on host immunity and pathogenesis.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"83 ","pages":"Article 102581"},"PeriodicalIF":5.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143360567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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