Pub Date : 2025-06-03DOI: 10.1016/j.mib.2025.102614
Yein Ra, Arash Komeili
Bacteria contain multiple subcellular compartments that enable a variety of biochemical activities and behaviors. In many cases, the organization of these organelles is not random and is directly linked to their function. In the last decade, mechanistic studies have uncovered the machinery responsible for organelle positioning in some bacterial systems. Here, we review several such positioning systems with an emphasis on two arrangement patterns and the molecular mechanisms used to achieve them. We start with carboxysomes as an illustration of how a ParA/MinD ATPase system is used to equally distribute organelles in a cell. We follow with an example of an actin-like cytoskeletal system that links lipid-bounded magnetosome organelles into a continuous chain. We finally explore emerging models of bacterial organelle positioning and conclude with an outlook on the future opportunities in the study of bacterial organelle cell biology.
{"title":"Organizing organelles: bacterial strategies for localizing intracellular compartments","authors":"Yein Ra, Arash Komeili","doi":"10.1016/j.mib.2025.102614","DOIUrl":"10.1016/j.mib.2025.102614","url":null,"abstract":"<div><div>Bacteria contain multiple subcellular compartments that enable a variety of biochemical activities and behaviors. In many cases, the organization of these organelles is not random and is directly linked to their function. In the last decade, mechanistic studies have uncovered the machinery responsible for organelle positioning in some bacterial systems. Here, we review several such positioning systems with an emphasis on two arrangement patterns and the molecular mechanisms used to achieve them. We start with carboxysomes as an illustration of how a ParA/MinD ATPase system is used to equally distribute organelles in a cell. We follow with an example of an actin-like cytoskeletal system that links lipid-bounded magnetosome organelles into a continuous chain. We finally explore emerging models of bacterial organelle positioning and conclude with an outlook on the future opportunities in the study of bacterial organelle cell biology.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"86 ","pages":"Article 102614"},"PeriodicalIF":5.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144205485","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 : 2025-05-30DOI: 10.1016/j.mib.2025.102613
Landon J Getz , Pramalkumar H Patel , Karen L Maxwell
Antibiotic-resistant bacterial infections pose a significant global health challenge. Phage therapy provides a promising alternative to antibiotics that enables the specific targeting of pathogenic bacteria while preserving the healthy microbiome. Recent advances in genetic engineering, synthetic biology, and artificial intelligence have rekindled interest in phage therapy, as they move phages into the realm of precision medicine. Engineered phages can be customized to have a broader host range, encode counter-defenses that overcome bacterial immune systems, or express other proteins that modulate the bacterial host to their advantage. Innovations in artificial intelligence and machine learning promise to speed up the identification of optimal phage candidates and create tailored cocktails for individualized therapies — advances that will transform phage therapy and provide a solution to the antibiotic resistance crisis.
{"title":"A solution to the postantibiotic era: phages as precision medicine","authors":"Landon J Getz , Pramalkumar H Patel , Karen L Maxwell","doi":"10.1016/j.mib.2025.102613","DOIUrl":"10.1016/j.mib.2025.102613","url":null,"abstract":"<div><div>Antibiotic-resistant bacterial infections pose a significant global health challenge. Phage therapy provides a promising alternative to antibiotics that enables the specific targeting of pathogenic bacteria while preserving the healthy microbiome. Recent advances in genetic engineering, synthetic biology, and artificial intelligence have rekindled interest in phage therapy, as they move phages into the realm of precision medicine. Engineered phages can be customized to have a broader host range, encode counter-defenses that overcome bacterial immune systems, or express other proteins that modulate the bacterial host to their advantage. Innovations in artificial intelligence and machine learning promise to speed up the identification of optimal phage candidates and create tailored cocktails for individualized therapies — advances that will transform phage therapy and provide a solution to the antibiotic resistance crisis.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"86 ","pages":"Article 102613"},"PeriodicalIF":5.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144178739","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 : 2025-05-22DOI: 10.1016/j.mib.2025.102612
Adedayo E Ogunware, Tammy Kielian
Staphylococcus aureus is both a commensal bacterium and versatile pathogen, capable of transitioning from a benign colonizer to cause invasive disease. Its ability to form biofilm — a resilient, highly structured bacterial community — plays a key role in chronic infections, including those associated with medical implants and native tissues. The unique microenvironments of these biofilm niches create challenges for the host immune system, complicating pathogen clearance. Immunometabolism, the interplay between immune function and metabolic programming, plays a crucial role in dictating how the host combats S. aureus biofilms. Leukocytes undergo profound metabolic changes in response to biofilm, which can lead to dysregulated immune responses and persistent infection. This review explores recent insights defining the metabolic landscape of immune responses to S. aureus biofilm with a focus on two clinically relevant models, namely, craniotomy and prosthetic joint infection.
{"title":"Immunometabolism shapes chronic Staphylococcus aureus infection: insights from biofilm infection models","authors":"Adedayo E Ogunware, Tammy Kielian","doi":"10.1016/j.mib.2025.102612","DOIUrl":"10.1016/j.mib.2025.102612","url":null,"abstract":"<div><div><em>Staphylococcus aureus</em> is both a commensal bacterium and versatile pathogen, capable of transitioning from a benign colonizer to cause invasive disease. Its ability to form biofilm — a resilient, highly structured bacterial community — plays a key role in chronic infections, including those associated with medical implants and native tissues. The unique microenvironments of these biofilm niches create challenges for the host immune system, complicating pathogen clearance. Immunometabolism, the interplay between immune function and metabolic programming, plays a crucial role in dictating how the host combats <em>S. aureus</em> biofilms. Leukocytes undergo profound metabolic changes in response to biofilm, which can lead to dysregulated immune responses and persistent infection. This review explores recent insights defining the metabolic landscape of immune responses to <em>S. aureus</em> biofilm with a focus on two clinically relevant models, namely, craniotomy and prosthetic joint infection.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"86 ","pages":"Article 102612"},"PeriodicalIF":5.9,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115531","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 : 2025-04-28DOI: 10.1016/j.mib.2025.102611
Matthew J Bush , Bastien Casu , Susan Schlimpert
Bacteria display diverse strategies for cell division, exemplified by the multicellular life cycle of Streptomyces, a genus within the Actinomycetota phylum. Filamentous growing Streptomyces utilise two distinct division modes: during vegetative growth, nonconstricting cross-walls divide the mycelial network into long multinucleate compartments, while during reproductive growth, sporulation septation results in a ‘multiple division event’ that produces dozens of unigenomic spores that can separate and disperse in the environment.
The cellular mechanisms governing these two types of cell division in Streptomyces are inherently complex and present specific biological challenges that involve core cell division proteins and several genus-specific factors. This review highlights recent advances and open questions in our understanding of Streptomyces cell biology, with a focus on key cell division components and the interplay of the chromosome with the division machinery, enabling these organisms to grow as multicellular filaments and form unicellular spores.
{"title":"Dividing lines: compartmentalisation and division in Streptomyces","authors":"Matthew J Bush , Bastien Casu , Susan Schlimpert","doi":"10.1016/j.mib.2025.102611","DOIUrl":"10.1016/j.mib.2025.102611","url":null,"abstract":"<div><div>Bacteria display diverse strategies for cell division, exemplified by the multicellular life cycle of <em>Streptomyces</em>, a genus within the Actinomycetota phylum. Filamentous growing <em>Streptomyces</em> utilise two distinct division modes: during vegetative growth, nonconstricting cross-walls divide the mycelial network into long multinucleate compartments, while during reproductive growth, sporulation septation results in a ‘multiple division event’ that produces dozens of unigenomic spores that can separate and disperse in the environment.</div><div>The cellular mechanisms governing these two types of cell division in <em>Streptomyces</em> are inherently complex and present specific biological challenges that involve core cell division proteins and several genus-specific factors. This review highlights recent advances and open questions in our understanding of <em>Streptomyces</em> cell biology, with a focus on key cell division components and the interplay of the chromosome with the division machinery, enabling these organisms to grow as multicellular filaments and form unicellular spores.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102611"},"PeriodicalIF":5.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143883025","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 : 2025-04-25DOI: 10.1016/j.mib.2025.102610
Philip J Spence , Wiebke Nahrendorf , Florian A Bach
We’ve had more than a hundred years of discovery-based human malaria research that has made steady progress in observing disease processes (such as sequestration and vascular occlusion) as well as potential mechanisms of immunity. These observations now take centre stage as we enter an era of mass vaccination that will alter the natural history and epidemiology of malaria. We will need to understand how to protect individuals from breakthrough infections and populations from a shift in the mean age of exposure. It is therefore paramount that we start to directly test our long-standing hypotheses about the causes of disease and the pathways to protection. This is now made possible by improvements to complex cellular model systems as well as a sea-change in our attitude towards human intervention studies. Mechanistic insight is therefore no longer limited to animal models, which are always imperfect, but can be achieved in people and in vivo.
{"title":"Moving beyond discovery science to a mechanistic understanding of human malaria","authors":"Philip J Spence , Wiebke Nahrendorf , Florian A Bach","doi":"10.1016/j.mib.2025.102610","DOIUrl":"10.1016/j.mib.2025.102610","url":null,"abstract":"<div><div>We’ve had more than a hundred years of discovery-based human malaria research that has made steady progress in observing disease processes (such as sequestration and vascular occlusion) as well as potential mechanisms of immunity. These observations now take centre stage as we enter an era of mass vaccination that will alter the natural history and epidemiology of malaria. We will need to understand how to protect individuals from breakthrough infections and populations from a shift in the mean age of exposure. It is therefore paramount that we start to directly test our long-standing hypotheses about the causes of disease and the pathways to protection. This is now made possible by improvements to complex cellular model systems as well as a sea-change in our attitude towards human intervention studies. Mechanistic insight is therefore no longer limited to animal models, which are always imperfect, but can be achieved in people and <em>in vivo</em>.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102610"},"PeriodicalIF":5.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874772","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 : 2025-04-18DOI: 10.1016/j.mib.2025.102609
Megha Shrivastava , Deeptodeep Roy , Rachna Chaba
Bacteria use host-derived long-chain fatty acids (LCFAs) as nutrients, signals, and membrane building blocks. Although the impact of LCFAs on the pathogenesis of Gram-negative bacteria via membrane remodeling or signaling is well-documented, their importance as a nutrient source for bacterial proliferation and virulence is an emerging research area with definitive studies reported only for Salmonella Typhimurium, Vibrio cholerae, and Pseudomonas aeruginosa. Moreover, recent studies in Escherichia coli have shown that LCFA degradation confers redox stress. Here, we review the known role of LCFAs as nutrients during infection in Gram-negative human pathogens and the association of LCFA degradation with redox stress and stress response mechanisms. We suggest that for understanding how, as nutrients, LCFAs influence host–bacterial interactions, it is necessary to resolve whether LCFA utilization also causes redox stress in pathogens, with defense mechanisms preconditioning them for challenging host environments, or if pathogens have pre-existing mechanisms that prevent LCFA-induced stress.
{"title":"Long-chain fatty acids as nutrients for Gram-negative bacteria: stress, proliferation, and virulence","authors":"Megha Shrivastava , Deeptodeep Roy , Rachna Chaba","doi":"10.1016/j.mib.2025.102609","DOIUrl":"10.1016/j.mib.2025.102609","url":null,"abstract":"<div><div>Bacteria use host-derived long-chain fatty acids (LCFAs) as nutrients, signals, and membrane building blocks. Although the impact of LCFAs on the pathogenesis of Gram-negative bacteria via membrane remodeling or signaling is well-documented, their importance as a nutrient source for bacterial proliferation and virulence is an emerging research area with definitive studies reported only for <em>Salmonella</em> Typhimurium, <em>Vibrio cholerae</em>, and <em>Pseudomonas aeruginosa</em>. Moreover, recent studies in <em>Escherichia coli</em> have shown that LCFA degradation confers redox stress. Here, we review the known role of LCFAs as nutrients during infection in Gram-negative human pathogens and the association of LCFA degradation with redox stress and stress response mechanisms. We suggest that for understanding how, as nutrients, LCFAs influence host–bacterial interactions, it is necessary to resolve whether LCFA utilization also causes redox stress in pathogens, with defense mechanisms preconditioning them for challenging host environments, or if pathogens have pre-existing mechanisms that prevent LCFA-induced stress.</div></div>","PeriodicalId":10921,"journal":{"name":"Current opinion in microbiology","volume":"85 ","pages":"Article 102609"},"PeriodicalIF":5.9,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143842520","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 : 2025-04-02DOI: 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}
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