Pub Date : 2025-10-08DOI: 10.1016/j.chom.2025.09.011
Simona Seizova, Christopher J. Tonkin
In recent papers published in Cell and Cell Host and Microbe, Marzook et al. and Huang et al. investigate how Cryptosporidium, an enteric parasite, can acquire nutrients from its host and deals with potentially toxic products. These studies highlight that transporters are likely key to the success of this parasite.
在最近发表在Cell and Cell Host and Microbe杂志上的论文中，Marzook等人和Huang等人研究了肠道寄生虫隐孢子虫（Cryptosporidium）如何从宿主那里获取营养并处理潜在的有毒产物。这些研究强调，转运蛋白可能是这种寄生虫成功的关键。
{"title":"Metabolic clash of Cryptosporidium and its host","authors":"Simona Seizova, Christopher J. Tonkin","doi":"10.1016/j.chom.2025.09.011","DOIUrl":"https://doi.org/10.1016/j.chom.2025.09.011","url":null,"abstract":"In recent papers published in <em>Cell</em> and <em>Cell Host and Microbe</em>, Marzook et al. and Huang et al. investigate how <em>Cryptosporidium</em>, an enteric parasite, can acquire nutrients from its host and deals with potentially toxic products. These studies highlight that transporters are likely key to the success of this parasite.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"22 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145241324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-30DOI: 10.1016/j.chom.2025.09.009
Rodrigo de Oliveira Formiga, Qing Li, Yining Zhao, Márcio Augusto Campos Ribeiro, Perle Guarino-Vignon, Rand Fatouh, Leonard Dubois, Laura Creusot, Virginie Puchois, Salomé Amouyal, Iria Alonso Salgueiro, Marius Bredon, Loïc Chollet, Tatiana Ledent, Cyril Scandola, Jean-Philippe Auger, Camille Danne, Gerhard Krönke, Emma Tkacz, Patrick Emond, Harry Sokol
Cadaverine is a polyamine produced by the gut microbiota with links to health and disease, notably inflammatory bowel disease (IBD). Here, we show that cadaverine shapes monocyte-macrophage immunometabolism in a context- and concentration-dependent fashion to impact macrophage functionality. At baseline, cadaverine is taken up via L-lysine transporters and activates the thioredoxin system, while during inflammation, cadaverine signals through aconitate decarboxylase 1 (Acod1)-itaconate. Both pathways induce activation of transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), which supports mitochondrial respiration and promotes immunoregulatory macrophage polarization. Conversely, under higher concentrations, cadaverine acts via histamine 4 receptor, leading to glycolysis-driven inflammation and pro-inflammatory functions in macrophages. Likewise, cadaverine exhibits paradoxical effects in experimental colitis, either protective or detrimental, evoking opposite fates on macrophages depending on levels dictated by Enterobacteriaceae. In IBD patients, elevated cadaverine correlated with higher flare risk. Our findings implicate cadaverine as a microbiota-derived metabolite manipulating macrophage energy metabolism with consequences in intestinal inflammation and implications for IBD pathogenesis.
{"title":"Immunometabolic reprogramming of macrophages by gut microbiota-derived cadaverine controls colon inflammation","authors":"Rodrigo de Oliveira Formiga, Qing Li, Yining Zhao, Márcio Augusto Campos Ribeiro, Perle Guarino-Vignon, Rand Fatouh, Leonard Dubois, Laura Creusot, Virginie Puchois, Salomé Amouyal, Iria Alonso Salgueiro, Marius Bredon, Loïc Chollet, Tatiana Ledent, Cyril Scandola, Jean-Philippe Auger, Camille Danne, Gerhard Krönke, Emma Tkacz, Patrick Emond, Harry Sokol","doi":"10.1016/j.chom.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.chom.2025.09.009","url":null,"abstract":"Cadaverine is a polyamine produced by the gut microbiota with links to health and disease, notably inflammatory bowel disease (IBD). Here, we show that cadaverine shapes monocyte-macrophage immunometabolism in a context- and concentration-dependent fashion to impact macrophage functionality. At baseline, cadaverine is taken up via L-lysine transporters and activates the thioredoxin system, while during inflammation, cadaverine signals through aconitate decarboxylase 1 (Acod1)-itaconate. Both pathways induce activation of transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), which supports mitochondrial respiration and promotes immunoregulatory macrophage polarization. Conversely, under higher concentrations, cadaverine acts via histamine 4 receptor, leading to glycolysis-driven inflammation and pro-inflammatory functions in macrophages. Likewise, cadaverine exhibits paradoxical effects in experimental colitis, either protective or detrimental, evoking opposite fates on macrophages depending on levels dictated by <em>Enterobacteriaceae</em>. In IBD patients, elevated cadaverine correlated with higher flare risk. Our findings implicate cadaverine as a microbiota-derived metabolite manipulating macrophage energy metabolism with consequences in intestinal inflammation and implications for IBD pathogenesis.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"2 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145189273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Plant-associated microorganisms interact with each other and with host plants via intricate chemical signals, offering multiple benefits, including enhanced nutrition. We report a mechanism through which the rhizosphere microbiome improves plant growth under sulfur (S) deficiency. Disruption of plant S homeostasis caused a coordinated shift in the composition and S-metabolism of the rhizosphere microbiome. Leveraging this, we developed an 18-membered synthetic rhizosphere bacterial community (SynCom) that rescued the growth of Arabidopsis and a leafy Brassicaceae vegetable under S-deficiency. This beneficial trait is taxonomically widespread among SynCom members, with bacterial pairs providing both synergistic and neutral effects on host growth. Notably, stronger competitive interactions among SynCom members conferred greater fitness benefits to the host, suggesting a trans-kingdom (plant-microbe) fitness trade-off. Finally, guided chemical screening, deletion knockout mutants, and targeted metabolomics identified and validated microbially released glutathione (GSH) as the necessary bioactive signal that coordinates the trans-kingdom fitness trade-off and improves plant growth under sulfur limitation.
{"title":"A bacterial signal coordinates plant-microbe fitness trade-off to enhance sulfur deficiency tolerance in plants","authors":"Arijit Mukherjee, Mrinmoy Mazumder, Arun Verma, Hitesh Tikariha, Raktim Bhattacharya, Qi En Ooi, Sanjay Swarup","doi":"10.1016/j.chom.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.chom.2025.09.007","url":null,"abstract":"Plant-associated microorganisms interact with each other and with host plants via intricate chemical signals, offering multiple benefits, including enhanced nutrition. We report a mechanism through which the rhizosphere microbiome improves plant growth under sulfur (S) deficiency. Disruption of plant S homeostasis caused a coordinated shift in the composition and S-metabolism of the rhizosphere microbiome. Leveraging this, we developed an 18-membered synthetic rhizosphere bacterial community (SynCom) that rescued the growth of <em>Arabidopsis</em> and a leafy Brassicaceae vegetable under S-deficiency. This beneficial trait is taxonomically widespread among SynCom members, with bacterial pairs providing both synergistic and neutral effects on host growth. Notably, stronger competitive interactions among SynCom members conferred greater fitness benefits to the host, suggesting a trans-kingdom (plant-microbe) fitness trade-off. Finally, guided chemical screening, deletion knockout mutants, and targeted metabolomics identified and validated microbially released glutathione (GSH) as the necessary bioactive signal that coordinates the trans-kingdom fitness trade-off and improves plant growth under sulfur limitation.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"18 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-26DOI: 10.1016/j.chom.2025.09.010
Markus Lakemeyer, Rocco Latorre, Kristyna Blazkova, Hannah M. Wood, Dane D. Jensen, Nayab Shakil, Scott C. Thomas, Deepak Saxena, Yatendra Mulpuri, David Poolman, Paz Duran, Laura J. Keller, David E. Reed, Brian L. Schmidt, Néstor N. Jiménez-Vargas, Fangxi Xu, Alan E. Lomax, Nigel W. Bunnett, Matthew Bogyo
Protease-activated receptor 2 (PAR2) is a central regulator of intestinal barrier function, inflammation, and pain. Upregulated intestinal proteolysis and PAR2 signaling are implicated in inflammatory bowel diseases (IBDs) and irritable bowel syndrome (IBS), conditions often associated with gut microbiome alterations. To identify potential bacterial regulators of PAR2 activity, we developed a functional assay for PAR2 processing to screen a library of diverse gut microbes. We identify multiple bacteria that secrete proteases capable of cleaving host PAR2. Using chemoproteomic profiling with a covalent irreversible inhibitor, we uncovered a previously uncharacterized Bacteroides fragilis serine protease 1 (Bfp1) and show that it cleaves and activates PAR2 in multicellular and murine models. PAR2 cleavage by Bfp1 disrupts the intestinal barrier, sensitizes nociceptors, and triggers colonic inflammation and abdominal pain. Collectively, our findings uncover Bfp1-mediated PAR2 processing as an axis of host-commensal interaction in the gut that has the potential to be targeted for therapeutic intervention in IBD or IBS.
{"title":"A Bacteroides fragilis protease activates host PAR2 to induce intestinal pain and inflammation","authors":"Markus Lakemeyer, Rocco Latorre, Kristyna Blazkova, Hannah M. Wood, Dane D. Jensen, Nayab Shakil, Scott C. Thomas, Deepak Saxena, Yatendra Mulpuri, David Poolman, Paz Duran, Laura J. Keller, David E. Reed, Brian L. Schmidt, Néstor N. Jiménez-Vargas, Fangxi Xu, Alan E. Lomax, Nigel W. Bunnett, Matthew Bogyo","doi":"10.1016/j.chom.2025.09.010","DOIUrl":"https://doi.org/10.1016/j.chom.2025.09.010","url":null,"abstract":"Protease-activated receptor 2 (PAR<sub>2</sub>) is a central regulator of intestinal barrier function, inflammation, and pain. Upregulated intestinal proteolysis and PAR<sub>2</sub> signaling are implicated in inflammatory bowel diseases (IBDs) and irritable bowel syndrome (IBS), conditions often associated with gut microbiome alterations. To identify potential bacterial regulators of PAR<sub>2</sub> activity, we developed a functional assay for PAR<sub>2</sub> processing to screen a library of diverse gut microbes. We identify multiple bacteria that secrete proteases capable of cleaving host PAR<sub>2</sub>. Using chemoproteomic profiling with a covalent irreversible inhibitor, we uncovered a previously uncharacterized <em>Bacteroides fragilis</em> serine protease 1 (Bfp1) and show that it cleaves and activates PAR<sub>2</sub> in multicellular and murine models. PAR<sub>2</sub> cleavage by Bfp1 disrupts the intestinal barrier, sensitizes nociceptors, and triggers colonic inflammation and abdominal pain. Collectively, our findings uncover Bfp1-mediated PAR<sub>2</sub> processing as an axis of host-commensal interaction in the gut that has the potential to be targeted for therapeutic intervention in IBD or IBS.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"100 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-25DOI: 10.1016/j.chom.2025.09.006
Sarah K. Munyoki, Julie P. Goff, Amanda Reshke, Erin Wilderoter, Nyasha Mafarachisi, Antonija Kolobaric, Yi Sheng, Steven J. Mullett, Gabrielle E. King, Jacob D. DeSchepper, Richard J. Bookser, Carlos A. Castro, Stacy L. Gelhaus, Mayara Grizotte-Lake, Kathleen E. Morrison, Anthony J. Zeleznik, Timothy W. Hand, Miguel A. Brieño-Enriquez, Eldin Jašarević
Infertility affects one in six people, but the underlying mechanisms remain unclear. We show that the microbiota governs female reproductive longevity in mice. Germ-free mice have fewer primordial follicles, increased atresia, and ovarian fibrosis, leading to smaller litters, fewer offspring, and a shorter reproductive lifespan. Germ-free mice are born with a similar ovarian reserve but display excessive activation, impaired progression, and increased atresia during post-natal development. Microbiome colonization during a critical post-natal window rescues premature ovarian reserve loss by normalizing follicle kinetics and gene expression patterns. These changes parallel increased short-chain fatty acids (SCFAs), and SCFA administration mitigates ovarian dysfunction in germ-free mice. Similar oocyte dysfunction occurred in conventionally raised mice fed a high-fat diet, but additional dietary fiber helped preserve oocyte quality and embryo competence. Thus, host-microbe interactions shape female fertility, and microbiota-targeted interventions may offer strategies to address reproductive disorders.
{"title":"The microbiota extends the reproductive lifespan of mice by safeguarding the ovarian reserve","authors":"Sarah K. Munyoki, Julie P. Goff, Amanda Reshke, Erin Wilderoter, Nyasha Mafarachisi, Antonija Kolobaric, Yi Sheng, Steven J. Mullett, Gabrielle E. King, Jacob D. DeSchepper, Richard J. Bookser, Carlos A. Castro, Stacy L. Gelhaus, Mayara Grizotte-Lake, Kathleen E. Morrison, Anthony J. Zeleznik, Timothy W. Hand, Miguel A. Brieño-Enriquez, Eldin Jašarević","doi":"10.1016/j.chom.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.chom.2025.09.006","url":null,"abstract":"Infertility affects one in six people, but the underlying mechanisms remain unclear. We show that the microbiota governs female reproductive longevity in mice. Germ-free mice have fewer primordial follicles, increased atresia, and ovarian fibrosis, leading to smaller litters, fewer offspring, and a shorter reproductive lifespan. Germ-free mice are born with a similar ovarian reserve but display excessive activation, impaired progression, and increased atresia during post-natal development. Microbiome colonization during a critical post-natal window rescues premature ovarian reserve loss by normalizing follicle kinetics and gene expression patterns. These changes parallel increased short-chain fatty acids (SCFAs), and SCFA administration mitigates ovarian dysfunction in germ-free mice. Similar oocyte dysfunction occurred in conventionally raised mice fed a high-fat diet, but additional dietary fiber helped preserve oocyte quality and embryo competence. Thus, host-microbe interactions shape female fertility, and microbiota-targeted interventions may offer strategies to address reproductive disorders.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"99 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145134464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-18DOI: 10.1016/j.chom.2025.08.011
Aleksander Czauderna, Grishma Kulkarni, Niccolò Bianchi, Liqing Cheng, Marissa Sim, Nicola R. Realini, Joanna Gach, Aurelie Caillon, Joachim Kloehn, Gérard Lambeau, Annika Hausmann, Stefano Serra, Matthew T. Sorbara, Simone Becattini
Immune responses can significantly alter the structure and function of the gut microbiota, leading to rapid transcriptional and metabolic shifts in commensal microbes. However, the host mediators involved in this process and their effects on bacteria remain poorly elucidated. Here, using a flagellin injection model to induce immune activation, we identified unsaturated long-chain fatty acids (uLCFAs) as broad modulators that are released into the gut lumen and alter bacterial gene expression. Luminal release of uLCFAs is partially mediated by host phospholipases, including PLA2G5. In response to uLCFAs, commensals such as Blautia trigger the expression of ohyA, encoding oleate hydratase, which converts toxic uLCFAs to non-toxic hydroxy fatty acids with immunomodulatory properties. Remarkably, oral administration of uLCFAs to mice replicates many of the bacterial transcriptional changes induced by flagellin. This molecular loop underscores the sophisticated interactions between host and microbiota and sheds light on how immune responses affect gut commensal functions.
{"title":"Long-chain unsaturated fatty acids released during immune responses stimulate host-microbe trans-kingdom communication","authors":"Aleksander Czauderna, Grishma Kulkarni, Niccolò Bianchi, Liqing Cheng, Marissa Sim, Nicola R. Realini, Joanna Gach, Aurelie Caillon, Joachim Kloehn, Gérard Lambeau, Annika Hausmann, Stefano Serra, Matthew T. Sorbara, Simone Becattini","doi":"10.1016/j.chom.2025.08.011","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.011","url":null,"abstract":"Immune responses can significantly alter the structure and function of the gut microbiota, leading to rapid transcriptional and metabolic shifts in commensal microbes. However, the host mediators involved in this process and their effects on bacteria remain poorly elucidated. Here, using a flagellin injection model to induce immune activation, we identified unsaturated long-chain fatty acids (uLCFAs) as broad modulators that are released into the gut lumen and alter bacterial gene expression. Luminal release of uLCFAs is partially mediated by host phospholipases, including PLA2G5. In response to uLCFAs, commensals such as <em>Blautia</em> trigger the expression of <em>ohyA</em>, encoding oleate hydratase, which converts toxic uLCFAs to non-toxic hydroxy fatty acids with immunomodulatory properties. Remarkably, oral administration of uLCFAs to mice replicates many of the bacterial transcriptional changes induced by flagellin. This molecular loop underscores the sophisticated interactions between host and microbiota and sheds light on how immune responses affect gut commensal functions.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"68 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145078378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-17DOI: 10.1016/j.chom.2025.08.015
Qian Zhang, Wenyue Zheng, Haoxiang Huang, Shuchen Wang, Sizhe Li, Kaixiang Wang, Haixia You, Hao Gong, Xiayan Pan, Zhongqiang Qi, Yan Du, Junjie Yu, Mina Yu, Huijuan Cao, Rongsheng Zhang, Yuanchao Wang, Daolong Dou, Zhenchuan Ma, Yongfeng Liu, Tianqiao Song
The interfamily transfer of pattern-recognition receptors (PRRs) offers a promising strategy to enhance plant immunity; however, factors causing functional limitations across species remain unknown. Here, we identify secreted TOM20 domain-containing protein (STOM), a previously uncharacterized fungal microbe-associated molecular pattern (MAMP) that triggers immunity in Nicotiana benthamiana but not in rice (Oryza sativa). We identify NbSTOMR as the receptor that recognizes and binds STOM, and NbSTOMRh as the co-receptor that, despite lacking ligand-binding ability, is essential through its extracellular interaction with NbSTOMR. Transferring NbSTOMR to rice fails to confer resistance, but NbSTOMRh alone enhances resistance to false smut and blast disease. Evolutionary analyses reveal that while STOMR is conserved, monocots have lost STOMRh due to transposon-mediated chromosomal separation of its extracellular domain. Although OsSTOMR binds STOM, OsSTOMRh is non-functional; however, NbSTOMRh promotes OsSTOMR-dependent STOM recognition. These findings highlight the critical role of co-receptors in overcoming taxonomic barriers and provide a strategy for reconstituting PRR-mediated immunity in monocot crops.
{"title":"Fungal resistance in rice is restored by interfamily transfer of an evolutionarily lost co-receptor","authors":"Qian Zhang, Wenyue Zheng, Haoxiang Huang, Shuchen Wang, Sizhe Li, Kaixiang Wang, Haixia You, Hao Gong, Xiayan Pan, Zhongqiang Qi, Yan Du, Junjie Yu, Mina Yu, Huijuan Cao, Rongsheng Zhang, Yuanchao Wang, Daolong Dou, Zhenchuan Ma, Yongfeng Liu, Tianqiao Song","doi":"10.1016/j.chom.2025.08.015","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.015","url":null,"abstract":"The interfamily transfer of pattern-recognition receptors (PRRs) offers a promising strategy to enhance plant immunity; however, factors causing functional limitations across species remain unknown. Here, we identify secreted TOM20 domain-containing protein (STOM), a previously uncharacterized fungal microbe-associated molecular pattern (MAMP) that triggers immunity in <em>Nicotiana benthamiana</em> but not in rice (<em>Oryza sativa</em>). We identify NbSTOMR as the receptor that recognizes and binds STOM, and NbSTOMRh as the co-receptor that, despite lacking ligand-binding ability, is essential through its extracellular interaction with NbSTOMR. Transferring NbSTOMR to rice fails to confer resistance, but NbSTOMRh alone enhances resistance to false smut and blast disease. Evolutionary analyses reveal that while STOMR is conserved, monocots have lost STOMRh due to transposon-mediated chromosomal separation of its extracellular domain. Although OsSTOMR binds STOM, OsSTOMRh is non-functional; however, NbSTOMRh promotes OsSTOMR-dependent STOM recognition. These findings highlight the critical role of co-receptors in overcoming taxonomic barriers and provide a strategy for reconstituting PRR-mediated immunity in monocot crops.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"52 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145072169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-16DOI: 10.1016/j.chom.2025.08.016
Xianhong Zhang, Xue Jin, Jiawei Li, Francisco Dini-Andreote, Hongyu Li, Muhammad Khashi u Rahman, Minmin Du, Fengzhi Wu, Zhong Wei, Xingang Zhou, Marcel G.A. van der Heijden, Matthias C. Rillig
Arbuscular mycorrhizal fungi can interconnect the roots of individual plants by forming common mycorrhizal networks (CMNs). These symbiotic structures can act as conduits for interplant communication. Despite their importance, the mechanisms of signal transfer via CMNs and their implications for plant community performance remain unknown. Here, we demonstrate that CMNs act as a pathway to elicit defense responses in healthy receiver plants connected to pathogen-infected donors. Specifically, we show that donor plants infected by the phytopathogen Botrytis cinerea transfer jasmonic acid via CMNs, which then act as a chemical signal in receiver plants. This signal transfer to receiver plants induces shifts in root exudates, promoting the recruitment of specific microbial taxa (Streptomyces and Actinoplanes) that are directly linked to the suppression of B. cinerea infection. Collectively, our study reveals that CMNs act as interplant chemical communication conduits, transferring signals that contribute to plant disease resistance via modulation of the rhizosphere microbiota.
{"title":"Common mycorrhizal networks facilitate plant disease resistance by altering rhizosphere microbiome assembly","authors":"Xianhong Zhang, Xue Jin, Jiawei Li, Francisco Dini-Andreote, Hongyu Li, Muhammad Khashi u Rahman, Minmin Du, Fengzhi Wu, Zhong Wei, Xingang Zhou, Marcel G.A. van der Heijden, Matthias C. Rillig","doi":"10.1016/j.chom.2025.08.016","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.016","url":null,"abstract":"Arbuscular mycorrhizal fungi can interconnect the roots of individual plants by forming common mycorrhizal networks (CMNs). These symbiotic structures can act as conduits for interplant communication. Despite their importance, the mechanisms of signal transfer via CMNs and their implications for plant community performance remain unknown. Here, we demonstrate that CMNs act as a pathway to elicit defense responses in healthy receiver plants connected to pathogen-infected donors. Specifically, we show that donor plants infected by the phytopathogen <em>Botrytis cinerea</em> transfer jasmonic acid via CMNs, which then act as a chemical signal in receiver plants. This signal transfer to receiver plants induces shifts in root exudates, promoting the recruitment of specific microbial taxa (<em>Streptomyces</em> and <em>Actinoplanes</em>) that are directly linked to the suppression of <em>B. cinerea</em> infection. Collectively, our study reveals that CMNs act as interplant chemical communication conduits, transferring signals that contribute to plant disease resistance via modulation of the rhizosphere microbiota.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"19 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-16DOI: 10.1016/j.chom.2025.08.012
Amanda M. Brandow, Samantha N. Atkinson, Zulmary Manjarres, Vanessa L. Ehlers, McKenna L. Pratt, Iti Mehta, Sruthi Mudunuri, Aishwarya Kappagantu, Stephanie I. Shiers, Khadijah Mazhar, Mackenzie A. Simms, Sahar Alhendi, Anagha Sheshadri, Anna M. Cervantes, Jeffrey C. Reese, Diana Tavares-Ferreira, Ishwarya Sankaranarayanan, Mandee K. Schaub, Tyler B. Waltz, Michael Hayward, Katelyn E. Sadler
Individuals with sickle cell disease (SCD) suffer from debilitating chronic pain that does not have a clear etiology. Recent 16S ribosomal RNA gene sequencing studies revealed gut dysbiosis in individuals with SCD. It is unclear, however, whether these intestinal microbial changes contribute to chronic SCD pain. Using transgenic SCD mice, we determined that chronic SCD pain is alleviated following fecal microbiota transplantation from healthy controls, specifically by increasing the relative abundance of probiotic Akkermansia muciniphila. Reciprocally, transplantation of the SCD gut microbiome induced persistent pain in wild-type recipients via bilirubin-vagus nerve TRPM2 signaling. Biospecimens from individuals with SCD and spatial transcriptomic analysis of human nodose ganglia tissue identified additional bacterial species and neuronally expressed transcripts that should be explored as novel SCD analgesic targets.
{"title":"Gut microbiota and metabolites drive chronic sickle cell disease pain in mice","authors":"Amanda M. Brandow, Samantha N. Atkinson, Zulmary Manjarres, Vanessa L. Ehlers, McKenna L. Pratt, Iti Mehta, Sruthi Mudunuri, Aishwarya Kappagantu, Stephanie I. Shiers, Khadijah Mazhar, Mackenzie A. Simms, Sahar Alhendi, Anagha Sheshadri, Anna M. Cervantes, Jeffrey C. Reese, Diana Tavares-Ferreira, Ishwarya Sankaranarayanan, Mandee K. Schaub, Tyler B. Waltz, Michael Hayward, Katelyn E. Sadler","doi":"10.1016/j.chom.2025.08.012","DOIUrl":"https://doi.org/10.1016/j.chom.2025.08.012","url":null,"abstract":"Individuals with sickle cell disease (SCD) suffer from debilitating chronic pain that does not have a clear etiology. Recent 16S ribosomal RNA gene sequencing studies revealed gut dysbiosis in individuals with SCD. It is unclear, however, whether these intestinal microbial changes contribute to chronic SCD pain. Using transgenic SCD mice, we determined that chronic SCD pain is alleviated following fecal microbiota transplantation from healthy controls, specifically by increasing the relative abundance of probiotic <em>Akkermansia muciniphila</em>. Reciprocally, transplantation of the SCD gut microbiome induced persistent pain in wild-type recipients via bilirubin-vagus nerve TRPM2 signaling. Biospecimens from individuals with SCD and spatial transcriptomic analysis of human nodose ganglia tissue identified additional bacterial species and neuronally expressed transcripts that should be explored as novel SCD analgesic targets.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"35 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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