Journal of Innate Immunity最新文献_第5页

Serine Protease Networks Mediate Immune Responses in Extra-Embryonic Tissues of Eggs in the Tobacco Hornworm, Manduca sexta. 丝氨酸蛋白酶网络介导烟草角虫卵胚外组织的免疫应答。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2022-12-13 DOI: 10.1159/000527974

Tisheng Shan, Yang Wang, Neal T Dittmer, Michael R Kanost, Haobo Jiang

{"title":"Serine Protease Networks Mediate Immune Responses in Extra-Embryonic Tissues of Eggs in the Tobacco Hornworm, Manduca sexta.","authors":"Tisheng Shan, Yang Wang, Neal T Dittmer, Michael R Kanost, Haobo Jiang","doi":"10.1159/000527974","DOIUrl":"10.1159/000527974","url":null,"abstract":"The melanization and Toll pathways, regulated by a network of serine proteases and noncatalytic serine protease homologs (SPHs), have been investigated mostly in adult and larval insects. However, how these innate immune reactions are regulated in insect eggs remains unclear. Here we present evidence from transcriptome and proteome analyses that extra-embryonic tissues (yolk and serosa) of early-stage Manduca sexta eggs are immune competent, with expression of immune effector genes including prophenoloxidase and antimicrobial peptides. We identified gene products of the melanization and Toll pathways in M. sexta eggs. Through in vitro reconstitution experiments, we demonstrated that constitutive and infection-induced serine protease cascade modules that stimulate immune responses exist in the extra-embryonic tissues of M. sexta eggs. The constitutive module (HP14b-SP144-GP6) may promote rapid early immune signaling by forming a cascade activating the cytokine Spätzle and regulating melanization by activating prophenoloxidase (proPO). The inducible module (HP14a-HP21-HP5) may trigger enhanced activation of Spätzle and proPO at a later phase of infection. Crosstalk between the two modules may occur in transition from the constitutive to the induced response in eggs inoculated with bacteria. Examination of data from two other well-studied insect species, Tribolium castaneum and Drosophila melanogaster, supports a role for a serosa-dependent constitutive protease cascade in protecting early embryos against invading pathogens.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"365-379"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10493118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Immunothrombosis and Complement Activation Contribute to Disease Severity and Adverse Outcome in COVID-19. 免疫血栓形成和补体激活会导致新冠肺炎的疾病严重程度和不良后果。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-11-08 DOI: 10.1159/000533339

Tiphaine Ruggeri, Yasmin De Wit, Noëlia Schärz, Gerard van Mierlo, Anne Angelillo-Scherrer, Justine Brodard, Joerg C Schefold, Cédric Hirzel, Ilse Jongerius, Sacha Zeerleder

{"title":"Immunothrombosis and Complement Activation Contribute to Disease Severity and Adverse Outcome in COVID-19.","authors":"Tiphaine Ruggeri, Yasmin De Wit, Noëlia Schärz, Gerard van Mierlo, Anne Angelillo-Scherrer, Justine Brodard, Joerg C Schefold, Cédric Hirzel, Ilse Jongerius, Sacha Zeerleder","doi":"10.1159/000533339","DOIUrl":"10.1159/000533339","url":null,"abstract":"Severe COVID-19 is characterized by systemic inflammation and multiple organ dysfunction syndrome (MODS). Arterial and venous thrombosis are involved in the pathogenesis of MODS and fatality in COVID-19. There is evidence that complement and neutrophil activation in the form of neutrophil extracellular traps are main drivers for development of microvascular complications in COVID-19. Plasma and serum samples were collected from 83 patients infected by SARS-CoV-2 during the two first waves of COVID-19, before the availability of SARS-CoV-2 vaccination. Samples were collected at enrollment, day 11, and day 28; and patients had differing severity of disease. In this comprehensive study, we measured cell-free DNA, neutrophil activation, deoxyribonuclease I activity, complement activation, and D-dimers in longitudinal samples of COVID-19 patients. We show that all the above markers, except deoxyribonuclease I activity, increased with disease severity. Moreover, we provide evidence that in severe disease there is continued neutrophil and complement activation, as well as D-dimer formation and nucleosome release, whereas in mild and moderate disease all these markers decrease over time. These findings suggest that neutrophil and complement activation are important drivers of microvascular complications and that they reflect immunothrombosis in these patients. Neutrophil activation, complement activation, cell-free DNA, and D-dimer levels have the potential to serve as reliable biomarkers for disease severity and fatality in COVID-19. They might also serve as suitable markers with which to monitor the efficacy of therapeutic interventions in COVID-19.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"850-864"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10699833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perilipin 1 Deficiency Prompts Lipolysis in Lipid Droplets and Aggravates the Pathogenesis of Persistent Immune Activation in Drosophila. 脂周蛋白1缺乏促进脂滴的脂解，并加重果蝇持续免疫激活的发病机制。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-09-23 DOI: 10.1159/000534099

Lei Wang, Jiaxin Lin, Kaiyan Yang, Weina Wang, Yan Lv, Xiangkang Zeng, Yaya Zhao, Junjing Yu, Lei Pan

{"title":"Perilipin 1 Deficiency Prompts Lipolysis in Lipid Droplets and Aggravates the Pathogenesis of Persistent Immune Activation in Drosophila.","authors":"Lei Wang, Jiaxin Lin, Kaiyan Yang, Weina Wang, Yan Lv, Xiangkang Zeng, Yaya Zhao, Junjing Yu, Lei Pan","doi":"10.1159/000534099","DOIUrl":"10.1159/000534099","url":null,"abstract":"Lipid droplets (LDs) are highly dynamic intracellular organelles, which are involved in lots of biological processes. However, the dynamic morphogenesis and functions of intracellular LDs during persistent innate immune responses remain obscure. In this study, we induce long-term systemic immune activation in Drosophila through genetic manipulation. Then, the dynamic pattern of LDs is traced in the Drosophila fat body. We find that deficiency of Plin1, a key regulator of LDs' reconfiguration, blocks LDs minimization at the initial stage of immune hyperactivation but enhances LDs breakdown at the later stage of sustained immune activation via recruiting the lipase Brummer (Bmm, homologous to human ATGL). The high wasting in LDs shortens the lifespan of flies with high-energy-cost immune hyperactivation. Therefore, these results suggest a critical function of LDs during long-term immune activation and provide a potential treatment for the resolution of persistent inflammation.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"697-708"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4d/d4/jin-2023-0015-0001-534099.PMC10601664.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41114840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of Piezo1 Ameliorates Intestinal Inflammation and Limits the Activation of Group 3 Innate Lymphoid Cells in Experimental Colitis. 在实验性结肠炎中，抑制Piezo1可改善肠道炎症并限制第3组固有淋巴细胞的激活。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-09-19 DOI: 10.1159/000533525

Chang Liu, Yanan Xia, Shichen Fu, Fanyi Meng, Bingcheng Feng, Leiqi Xu, Lixiang Li, Xiuli Zuo

{"title":"Inhibition of Piezo1 Ameliorates Intestinal Inflammation and Limits the Activation of Group 3 Innate Lymphoid Cells in Experimental Colitis.","authors":"Chang Liu, Yanan Xia, Shichen Fu, Fanyi Meng, Bingcheng Feng, Leiqi Xu, Lixiang Li, Xiuli Zuo","doi":"10.1159/000533525","DOIUrl":"10.1159/000533525","url":null,"abstract":"Piezo1, the mechanosensory ion channel, has attracted increasing attention for its essential roles in various inflammatory responses and immune-related diseases. Although most of the key immune cells in inflammatory bowel disease (IBD) have been reported to be regulated by Piezo1, the specific role of Piezo1 in colitis has yet to be intensively studied. The present study investigated the impact of pharmacological inhibition of Piezo1 on dextran sulfate sodium (DSS)-induced colitis and explored the role of Piezo1 in intestinal immune cells in the context of colitis. We observed upregulated expression of Piezo1 in the colon tissue of mice with DSS-induced colitis. Pharmacological inhibition of Piezo1 by GsMTx4 diminished the severity of colitis. Piezo1 inhibition downregulated the expression of pro-inflammatory mediators Il1b, Il6, and Ptgs2 in colonic tissue and suppressed the production of IL-6 from macrophages and dendritic cells without altering the balance of T helper (Th) cells. In particular, Piezo1 did not affect cell viability but regulated cell proliferation and production of IL-17A in group 3 innate lymphoid cells (ILC3s), which is dependent on the PI3K-Akt-mTOR signaling pathway. Our findings uncover Piezo1 as an effective regulator of gut inflammation. Targeting Piezo1 could be a promising strategy to modulate intestinal immunity in IBD.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"709-723"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/84/c3/jin-2023-0015-0001-533525.PMC10601687.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41124956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tryptophol Acetate and Tyrosol Acetate, Small-Molecule Metabolites Identified in a Probiotic Mixture, Inhibit Hyperinflammation. 在益生菌混合物中发现的小分子代谢物乙酸色醇酯和乙酸酪醇酯可抑制炎症反应。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-02-21 DOI: 10.1159/000529782

Orit Malka, Ravit Malishev, Marina Bersudsky, Manikandan Rajendran, Mathumathi Krishnamohan, Jakeer Shaik, Daniel A Chamovitz, Evgeni Tikhonov, Eliya Sultan, Omry Koren, Ron N Apte, Benyamin Rosental, Elena Voronov, Raz Jelinek

{"title":"Tryptophol Acetate and Tyrosol Acetate, Small-Molecule Metabolites Identified in a Probiotic Mixture, Inhibit Hyperinflammation.","authors":"Orit Malka, Ravit Malishev, Marina Bersudsky, Manikandan Rajendran, Mathumathi Krishnamohan, Jakeer Shaik, Daniel A Chamovitz, Evgeni Tikhonov, Eliya Sultan, Omry Koren, Ron N Apte, Benyamin Rosental, Elena Voronov, Raz Jelinek","doi":"10.1159/000529782","DOIUrl":"10.1159/000529782","url":null,"abstract":"Probiotic fermented foods are perceived as contributing to human health; however, solid evidence for their presumptive therapeutic systemic benefits is generally lacking. Here we report that tryptophol acetate and tyrosol acetate, small-molecule metabolites secreted by the probiotic milk-fermented yeast Kluyveromyces marxianus, inhibit hyperinflammation (e.g., \"cytokine storm\"). Comprehensive in vivo and in vitro analyses, employing LPS-induced hyperinflammation models, reveal dramatic effects of the molecules, added in tandem, on mice morbidity, laboratory parameters, and mortality. Specifically, we observed attenuated levels of the proinflammatory cytokines IL-6, IL-1α, IL-1β, and TNF-α and reduced reactive oxygen species. Importantly, tryptophol acetate and tyrosol acetate did not completely suppress proinflammatory cytokine generation, rather brought their concentrations back to baseline levels, thus maintaining core immune functions, including phagocytosis. The anti-inflammatory effects of tryptophol acetate and tyrosol acetate were mediated through downregulation of TLR4, IL-1R, and TNFR signaling pathways and increased A20 expression, leading to NF-kB inhibition. Overall, this work illuminates phenomenological and molecular details underscoring anti-inflammatory properties of small molecules identified in a probiotic mixture, pointing to potential therapeutic avenues against severe inflammation.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"531-547"},"PeriodicalIF":4.7,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10101109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of Macrophage Cell Surface GAPDH Alters LL-37 Internalization and Downstream Effects in the Cell. 巨噬细胞表面 GAPDH 的调节改变了 LL-37 在细胞中的内化和下游效应。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-04-20 DOI: 10.1159/000530083

Asmita Dhiman, Sharmila Talukdar, Gaurav Kumar Chaubey, Rahul Dilawari, Radheshyam Modanwal, Surbhi Chaudhary, Anil Patidar, Vishant Mahendra Boradia, Pradeep Kumbhar, Chaaya Iyengar Raje, Manoj Raje

{"title":"Regulation of Macrophage Cell Surface GAPDH Alters LL-37 Internalization and Downstream Effects in the Cell.","authors":"Asmita Dhiman, Sharmila Talukdar, Gaurav Kumar Chaubey, Rahul Dilawari, Radheshyam Modanwal, Surbhi Chaudhary, Anil Patidar, Vishant Mahendra Boradia, Pradeep Kumbhar, Chaaya Iyengar Raje, Manoj Raje","doi":"10.1159/000530083","DOIUrl":"10.1159/000530083","url":null,"abstract":"Mycobacterium tuberculosis (M.tb), the major causative agent of tuberculosis, has evolved mechanisms to evade host defenses and persist within host cells. Host-directed therapies against infected cells are emerging as an effective option. Cationic host defense peptide LL-37 is known to internalize into cells and induce autophagy resulting in intracellular killing of M.tb. This peptide also regulates the immune system and interacts with the multifunctional protein glyceraldehyde-3-phosphate dehydrogenase (GAPDH) inside macrophages. Our investigations revealed that GAPDH moonlights as a mononuclear cell surface receptor that internalizes LL-37. We confirmed that the surface levels of purinergic receptor 7, the receptor previously reported for this peptide, remained unaltered on M.tb infected macrophages. Upon infection or cellular activation with IFNγ, surface recruited GAPDH bound to and internalized LL-37 into endocytic compartments via a lipid raft-dependent process. We also discovered a role for GAPDH in LL-37-mediated autophagy induction and clearance of intracellular pathogens. In infected macrophages wherein GAPDH had been knocked down, we observed an inhibition of LL-37-mediated autophagy which was rescued by GAPDH overexpression. This process was dependent on intracellular calcium and p38 MAPK pathways. Our findings reveal a previously unknown process by which macrophages internalize an antimicrobial peptide via cell surface GAPDH and suggest a moonlighting role of GAPDH in regulating cellular phenotypic responses of LL-37 resulting in reduction of M.tb burden.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"581-598"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9742541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex. 抑制膜攻击复合物的人源化C6单克隆抗体的开发、鉴定和体内验证。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2022-05-12 DOI: 10.1159/000524587

Heidi Gytz Olesen, Iliana Michailidou, Wioleta M Zelek, Jeroen Vreijling, Patrick Ruizendaal, Ferry de Klein, J Arnoud Marquart, Thomas B Kuipers, Hailiang Mei, Yuchun Zhang, Muhammad Ahasan, Krista K Johnson, Yi Wang, B Paul Morgan, Marcus van Dijk, Kees Fluiter, Gregers Rom Andersen, Frank Baas

{"title":"Development, Characterization, and in vivo Validation of a Humanized C6 Monoclonal Antibody that Inhibits the Membrane Attack Complex.","authors":"Heidi Gytz Olesen, Iliana Michailidou, Wioleta M Zelek, Jeroen Vreijling, Patrick Ruizendaal, Ferry de Klein, J Arnoud Marquart, Thomas B Kuipers, Hailiang Mei, Yuchun Zhang, Muhammad Ahasan, Krista K Johnson, Yi Wang, B Paul Morgan, Marcus van Dijk, Kees Fluiter, Gregers Rom Andersen, Frank Baas","doi":"10.1159/000524587","DOIUrl":"10.1159/000524587","url":null,"abstract":"Damage and disease of nerves activates the complement system. We demonstrated that activation of the terminal pathway of the complement system leads to the formation of the membrane attack complex (MAC) and delays regeneration in the peripheral nervous system. Animals deficient in the complement component C6 showed improved recovery after neuronal trauma. Thus, inhibitors of the MAC might be of therapeutic use in neurological disease. Here, we describe the development, structure, mode of action, and properties of a novel therapeutic monoclonal antibody, CP010, against C6 that prevents formation of the MAC in vivo. The monoclonal antibody is humanized and specific for C6 and binds to an epitope in the FIM1-2 domain of human and primate C6 with sub-nanomolar affinity. Using biophysical and structural studies, we show that the anti-C6 antibody prevents the interaction between C6 and C5/C5b by blocking the C6 FIM1-2:C5 C345c axis. Systemic administration of the anti-C6 mAb caused complete depletion of free C6 in circulation in transgenic rats expressing human C6 and thereby inhibited MAC formation. The antibody prevented disease in experimental autoimmune myasthenia gravis and ameliorated relapse in chronic relapsing experimental autoimmune encephalomyelitis in human C6 transgenic rats. CP010 is a promising complement C6 inhibitor that prevents MAC formation. Systemic administration of this C6 monoclonal antibody has therapeutic potential in the treatment of neuronal disease.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":"1 1","pages":"16-36"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42867411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Bruton's Tyrosine Kinase in Neutrophils Is Crucial for Host Defense against Klebsiella pneumoniae. 中性粒细胞中的布鲁顿酪氨酸激酶对宿主防御肺炎克雷伯菌至关重要。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2022-05-10 DOI: 10.1159/000524583

Zhe Liu, Alexander P N A De Porto, Regina De Beer, Joris J T H Roelofs, Onno J De Boer, Sandrine Florquin, Cornelis Van't Veer, Rudi W Hendriks, Tom Van der Poll, Alex F De Vos

{"title":"Bruton's Tyrosine Kinase in Neutrophils Is Crucial for Host Defense against Klebsiella pneumoniae.","authors":"Zhe Liu, Alexander P N A De Porto, Regina De Beer, Joris J T H Roelofs, Onno J De Boer, Sandrine Florquin, Cornelis Van't Veer, Rudi W Hendriks, Tom Van der Poll, Alex F De Vos","doi":"10.1159/000524583","DOIUrl":"10.1159/000524583","url":null,"abstract":"Humans with dysfunctional Bruton's tyrosine kinase (Btk) are highly susceptible to bacterial infections. Compelling evidence indicates that Btk is essential for B cell-mediated immunity, whereas its role in myeloid cell-mediated immunity against infections is controversial. In this study, we determined the contribution of Btk in B cells and neutrophils to host defense against the extracellular bacterial pathogen Klebsiella pneumoniae, a common cause of pulmonary infections and sepsis. Btk-/- mice were highly susceptible to Klebsiella infection, which was not reversed by Btk re-expression in B cells and restoration of natural antibody levels. Neutrophil-specific Btk deficiency impaired host defense against Klebsiella to a similar extent as complete Btk deficiency. Neutrophil-specific Btk deficiency abolished extracellular reactive oxygen species production in response to Klebsiella. These data indicate that expression of Btk in neutrophils is crucial, while in B cells, it is dispensable for in vivo host defense against K. pneumoniae.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":"1 1","pages":"1-15"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45364696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Intersection between Bacterial Metabolism and Innate Immunity. 细菌代谢和先天免疫之间的交叉点。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-10-27 DOI: 10.1159/000534872

Ivan C Acosta, Francis Alonzo

{"title":"The Intersection between Bacterial Metabolism and Innate Immunity.","authors":"Ivan C Acosta, Francis Alonzo","doi":"10.1159/000534872","DOIUrl":"10.1159/000534872","url":null,"abstract":"Background: The innate immune system is the first line of defense against microbial pathogens and is essential for maintaining good health. If pathogens breach innate barriers, the likelihood of infection is significantly increased. Many bacterial pathogens pose a threat to human health on account of their ability to evade innate immunity and survive in growth-restricted environments. These pathogens have evolved sophisticated strategies to obtain nutrients as well as manipulate innate immune responses, resulting in disease or chronic infection.Summary: The relationship between bacterial metabolism and innate immunity is complex. Although aspects of bacterial metabolism can be beneficial to the host, particularly those related to the microbiota and barrier integrity, others can be harmful. Several bacterial pathogens harness metabolism to evade immune responses and persist during infection. The study of these adaptive traits provides insight into the roles of microbial metabolism in pathogenesis that extend beyond energy balance. This review considers recent studies on bacterial metabolic pathways that promote infection by circumventing several facets of the innate immune system. We also discuss relationships between innate immunity and antibiotics and highlight future directions for research in this field.Key messages: Pathogenic bacteria have a remarkable capacity to harness metabolism to manipulate immune responses and promote pathogenesis. While we are beginning to understand the multifaceted and complex metabolic adaptations that occur during infection, there is still much to uncover with future research.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"782-803"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10663042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71412551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Human Ribonuclease 6 Has a Protective Role during Experimental Urinary Tract Infection. 人核糖核酸酶6在实验性尿路感染中的保护作用

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-01-01 Epub Date: 2023-11-18 DOI: 10.1159/000534736

Juan de Dios Ruiz-Rosado, Hanna Cortado, Macie Kercsmar, Birong Li, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Sudipti Gupta, Christina Ching, Ester Boix, Ashley R Jackson, John David Spencer, Brian Becknell

{"title":"Human Ribonuclease 6 Has a Protective Role during Experimental Urinary Tract Infection.","authors":"Juan de Dios Ruiz-Rosado, Hanna Cortado, Macie Kercsmar, Birong Li, Gregory Ballash, Israel Cotzomi-Ortega, Yuriko I Sanchez-Zamora, Sudipti Gupta, Christina Ching, Ester Boix, Ashley R Jackson, John David Spencer, Brian Becknell","doi":"10.1159/000534736","DOIUrl":"10.1159/000534736","url":null,"abstract":"Mounting evidence suggests that antimicrobial peptides and proteins (AMPs) belonging to the RNase A superfamily have a critical role in defending the bladder and kidney from bacterial infection. RNase 6 has been identified as a potent, leukocyte-derived AMP, but its impact on urinary tract infection (UTI) in vivo has not been demonstrated. To test the functional role of human RNase 6, we generated RNASE6 transgenic mice and studied their susceptibility to experimental UTI. In addition, we generated bone marrow-derived macrophages to study the impact of RNase 6 on antimicrobial activity within a cellular context. When subjected to experimental UTI, RNASE6 transgenic mice developed reduced uropathogenic Escherichia coli (UPEC) burden, mucosal injury, and inflammation compared to non-transgenic controls. Monocytes and macrophages were the predominant cellular sources of RNase 6 during UTI, and RNASE6 transgenic macrophages were more proficient at intracellular UPEC killing than non-transgenic controls. Altogether, our findings indicate a protective role for human RNase 6 during experimental UTI.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"865-875"},"PeriodicalIF":5.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10699853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138047148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0