Infection and Immunity最新文献

{"title":"Erratum for Honorato et al., \"Extracellular vesicles of <i>Emergomyces africanus</i> modulate host immune responses and reflect metabolic adaptations to nutrient availability\".","authors":"Leandro Honorato, Albaniza Liuane Ribeiro do Nascimento Sabino, Jhon Jhamilton Artunduaga Bonilla, Susana Ruiz Mendoza, Julio Kornetz, Flavia C G Dos Reis, Elaine C Albergoni, Vinicius Alves, Susana Frases, Allan Jefferson Guimarães, Daniel Zamith-Miranda, Simone Sidoli, Joshua D Nosanchuk, Marcio L Rodrigues, Leonardo Nimrichter","doi":"10.1128/iai.00434-26","DOIUrl":"10.1128/iai.00434-26","url":null,"abstract":"","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0043426"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760140","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}

{"title":"Growing <i>Staphylococcus aureus</i> in synthetic cystic fibrosis medium promotes colonization in a murine pneumonia model.","authors":"Justin M Luu, Ian N Moore, Dina A Moustafa, Joanna B Goldberg","doi":"10.1128/iai.00283-26","DOIUrl":"10.1128/iai.00283-26","url":null,"abstract":"<p><p><i>Staphylococcus aureus</i> is a leading cause of bacterial infections worldwide and can lead to diseases, such as osteomyelitis, skin, and lung infections in humans. Murine infection models have been an essential tool to the study of <i>S. aureus</i> virulence, although they do have their limitations. In murine pneumonia models, <i>S. aureus</i> infections are generally not well maintained. We hypothesize that culturing <i>S. aureus</i> under different conditions, such as in Synthetic CF Medium 2 (SCFM2), would increase bacterial respiratory loads compared to growing the bacteria on standard rich medium agar plates. We observed that culturing six <i>S. aureus</i> strains from various sources in SCFM2 resulted in a neutral or increased level of bacterial lung load compared with those cultured on agar plates. Focusing on one strain, WU1, we found that culturing in SCFM2 improved bacterial persistence in the oropharynx and led to a sustained long-term lung infection compared with agar plates. We further noted that mice experienced increased inflammation in both lobes of the lungs when infected with WU1 cultured in SCFM2 compared with agar plates. Overall, we have shown that culturing <i>S. aureus</i> under different conditions prior to infection impacts the level of colonization and host response.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0028326"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678334","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}

{"title":"Characterization of <i>Pasteurella multocida</i> type B capsule biosynthesis proteins.","authors":"Thomas R Smallman, Chantelle M Cairns, Frank St Michael, Xiaochu Wang, Manon Sabouraud, Andrew D Cox, Marina Harper, John D Boyce","doi":"10.1128/iai.00049-26","DOIUrl":"10.1128/iai.00049-26","url":null,"abstract":"<p><p><i>Pasteurella multocida</i> causes several severe animal diseases, including hemorrhagic septicemia in ungulates. Strains of <i>P. multocida</i> are differentiated into five capsular and nine lipopolysaccharide genotypes. To date, only <i>P. multocida</i> strains that produce capsule types B and E have been recovered from cases of hemorrhagic septicemia. The structure of the type B capsule has recently been determined to be a repeating main chain of N-acetyl glucosamine (GlcNAc) and N-acetyl mannosaminuronic acid (ManNAcA), with a fructose and glycine side chain. In this study, we investigated the role of proteins involved in capsule biosynthesis in <i>P. multocida</i> strain M1404, a bison hemorrhagic septicemia isolate that produces a type B capsule. Using capsule absorbance assays, Alcian blue stains, and capsule Western blots to assess capsule production and export, as well as in-source collision-induced dissociation mass spectrometry to determine capsule structure, we show that BcbC is likely the capsule synthase; BcbE and BcbG are involved in fructose side chain addition, and BcbH is likely the glycine transferase. Furthermore, we show that inactivation of <i>bcbE</i>, <i>bcbG</i>, or <i>bcbH</i> significantly decreases overall capsule production in <i>P. multocida</i> strain M1404. Additionally, heterologous expression of <i>bcbABCDI</i> in a <i>P. multocida</i> strain VP161 (type A) capsule mutant allowed production of a repeating GlcNAc-ManNAcA monomer in this strain background that was indistinguishable from the type B main chain, indicating that these genes are necessary and sufficient for synthesis of the main repeating type B polysaccharide.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0004926"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678398","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}

{"title":"Early enhanced control of <i>Plasmodium yoelii</i> infection in IL-10-deficient mice is independent of IFN-γ, IL-12, and the humoral response.","authors":"Meghan D Jones, Kara A O'Neal, Sheldon L Zeltner, Alison R Gouch, Jeanette M Ramos, Jason S Stumhofer","doi":"10.1128/iai.00196-26","DOIUrl":"10.1128/iai.00196-26","url":null,"abstract":"<p><p>The outcome of a <i>Plasmodium</i> infection depends on the timely regulation of the robust pro-inflammatory response required to eliminate the parasite, but this response can cause tissue damage if not properly controlled. Interleukin-10 (IL-10) is an important regulatory cytokine that prevents immunopathology during many <i>Plasmodium</i> infections; however, this protection comes at the expense of less effective parasite control. This is illustrated by infection with blood-stage <i>Plasmodium yoelii</i>, in which mice exhibit a lower parasite load in the absence of IL-10. However, the immune components that limit parasite burden in the absence of IL-10 remain poorly understood. Abolishing IL-10 led to a predicted increase in T_H1 polarization and a higher production of IL-12 and interferon-γ (IFN-γ). However, the enhanced production of these cytokines did not explain the improved parasite control seen in <i>Il10^-/-</i> mice. Loss of IL-10 signaling reduced the accumulation of germinal center B cells and plasmablasts in the spleen, indicating a role for IL-10 in supporting the humoral response. However, although B cells are essential for survival, they do not play a critical role in early parasite control in IL-10-deficient mice. Moreover, <i>Il10^-/-</i> mice lacking IFN-γ and B cells can limit early parasite expansion, suggesting that IL-10 suppresses host-protective pathways beyond the functions of B cells and IFN-γ in parasite control.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0019626"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678364","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}

{"title":"Innate immune recognition of <i>Debaryomyces hansenii</i> requires Dectin-1-Card9 signaling.","authors":"Kevin P Newhall, Sarah K McNeer, Scott T Espenschied, Elora G Dolan, Julie Y Zhou, Deborah A Hogan, Thaddeus S Stappenbeck","doi":"10.1128/iai.00157-26","DOIUrl":"10.1128/iai.00157-26","url":null,"abstract":"<p><p>Innate immune signaling plays a key role in host response to infection, yet the pattern recognition receptors that detect non-model gut-associated yeasts remain poorly defined. Here, we investigated macrophage sensing of <i>Debaryomyces hansenii</i>, a food-derived yeast that we found to be enriched within intestinal ulcers of Crohn disease (CD) patients. Using a cell surface receptor antibody screen of bone marrow-derived macrophages infected with a CD patient isolate of <i>D. hansenii</i>, we showed that <i>D. hansenii</i>-induced macrophage activation characterized by increased expression of co-stimulatory molecules, MHC-II, and pattern recognition receptors, including the C-type lectin receptor Dectin-1. Antibody blockade experiments showed both Dectin-1 and complement receptor 3 subunit CD11b were required for phagocytosis of <i>D. hansenii</i>, while Dectin-1 was uniquely required for production of the pro-inflammatory cytokine tumor necrosis factor (Tnf). CRISPR-Cas9-mediated deletion of Dectin-1 phenocopied antibody neutralization effects on phagocytosis. Furthermore, deletion of Dectin-1 or its downstream signaling adaptor molecule Card9 resulted in reduced Tnf secretion in response to <i>D. hansenii</i>. Dectin-1-mediated uptake of <i>D. hansenii</i> was observed in primary bone marrow-derived macrophage and dendritic cells, as well as across the spectrum of macrophage polarization states. Together, these findings define the role of Dectin-1-Card9 signaling axis in innate immune cell sensing of <i>D. hansenii</i>. These findings support the emerging relevance of innate immune recognition of a yeast in Crohn disease pathogenesis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0015726"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669369","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}

{"title":"A multivalent subunit vaccine augments pre-existing immunity to protect against T3SS-positive <i>Pseudomonas aeruginosa</i> but reveals immunological interference against ExlA-positive strains.","authors":"Debaki R Howlader, Sayan Das, Satabdi Biswas, Zackary K Dietz, Robert K Ernst, William D Picking, Wendy L Picking","doi":"10.1128/iai.00175-26","DOIUrl":"10.1128/iai.00175-26","url":null,"abstract":"<p><p><i>Pseudomonas aeruginosa</i> (Pa) is a ubiquitous, opportunistic nosocomial pathogen that poses a significant threat due to its innate and acquired multidrug resistance. Novel vaccine strategies are urgently needed for vulnerable populations, many of which harbor pre-existing immunity from prior encounters with Pa. Here, we evaluated a multivalent subunit vaccine combining type III secretion system (T3SS) antigens and exolysin A (ExlA) in a nanoemulsion formulation using a clinically relevant murine pulmonary pre-exposure model. This approach allowed us to determine whether vaccination could overcome the limitations of the host's initial, ineffective immune response. Vaccination fundamentally transforms suboptimal baseline memory into a potent, multi-faceted Th1/Th17-polarized response. This globally transformed signature was characterized by significantly enhanced antigen-specific IFN-<i>γ</i> and IL-17A production, both locally and systematically in the lung, with exceptionally large biological effect sizes (Cohen's <i>d</i> values reaching 21.35). By utilizing log10 transformation to accurately reflect pathogen growth kinetics, we demonstrated that this vaccine-augmented immunity conferred statistically significant protection following heterologous challenge. In the twice-exposed cohort, vaccination promoted superior bacterial clearance of the T3SS-positive strain, though clearance of the ExlA-positive strain was not enhanced, potentially due to immunological interference from pre-existing T3SS memory. In the thrice-exposed cohort, a functional protective threshold was observed, where high levels of natural immunity matched the vaccine-induced clearance levels. Our findings established that our vaccine formulation can effectively boost and redirect pre-existing immunity, offering a promising approach to overcome the limitations of natural exposure and protect at-risk individuals from diverse Pa infections.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0017526"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669265","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}

{"title":"Protein kinase F regulates the virulence of <i>Mycobacterium tuberculosis</i>.","authors":"Flor Torres-Juarez, Shivangi Rastogi, David Young, Ashton T Belew, Paul J Baker, Viplov K Biswas, Shannon E Khan, Najib M El-Sayed, D Branch Moody, Katrin D Mayer-Barber, Volker Briken","doi":"10.1128/iai.00698-25","DOIUrl":"10.1128/iai.00698-25","url":null,"abstract":"<p><p>The serine/threonine protein kinase F (PknF) of <i>Mycobacterium tuberculosis</i> (Mtb) has poorly defined targets and functions but is involved in limiting NLRP3 inflammasome activation in murine macrophages and dendritic cells <i>in vitro</i>. The importance of PknF for the virulence of Mtb <i>in vivo</i> is not known. Here, we demonstrate that the Mtb CDC1551 deletion mutant of <i>pknF</i> (∆<i>pknF</i>) expresses significantly increased levels of the lipid pthiocerol dimycoserosate (PDIM), a polyketide lipid with pro-virulence properties. The ∆<i>pknF</i> mutant strain compared with the Mtb and complemented strains showed a 100-fold increase in growth at day 28 and about a 10-fold increase in growth at days 90-98 in the lungs of mice. The increase in pulmonary bacterial loads after infection with the ∆<i>pknF</i> strain was conserved even in <i>Nlrp3</i>-deficient mice, arguing that PknF modulates Mtb virulence independently of NLRP3-inflammasome activation in mice. Staining of lung sections revealed increased inflammation in the lungs of ∆<i>pknF</i> strain-infected mice when compared with Mtb and the complemented mutant strain. Highly susceptible B6.Sst1^S mice displayed decreased host resistance, with significantly decreased survival when infected with the ∆<i>pknF</i> strain compared to the complemented strain or Mtb. In conclusion, our data suggest that expression of PknF, as a modulator of multiple downstream effector proteins, restricts the virulence of Mtb in the lungs of mice through an NLRP3 inflammasome-independent mechanism, but potentially via suppressing production of the virulence lipid, PDIM.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0069825"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148591344","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}

{"title":"Desiccation tolerance as a driver of environmental persistence and transmission in nosocomial bacterial pathogens.","authors":"Michael J Bucher, Alejandro Rivera-Madera, Erin R Green","doi":"10.1128/iai.00557-25","DOIUrl":"10.1128/iai.00557-25","url":null,"abstract":"<p><p>Hospital-acquired infections (HAIs) represent a major global health burden, leading to increased patient morbidity, mortality, and healthcare costs. These infections frequently occur following patient contact with microbial pathogens persisting on indwelling devices and other abiotic surfaces in the hospital environment. A key driver of this persistence is the ability to survive the total loss of water, a phenomenon known as desiccation tolerance. While desiccation tolerance has been studied across various kingdoms of life, comparatively little is known about the molecular mechanisms that enable bacterial pathogens to tolerate extreme water loss. In this review, we will examine the consequences of desiccation stress in bacteria and highlight conserved mechanisms by which bacterial cells tolerate drying, including spore formation, capsule synthesis, osmolyte accumulation, expression of intrinsically disordered proteins, and other protective mechanisms. We will also examine the mechanisms and consequences of desiccation tolerance in several clinically significant nosocomial pathogens and review emerging evidence that desiccation stress responses may influence other bacterial traits, such as antimicrobial resistance, polymicrobial community interactions, and virulence. Understanding the mechanisms by which nosocomial pathogens tolerate desiccation may reveal novel strategies to disrupt pathogen reservoirs and reduce future HAI transmission.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0055725"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669411","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}

{"title":"Subunits of adaptor protein complex-1 make distinct contributions to the virulence of <i>Cryptococcus neoformans</i>.","authors":"Kabir Bhalla, Eddy Sánchez-León, Yu-Hsuan Huang, Guanggan Hu, Anisha Neogi, Alba Torres-Cano, Oscar Zaragoza, Pauline Johnson, James W Kronstad","doi":"10.1128/iai.00100-26","DOIUrl":"10.1128/iai.00100-26","url":null,"abstract":"<p><p>Cryptococcal meningoencephalitis is among the most prevalent invasive fungal diseases, posing a threat to immunocompromised individuals and representing a growing global health concern. The mechanisms of cryptococcal trafficking of virulence factors during disease are incompletely understood. Adaptor protein (AP) complexes play crucial roles in intracellular trafficking by orchestrating the sorting of macromolecular cargo and serving as essential components of the endocytic and secretory pathways. In a recent study, we demonstrated that <i>Cryptococcus neoformans</i> cells lacking the AP-1 complex subunits exhibit impaired elaboration of virulence factors and fail to survive in the harsh conditions of the macrophage phagolysosome. Although we characterized the phenotypes of AP-1 deficient cells <i>in vitro</i>, the contribution of this complex to pathogenesis remains unexplored. In this study, we show that mutants deficient in AP-1 complex subunits are either avirulent or exhibit attenuated virulence in a murine inhalational model. Loss of the small subunit resulted in the formation of granuloma-like lesions in mouse lungs with early containment of infection but eventual mortality, whereas mutants lacking the large subunits were rapidly cleared by mice. The delayed onset of disease in mice caused by mutants lacking the small subunit was marked by delayed weight loss and increased respiration rate, yet the mutant exhibited enhanced dissemination during late-stage infection, coinciding with waning immune responses and elevated collagen deposition. These findings demonstrate that deficiencies in the AP-1 complex impair <i>C. neoformans</i> virulence, reveal distinct roles for individual subunits, and identify the complex as a potential target for therapeutic intervention in cryptococcosis.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0010026"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669356","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}

{"title":"Sero-epidemiological and functional evaluation of IgG specific for a cysteine protease inhibitor of <i>Plasmodium falciparum</i>, falstatin.","authors":"Jyoti Bhardwaj, Erik L Gaskin, Prasida Holla, Oscar De Los Santos, Safiatou Doumbo, Kassoum Kayentao, Aissata Ongoiba, Boubacar Traore, Peter D Crompton, Tuan M Tran","doi":"10.1128/iai.00202-26","DOIUrl":"10.1128/iai.00202-26","url":null,"abstract":"<p><p>Recently approved malaria pre-erythrocytic vaccines are important public health tools for the reduction of malaria morbidity and mortality. However, these vaccines have shown reduced protection in some of the most vulnerable age groups, require multiple dosing, and have the potential for parasite escape. These limitations have motivated the development of vaccines targeting multiple stages of the parasite life cycle. To ensure a robust pipeline, pre-clinical evaluation of additional malaria vaccine candidate antigens remains a key priority. The <i>P. falciparum</i> cysteine protease inhibitor falstatin can limit the cysteine protease activity of falcipains, controlling proteolysis at the site of merozoite entry on erythrocytes, thereby facilitating parasite invasion. Antibodies against falstatin have been shown to reduce the ability of merozoites to invade erythrocytes, raising the possibility that naturally acquired antibody responses could confer a similar advantage to the host. Here, IgG responses to full-length falstatin (falstatin_FL) and two smaller, conserved regions (falstatin_35-68 and falstatin_289-335) were determined at the pre-malaria season baseline in a prospective cohort study conducted in Kalifabougou, Mali. The presence of anti-falstatin IgG was not associated with reduced risk of clinical malaria overall. However, baseline falstatin seropositivity predicted a non-statistically significant reduction in risk of febrile malaria within the first 30 days after incident parasitemia (log-rank statistic 3.2, <i>P</i> = 0.072). Using <i>in vitro</i> growth inhibitory assays, neither affinity-purified anti-falstatin_289-335 IgG nor affinity-purified anti-falstatin_FL IgG consistently inhibited <i>P. falciparum</i> blood-stage parasites. Larger cohort studies would be needed to confirm whether pre-existing anti-falstatin antibodies can delay the progression of malaria symptoms after blood-stage infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0020226"},"PeriodicalIF":3.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669417","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}