Infection and Immunity最新文献

{"title":"Recombinant subunit vaccine against <i>Mycoplasma gallisepticum</i> disease confers cross-protection against multiple pathogenic strains.","authors":"Jeremy M Miller, Rosemary G Ozyck, Arlind B Mara, Esmeralda F Hernandez, Jessica B Malek, Edan R Tulman, Steven M Szczepanek, Steven J Geary","doi":"10.1128/iai.00025-26","DOIUrl":"10.1128/iai.00025-26","url":null,"abstract":"<p><p><i>Mycoplasma gallisepticum</i> (MG) is an avian respiratory pathogen of global concern, responsible for hundreds of millions of dollars in estimated economic damage each year. Given that MG is distributed across every continent except Antarctica, any globally applicable vaccine must provide protection against numerous strains. We previously published that an R_low-based subunit vaccine reduced both MG bacterial burden and tracheal pathology in a homologous infection model using virulent MG strain R_low. It remains unknown if the subunit vaccine could reduce disease burden induced by heterologous MG strains. To test this, we utilized a prime-boost schedule and challenged with either strain VA94 or Ap3AS. The vaccine significantly reduced disease burden induced by both heterologous strains as indicated by reduced MG burden and by reduced tracheal pathology. This demonstrates that an MG subunit vaccine has global potential.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0002526"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224749","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":"Implications of bacterial exposure to reactive oxygen and chlorine species.","authors":"Gracious Yoofi Donkor, Jan-Ulrik Dahl","doi":"10.1128/iai.00010-23","DOIUrl":"10.1128/iai.00010-23","url":null,"abstract":"<p><p>To inhabit aerobic environments, microbes must be able to cope with the reactive byproducts of aerobic growth. These toxic compounds, also named reactive oxygen species (ROS), damage a variety of cellular macromolecules, and thus demand universal adaptive responses in microorganisms. Beyond ROS, microbes must also contend with exogenous oxidants such as reactive chlorine species (RCS) and reactive nitrogen species (RNS). In the context of antimicrobial activity, discussions on exogenous reactive species have typically focused on pathogen clearance during the oxidative burst of activated leukocytes. However, the discovery that oxidative stress may contribute to the activity of bactericidal antibiotics presents new possibilities for targeting the antioxidant defenses of pathogens as an antimicrobial strategy for potentiating current antibiotics. Considering the emergence of antibiotic resistance in many clinically relevant bacteria, and the concurrent decline in antibiotic discovery efforts, such alternative treatment options are increasingly needed. In this minireview, we discuss the well-established pathways of oxidative stress resulting from endogenous and exogenous sources of ROS and RCS. We also contrast the macromolecular targets of ROS and RCS, as well as specialized detoxification mechanisms evolved by bacteria to minimize damage caused by each species. The implications of ROS/RCS exposure are then discussed in two facets: their contributions to antibiotic resistance and involvement in the activity of bactericidal antibiotics. Finally, we highlight antimicrobial strategies whose mode of action is proposed to depend on or involve ROS formation.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0001023"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211107","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":"Sedative choice alters <i>Klebsiella pneumoniae</i> lung pathogenesis and dissemination.","authors":"David R Mains, Ella R Rotman, Deanna K Aman, Denise A Ludvik, Anirudh Desikan, Acadia A Kocher, An N H Tran, Mark J Mandel, Nancy E Freitag","doi":"10.1128/iai.00069-26","DOIUrl":"10.1128/iai.00069-26","url":null,"abstract":"<p><p><i>Klebsiella pneumoniae</i> makes up 85% of carbapenem-resistant Enterobacteriaceae, bacteria that have become an urgent threat to public health. <i>K. pneumoniae</i> is largely transmitted in healthcare settings, where inpatients and outpatients are often anesthetized with the widely used anesthetic induction agent propofol. Recent evidence obtained from rodent infection models indicates that propofol exposure can dramatically increase host susceptibility to microbial infections. Given that intensive care patients who are at a greater risk for <i>K. pneumoniae</i> lung infections are often given propofol during their hospitalization, we investigated the outcome of <i>K. pneumoniae</i> infections in mice briefly sedated with either propofol or ketamine/xylazine as a control. Propofol-sedated mice experienced more rapid dissemination from the lungs to secondary sites of infection, and their lungs exhibited more severe pathology. Based on these observations, we investigated bacterial factors involved in infection and dissemination in mice with propofol or ketamine/xylazine sedation using a high-throughput insertion sequencing (INSeq) approach. We identified numerous novel potential virulence factors together with previously identified gene products, confirming the validity of our screen. We further characterized a mutant lacking the phospholipid retrograde trafficking chaperone MlaC and found that the degree of mutant attenuation was dependent upon the sedation method. These results highlight the importance of sedative choice when studying hospital-acquired microbial infections and suggest that sedation can influence the outcome of <i>K. pneumoniae</i> infection and dissemination in animal models.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0006926"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042142","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":"<i>Chlamydia pneumoniae</i> facilitates its development by recruiting PI4P to inclusion bodies via the Cpn0308-ACBD3-PI4KB pathway.","authors":"Xiaonan Feng, Tian'ai Cao, Xiaohui Jia, Zewei Jia, Ping Li, Yan Zhou, Tianjun Jia","doi":"10.1128/iai.00580-25","DOIUrl":"10.1128/iai.00580-25","url":null,"abstract":"<p><p><i>Chlamydia pneumoniae</i> (Cpn) is an obligate intracellular parasitic pathogen that replicates inside a membrane-bound vacuole termed the inclusion. This compartment is modified by chlamydial inclusion membrane proteins (Incs), which interact with host proteins to facilitate chlamydial development and pathogenicity. Among these, Cpn0308 localizes specifically to the inclusion membrane. Our previous study demonstrated that exogenously expressed Cpn0308 can interact with host protein ACBD3; here, we demonstrate this interaction during actual Cpn infection using endogenous proteins. This interplay proved critical for Cpn development, as ACBD3 knockout in HeLa cells led to significantly smaller inclusions, delayed transition from elementary bodies (EBs) to reticulate bodies (RBs), and reduced bacterial copy numbers. Mechanistically, the Cpn0308-ACBD3 interaction facilitates the recruitment of Phosphatidylinositol 4-kinase 3β (PI4KB) to the inclusion vicinity. This recruitment enhances the production and localization of Phosphatidylinositol 4-phosphate (PI4P) within Cpn<i>-</i>infected HeLa cells. Conversely, PI4KB and PI4P levels were markedly diminished in Cpn-infected ACBD3-knockout cells, whereas their expression remained unchanged in uninfected knockout cells. Furthermore, pharmacological inhibition of PI4KB with PIK93 impaired PI4P synthesis and suppressed Cpn replication. In conclusion, we propose a mechanism wherein the Cpn inclusion membrane protein Cpn0308 engages host ACBD3 to recruit PI4KB around the inclusion, which subsequently catalyzes PI4P production, thereby promoting the development and progression of <i>C. pneumoniae</i> infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0058025"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156032","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":"Protective efficacy of mutant strains of <i>Borrelia burgdorferi</i> as potential reservoir host-targeted biologics against Lyme disease.","authors":"Venkatesh Kumaresan, Trever C Smith, Miranda Lumbreras, Taylor MacMackin Ingle, Nathan Kilgore, Jolie F Starling-Lin, Elizabeth J Horn, J Seshu","doi":"10.1128/iai.00210-26","DOIUrl":"10.1128/iai.00210-26","url":null,"abstract":"<p><p>Lyme disease (LD), caused by <i>Borrelia burgdorferi</i> (<i>Bb</i>), is the most common vector-borne disease in the United States. Novel strategies to control transmission of <i>Bb</i> to humans via ticks are critical for the prevention of LD. One such strategy is to leverage non-infectious mutant strains of <i>Bb</i> for pathogen-derived biologics to block <i>Bb</i> transmission during the natural infectious cycle. Deletion of <u>B</u>orrelia host-<u>ad</u>aptation <u>R</u>egulator (<i>ΔbadR</i>) and replacement of eight conserved residues with alanines in Carbon Storage Regulator A of <i>Bb</i> (8S) resulted in mutants with upregulation of RpoS and several immunogenic lipoproteins, that were incapable of colonization in C3H/HeN mice. Intradermal vaccination of mice with the live mutant strains resulted in significant anti-borrelial antibody responses and a reduction in <i>Bb</i> acquisition by naïve <i>Ixodes scapularis</i> larvae following needle challenge with <i>Bb</i> B31-A3. While vaccination with the <i>ΔbadR</i> mutant conferred a significant reduction in the percentage of infected mice, ML23 and 8S mutants conferred variable levels of protection. Comparative proteomic analysis of purified borrelial lipoproteins (PBLs) from parental and mutant strains revealed similar and unique antigenic components. Infection-derived mouse serum and serum from Lyme disease patients exhibited reactivity to lysates and PBLs from these mutants. Immunization with PBLs from B31-A3 and 8S strains conferred significant protection against challenge with <i>Bb</i>-infected nymphs, underscoring the utility of PBLs as protective formulations. Overall, non-infectious mutant strains, or their lipoproteins, can be exploited as biologics to block the acquisition of <i>Bb</i> by naïve larvae from reservoir hosts, thereby disrupting the enzootic transmission cycle of the agent of Lyme disease.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0021026"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156006","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":"Phase variable colony morphotypes of <i>Clostridioides difficile</i> elicit distinct host responses during acute infection.","authors":"Jilarie A Santos-Santiago, Nicole C Gadda, Rani S Sellers, Rita Tamayo","doi":"10.1128/iai.00022-26","DOIUrl":"10.1128/iai.00022-26","url":null,"abstract":"<p><p>Many <i>Clostridioides difficile</i> strains can form two colony morphotypes: rough and smooth. The rough and smooth morphotypes differ in multiple phenotypes, including cell length and chaining, motility, biofilm production, and virulence in the hamster model of <i>C. difficile</i> infection (CDI). Colony morphology undergoes phase variation and is determined by the ON/OFF expression of <i>cmrRST</i>, which encodes a signal transduction system. Here, we test the hypothesis that differences in colony morphology and the associated phenotypes influence pathogenesis and the host response to infection. We first compared the rough and smooth colony variants of wild-type <i>C. difficile</i> in a mouse model of CDI. However, CmrRST phase varied during infection such that the <i>C. difficile</i> populations became indistinguishable in feces and tissues, and no differences in disease were observed in mice inoculated with these variants. We next circumvented phase variation using mutants that form only rough or only smooth colonies. Co-infection of mice with these phenotypically locked strains revealed that the smooth colony mutant has greater fitness than the rough mutant, which is outcompeted during late infection. In addition, NanoString analyses showed a higher number of differentially expressed pro-inflammatory genes and overall higher expression levels in mice infected with the rough colony mutant, independent of bacterial burden and toxin levels. Our results indicate that in a mouse model of CDI, cells from rough colonies are more immunostimulatory during early murine infection, potentially leading to reduced relative fitness compared to cells from smooth colonies.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0002226"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148204675","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":"Analysis of <i>in vivo</i> infection dynamics using bioluminescent <i>Giardia duodenalis</i>.","authors":"Rita Kosile, Bergeline C Nguemwo Tentokam, Peiran Shen, Nikki Farnham, Katherine McGowan, Scott Dawson, Steven M Singer","doi":"10.1128/iai.00144-26","DOIUrl":"10.1128/iai.00144-26","url":null,"abstract":"<p><p><i>Giardia duodenalis</i> is an intestinal protozoan transmitted through contaminated food and water and is a major cause of diarrheal disease worldwide and has been linked to post-infectious sequelae and growth impairment in children. Quantifying parasite burden <i>in vivo</i> is essential for studying infection dynamics and host responses, yet commonly used methods (stool PCR, antigen detection, and terminal trophozoite counts from segments of the intestine) are limited by intermittent stool shedding, uneven parasite distribution, sampling error, and lack of longitudinal data. We developed a bioluminescent reporter system for the assemblage B strain GS to enable noninvasive tracking of infection in mice without antibiotic pretreatment. Using <i>in vivo</i> bioluminescent imaging (BLI), we observed peak signal in immunocompetent C57BL/6J and BALB/c mice at days 6-8 post-infection, followed by return to baseline by ~day 10, consistent with the self-limiting nature of giardiasis. In immunodeficient mice, radiance increased and persisted over time, demonstrating stable luciferase expression during chronic infection <i>in vivo</i> without continuous antibiotic selection. Whole-animal radiance strongly correlated with direct trophozoite counts from excised intestinal segments (<i>r</i> = 0.915, <i>P</i> < 0.001), validating BLI as a useful alternative for determining parasite burden. Together, these findings establish BLI as a robust platform for longitudinal studies of <i>Giardia</i> infection dynamics and for future applications that may examine host immunity, the microbiota, nutrient-dependent effects, and drug testing.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0014426"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148251444","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":"Multiple TonB-dependent transport systems in <i>Helicobacter pylori</i>.","authors":"John T Loh, Chiamaka D Okoye, Dillon E Kunkle, W Hayes McDonald, Mark S McClain, Eric P Skaar, Timothy L Cover","doi":"10.1128/iai.00018-26","DOIUrl":"10.1128/iai.00018-26","url":null,"abstract":"<p><p>TonB-dependent transport systems (consisting of TonB-dependent transporters, TonB, ExbB, and ExbD) facilitate uptake of nutrients across the bacterial outer membrane. Tol-Pal systems contain components related to those of TonB systems. In this study, we investigated TonB-dependent transport systems in <i>Helicobacter pylori. H. pylori</i> genomes contain three <i>tonB</i> paralogs (designated <i>tonB1</i>, <i>tonB2</i>, and <i>tonB3/tolA</i>), three <i>exbB</i> paralogs, three <i>exbD</i> paralogs, six genes encoding putative TonB-dependent transporters, <i>tolB</i>, and <i>pal</i>. By using immunopurification and mass spectrometry methods, we show that TonB2, ExbB2, and ExbD2 co-purify with each other, consistent with the corresponding genes being in the same predicted operon. The <i>tonB1</i> gene is not linked to <i>exbB</i> or <i>exbD</i> genes, but we show that ExbB3 and ExbD3 co-purify with TonB1. The <i>tonB3/tolA</i> gene is in a predicted operon containing <i>exbB1/tolQ</i>, <i>exbD1/tolR</i>, <i>tolB</i>, and <i>pal</i>. We show that TonB3/TolA co-purifies with ExbB1/TolQ and ExbD1/TolR, suggesting that TonB3/TolA is a component of the Tol-Pal system. We show that <i>H. pylori tonB1</i> is essential for <i>H. pylori</i> growth, <i>tonB2</i> mutants require supplemental iron for growth, and <i>tonB3</i>/<i>tolA</i> is non-essential for growth <i>in vitro</i>. ICP-MS experiments showed that a <i>tonB2</i> mutant contains reduced levels of nickel compared to a wild-type strain, and correspondingly, the <i>tonB2</i> mutant exhibits reduced urease activity. These results indicate that the TonB2 system has an important role in <i>H. pylori</i> acquisition of nickel and iron. We propose that the TonB1 system has a key role in the acquisition of multiple nutrients required for <i>H. pylori</i> viability.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0001826"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156018","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":"The cholesterol-dependent cytolysin promotes <i>Streptococcus</i> systemic spread and induces arachidonic acid accumulation-mediated lethality in a murine intraperitoneal infection model.","authors":"Linya Xia, Xingyu Tian, Chen Yuan, Zhaoxuan Zhu, Fei Pan, Hongjie Fan, Karthik Hullahalli, Matthew K Waldor, Zhe Ma","doi":"10.1128/iai.00164-26","DOIUrl":"10.1128/iai.00164-26","url":null,"abstract":"<p><p>Streptococcal peritonitis is associated with a high mortality risk and sometimes accompanied by streptococcal toxic shock-like syndrome (STSLS). Here, we used a murine intraperitoneal model of <i>Streptococcus suis</i> serotype 2 (SS2) infection and applied bacterial lineage tracing to investigate the pathogen's population dynamics during streptococcal intraperitoneal infection. We found that the cholesterol-dependent cytolysin suilysin (SLY) was essential for acute lethality and facilitated bacterial systemic spread by mitigating infection bottlenecks and enabling vascular leakage in the peritoneal cavity. SLY induced marked accumulation of arachidonic acid (AA) in the peritoneal cavity. Although inhibition of AA synthesis alone did not prevent mortality, it widened the therapeutic window of antibiotic treatment, enhancing their efficacy and capacity to reduce lethality. These findings identify SLY as a critical virulence determinant linking inflammation-associated metabolic alterations, disruption of vascular integrity, and mortality and highlight AA metabolism as a promising adjunctive therapeutic target for acute SS2 intraperitoneal infection.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0016426"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148368309","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":"Dual host and pathogen targeting by MEK1/2 inhibitors.","authors":"Eryn Zuiker, Matthew E Long","doi":"10.1128/iai.00064-26","DOIUrl":"10.1128/iai.00064-26","url":null,"abstract":"<p><p>Therapeutic strategies that manipulate the host response to infection to reduce inflammation and host driven tissue damage may reduce disease pathogenesis. However, therapeutic approaches that have dual host-modulatory and antimicrobial therapeutic effects remain limited. Mammalian targeting MEK1/2 inhibitor compounds represent one class of small molecules that have now been recognized to have anti-viral effects through disruption of viral replication in epithelial cells and have direct anti-bacterial effects on gram-positive bacteria. MEK1/2 inhibitors elicit anti-inflammatory effects during <i>in vivo</i> infection and injury models that also include models of infection with gram-negative bacteria and parasites. This review aims to summarize progress made in understanding the effects of MEK1/2 inhibitor compounds on host innate immune cells and will highlight experimental models of infection or injury in which MEK1/2 inhibitors have been evaluated. The direct and indirect antimicrobial effects of MEK1/2 inhibitor compounds and the emerging recognition of different roles of MEK1 and MEK2 in programming cellular responses will be identified and discussed.</p>","PeriodicalId":13541,"journal":{"name":"Infection and Immunity","volume":" ","pages":"e0006426"},"PeriodicalIF":3.4,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156022","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}