Innate Immunity最新文献

{"title":"Retraction: Effect of berberine on LPS-induced expression of NF-κB/MAPK signalling pathway and related inflammatory cytokines in porcine intestinal epithelial cells.","authors":"","doi":"10.1177/17534259261435238","DOIUrl":"10.1177/17534259261435238","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261435238"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13018703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of trained immunity in chronic non-communicable inflammatory diseases.","authors":"Joseph Mucumbitsi, Jean Claude Hakizimana, Marie Gorette Kampire, Callixta Kaneza, Themistocles Bushobozi, Sophie Mukantwari, Jean Mfizi Ngaboyishema, Alex Butera, Abdullateef Isiaka Alagbonsi","doi":"10.1177/17534259261446050","DOIUrl":"10.1177/17534259261446050","url":null,"abstract":"<p><p>BackgroundTrained immunity, a form of long-term functional reprogramming of innate immune cells through epigenetic and metabolic changes, traditionally confers protection against infections. However, inappropriate activation by endogenous sterile stimuli can drive persistent maladaptive inflammation in non-communicable diseases (NCDs).ObjectiveThis systematic review synthesizes primary evidence for trained immunity in atherosclerosis, type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), and neurodegenerative disorders, focusing on endogenous inducers, cellular mediators, mechanisms, and translational implications.Data Sources and MethodsFollowing PRISMA guidelines, we included original studies demonstrating trained immunity induced by sterile endogenous signals in the targeted diseases. Narrative synthesis was performed due to heterogeneity precluding meta-analysis.ResultsTwelve primary studies met the inclusion criteria. In atherosclerosis (n = 8 studies), oxLDL, aldosterone, Western diet lipids, and post-myocardial infarction signals induced trained immunity in monocytes or macrophages and hematopoietic progenitors via H3K4me3 enrichment, mTOR/NLRP3 activation, and glycolytic/fatty acid shifts, leading to persistent cytokine hyperproduction (TNF-α, IL-6), foam cell formation, and transmissible plaque progression. In T2DM/hyperglycemia (n = 3), high glucose levels triggered MLL-mediated epigenetic reprogramming and glycolysis-dependent \"metabolic memory,\" which skewed myelopoiesis and accelerated atherosclerosis despite normoglycemia. In CKD (n = 1), indoxyl sulfate induced AhR-dependent arachidonic acid pathway activation with metabolic rewiring, sustaining systemic inflammation. In neurodegeneration (n = 1), peripheral stimuli caused epigenetic reprogramming in microglia, yielding hyperresponsive or tolerized states modulating amyloid-β pathology. Convergent mechanisms (H3K4me3, glycolysis, mTOR/AhR/NLRP3) highlight trained immunity as a shared driver of chronic sterile inflammation.ConclusionsTrained immunity emerges as a unifying maladaptive mechanism perpetuating low-grade inflammation across these diseases, bridging transient endogenous insults to sustained pathology. Targeting reprogramming pathways, such as glycolysis or epigenetic inhibitors, offers promising therapeutic strategies. Expanded human studies are needed to address preclinical dominance and data gaps, particularly in CKD and neurodegeneration, where evidence is preliminary.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261446050"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tn-Glycoconjugates engage MGL2 to potentiate TLR9-mediated dendritic cell maturation and Th1-skewed immune responses.","authors":"Carolina Chiale, Sylvie Bay, Christelle Ganneau, Teresa Freire","doi":"10.1177/17534259261449674","DOIUrl":"10.1177/17534259261449674","url":null,"abstract":"<p><p>Dendritic cells (DCs) orchestrate antitumor immunity by integrating signals from the tumor microenvironment to prime effective T cell responses. Many tumors display altered glycosylation patterns, including tumor-associated carbohydrate antigens (TACAs) such as the Tn antigen (GalNAcα1-<i>O</i>-Ser/Thr); yet how these structures influence DC function is not well defined. Here, we investigated how Tn-bearing glycoconjugates modulate DC activation and shape adaptive immunity. Bone marrow-derived DCs (BMDCs) efficiently internalized fluorescently labeled Tn-glycoconjugates, whereas uptake of non-glycosylated counterparts was negligible. Although Tn-glycoconjugates alone did not induce DC maturation, co-stimulation with the Toll-like receptor 9 (TLR9) agonist CpG markedly increased CD86 expression and the secretion of IL-12/23p40 and IL-6, with the multivalent construct MAG:Tn3-PV eliciting the strongest response. These conditioned BMDCs promoted strong IFN-γ production by allogeneic splenocytes, consistent with a Th1-polarizing phenotype. Mechanistically, both uptake and CpG-enhanced activation required the C-type lectin receptor MGL2, as blockade of MGL or competition with GalNAc abrogated glycoconjugate uptake and CpG-enhanced cytokine induction. Pharmacological inhibition revealed that MGL2 signaling synergizes with TLR9 through the Syk-Raf-1-NF-κB axis. <i>In vivo</i>, mice immunized with DCs conditioned with Tn-glycoconjugate- plus CpG displayed enhanced splenocyte proliferation, increased IFN-γ secretion, and elevated cytotoxic activity without IL-10 induction, confirming a Th1-skewed response. Collectively, these findings identify MGL2 as a critical mediator of Tn-glycoconjugate sensing and unveil a synergistic C-type lectin receptor (CLR)-TLR9 cross-talk that amplifies DC maturation and cytotoxic immunity. This study provides mechanistic insight into how specific glycan-lectin interactions fine-tune innate receptor signaling, highlighting the potential of Tn-based glycoconjugates as immunomodulatory tools for vaccine design and cancer immunotherapy.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261449674"},"PeriodicalIF":3.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13172724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineered neutrophil, an emerging immune therapeutic strategy.","authors":"Jingyi Wang, Teng Deng, Ruisi Chen, Lu Yang, Yan Teng, Junming Miao","doi":"10.1177/17534259251365803","DOIUrl":"10.1177/17534259251365803","url":null,"abstract":"<p><p>Neutrophils play a pivotal role in the host immune system, serving as the frontline defense against microbial infections. They eradicate pathogens through diverse mechanisms, encompassing degranulation, phagocytosis, and the release of reactive oxygen species. Moreover, they are acknowledged as crucial contributors to chronic inflammatory pathological processes, including conditions such as cancer and autoimmune diseases. An expanding body of research suggests that neutrophils, harnessing their innate immune characteristics, possess the potential to serve as carriers for therapeutic agents or be directly employed in disease treatment. This underscores their potential as a cell therapy platform for future applications. Consequently, we systematically investigate the potential applications of neutrophils in this review, with a primary emphasis on elucidating the research advancements in utilizing neutrophils, including those derived from stem cells, for therapeutic interventions in various diseases.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251365803"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical development of the TLR4 antagonist FP12 as a drug lead targeting the HMGB1/MD-2/TLR4 axis in lethal influenza infection.","authors":"Kari Ann Shirey, Alessio Romerio, Mohammed Monsoor Shaik, David S Leake, Charys Palmer, Natalia Skupinska, Jules Paton, Grisha Pirianov, Jorge Cg Blanco, Stefanie N Vogel, Francesco Peri","doi":"10.1177/17534259241313201","DOIUrl":"10.1177/17534259241313201","url":null,"abstract":"<p><strong>Background: </strong>Acute Lung Injuries (ALI) are a severe consequence of influenza-induced cytokine storm that can cause respiratory failure and death. It has been demonstrated that Toll-like Receptor 4 (TLR4) is involved in cytokine storm and that TLR4^-/- mice are protected against ALI. Therefore, TLR4 is a prime target for protection against ALI. FP12 is a known TLR4 antagonist that reduces TLR4-dependent immune activation and it is a promising lead compound for the treatment of innate immunity related pathologies.</p><p><strong>Objectives: </strong>We present here the preclinical development of FP12 as an anti-inflammatory lead compound acting on influenza-induced ALI.</p><p><strong>Methods: </strong><i>In vitro:</i> We pre-treated THP-1 cells with FP12 (10 μM) for 0.5 h, then exposed to LPS (100 ng/ml) for 0 to 16 h. In some experiments, cells were simultaneously incubated with FP12 and LPS, or FP12 was added 30 min after LPS. Cytokine levels were measured by Western blot and ELISA assays. <i>In vivo:</i> WT C57BL/6J mice were infected with mouse-adapted influenza virus (PR8). Two days after infection, mice received either vehicle, FP7 (200 µg/mouse), or FP12 (200 µg/mouse) once daily (Day 2 to Day 6). Mice were monitored daily for survival for 14 days. Data were collected through histological staining, qRT-PCR, and ELISA assay.</p><p><strong>Results: </strong>FP12 treatment inhibited both LPS- and HMGB1-induced TLR4 intracellular pathways (MyD88 and TRIF) leading to significantly reduced levels of a variety of proinflammatory cytokines including Type I interferon (IFN-β), highlighting its effectiveness in controlling proinflammatory protein production and reducing inflammation. FP12 protected mice therapeutically from influenza virus-induced lethality and reduced both cytokine gene expression and High Mobility Group Box 1 (HMGB1) levels in the lungs as well as ALI.</p><p><strong>Conclusion: </strong>FP12 can antagonize TLR4 activation in vitro and protects mice from severe influenza infection, most likely by reducing the TLR4-dependent cytokine storm mediated by danger-associated molecular patterns (DAMPs).</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259241313201"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutation within the transmembrane domain of oxidized low-density lipoprotein receptor 1 influences oxidized low-density lipoprotein-induced signal transduction.","authors":"Zhen Ma, Ran Xu, Jing Lu, Xiong Huang, Hao Jia, Zhiwen Ding, Jie Yuan, Yunzeng Zou","doi":"10.1177/17534259251350447","DOIUrl":"10.1177/17534259251350447","url":null,"abstract":"<p><p>ObjectiveTo investigate the important active sites within the NTFs to affect the <i>in vitro</i> interaction of oxidized low-density lipoprotein (ox-LDL) with its receptor, OLR1.MethodsSimulation analysis online was performed to generate various OLR1 chimeras, truncation mutants, and site-specific mutations. They were transfected in COS-7 cells and subjected to ox-LDL stimulations to observe the different reactions. Immunoprecipitation-mass spectrometry (IP-MS) was performed to show what proteins combined with OLR1 mutants in reaction to ox-LDL. Lipid uptake in human monocytes (THP-1) originated foam cells overexpressing somatic mutant of OLR1 were also determined. Further studies focusing on these regions were conducted using truncation mutants and site-specific mutants such as G43A, V44A, L45A, C46A, and L47A.ResultsAmino acids within the TM were highly conserved, spanning amino acids 35 to 57. The induction of intracellular p-ERK1/2 in response to ox-LDL stimulation was highly promoted in Chimera 3 possessing the TM from OLR1 like OLR1/WT (<i>p</i> < 0.05). Sequence alignment revealed two conserved regions within the TM of OLR1, Leu45-Cys46-Leu47 and Val55-Leu56-Gly57. Western blot showed that most of the TM changes ablated ERK1/2 activation in response to ox-LDL stimulation (<i>p</i> < 0.05). One human somatic mutation at L45F revealed significantly lower p-ERK1/2 levels with enhanced intake of ox-LDL in THP-1-derived foam cells than the control cells (<i>p</i> < 0.05). L45A and C46A molecular complexes were identified. After ox-LDL stimulation, these underlined interactions with keratins, namely KRT2 and KRT6A.ConclusionThese findings emphasize the vital role of the TM in the interactions between OLR1 and ox-LDL and point to an exciting possibility that signal transduction induced by ox-LDL through its receptor OLR1 may involve complex interactions with cytoskeletal proteins.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251350447"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunity's core reset: Synbiotics and gut microbiota in the COVID-19 era.","authors":"Dejana Bajić, Nemanja Todorović, Mladena Lalić Popović, Milica Plazačić, Andrea Mihajlović","doi":"10.1177/17534259251362023","DOIUrl":"10.1177/17534259251362023","url":null,"abstract":"<p><p>The gut microbiome plays a crucial role in shaping immune responses, and its connection to immunity has never been more relevant than in the COVID-19 era. The interaction between gut microbes and the immune system, known as microbiome-immunity crosstalk, influences both how the body responds to infections and how well it recovers. COVID-19, whether in its acute phase or lingering as long COVID, has been linked to disturbances in the gut microbiome. During infection, many patients experience dysbiosis-an imbalance in gut bacteria-that can contribute to immune dysfunction and excessive inflammation. This imbalance may not only worsen the severity of the disease but also prolong recovery, leading to persistent symptoms like fatigue, brain fog, and digestive issues. Long COVID, in particular, has been associated with ongoing immune dysregulation, where the body's defense system remains in a state of heightened activation, causing chronic inflammation. Given the strong link between gut health and immunity, there is growing interest in strategies to restore microbial balance. Synbiotics-combinations of probiotics (beneficial bacteria) and prebiotics (nutrients that support them)-are being explored as a potential therapeutic approach. By replenishing beneficial gut microbes, synbiotics may help regulate immune responses, reduce inflammation, and support overall recovery from COVID-19. Emerging research suggests that improving gut health could enhance the body's ability to fight infections and recover more efficiently. As we continue to understand the long-term impact of COVID-19, focusing on the gut microbiome offers a promising path forward. Supporting a balanced and diverse microbiome through diet, lifestyle, and targeted interventions like synbiotics may provide a natural way to strengthen immunity and improve health outcomes in both acute and long COVID cases.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251362023"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144730295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute-phase response- and inflammation-, but not extracellular matrix-related proteins in the amniotic fluid are associated with spontaneous preterm delivery in asymptomatic women with midtrimester short cervix.","authors":"Kyo Hoon Park, Bo Young Choi, Kyong-No Lee, Eunji Oh, Min Jung Lee, Hee Young Cho, Da Eun Jeong","doi":"10.1177/17534259251372138","DOIUrl":"10.1177/17534259251372138","url":null,"abstract":"<p><p><b>Background:</b> To determine whether (i) altered levels of acute-phase <i>response</i> (APR)-, inflammation-, and extracellular matrix (ECM)-related <i>proteins</i> in the amniotic fluid (AF) were associated with spontaneous preterm delivery (SPTD) in asymptomatic women with midtrimester short cervix (SCX) and (ii) if SPTD risk severity was related to the expression levels of inflammation-related proteins in the AF. <b>Methods:</b> This retrospective cohort study included 70 singleton pregnant women diagnosed with a SCX (<25 mm) at 17-25 weeks, who were subjected to amniocentesis to exclude intraamniotic inflammation (IAI; defined as AF interleukin [IL]-6 ≥ 2.6 ng/mL). APR (<i>i.e.,</i> h<i>epcidin,</i> kallistatin, MBL, pentraxin-2, RBP4<i>, and serpin A1)</i>, inflammatory (<i>i.e.,</i> <i>IL-6, IL-8, and resistin)</i>, and ECM-related (<i>i.e.,</i> lumican, MMP-8, TGFBI, and uPA) molecules were assayed in the AF by ELISA. The primary outcome measure was SPTD at <34 weeks. The levels of each identified dysregulated <i>inflammatory</i> mediator were divided into quartiles to assess the correlation between their AF expression profiles and SPTD risk severity. <b>Results:</b> Multivariable Firth logistic regression <i>analyses revealed that elevated AF levels of</i> IL-6, IL-8, kallistatin, pentraxin-2, <i>resistin,</i> and serpin A1, <i>and</i> IAI presence were independently associated with SPTD at <34 weeks after adjusting for baseline covariates. The areas under the curves of the aforementioned mediators ranged from 0.67 to 0.79 for outcome prediction. The odds of SPTD at <34 weeks, even after adjusting for confounders, significantly increased with each increasing quartile of baseline AF levels of IL-6/8, pentraxin-2, and resistin. <b>Conclusions:</b> APR (kallistatin, pentraxin-2, and serpin A1)- and inflammation (IL-6/8 and resistin)-, but not ECM-related mediators in the AF are involved in SPTD development in asymptomatic women with a midtrimester SCX. In particular, SPTD risk (especially risk severity) is associated with the degree of the inflammatory response in the AF, as categorized by inflammatory protein expression profiles, as well as IAI presence.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251372138"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12409065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bronchial pyroptosis promotes Th17 inflammation in steroid-insensitive asthma mouse.","authors":"Yun Lin, Jianhua Yin, Xia Yang, Jianghong Wei, Yaxi Liang, Chengfeng Zhou, Dongfang Zou, Shuyuan Chu","doi":"10.1177/17534259251372592","DOIUrl":"10.1177/17534259251372592","url":null,"abstract":"<p><p>Bronchial cell pyroptosis and IL-17 respectively contribute- to the pathogenesis of steroid-insensitive asthma. In this study, we aim to explore the relationship between bronchial cell pyroptosis and Th17 in airway inflammation of steroid-insensitive asthma. The steroid-insensitive asthma model of mice was induced by toluene diisocyanate (TDI), which was also intraperitoneally injected with NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inhibitor MCC950. The bronchial epithelial cell pyroptosis was identified in morphology by transmission electron microscope. Protein expressions of pyroptosis cytokines (pro-Caspase-1, Caspase-1 p20, pro-GSDMD, cleaved-GSDMD and HMGB1), IL-17A, IL-17F and phosphorylated STAT3 (p-STAT3) in lung tissues were assessed by western blotting. Th17 in lung tissues was measured by flow cytometry. IL-17A + and p-STAT3 + cells in airway were identified by immunohistochemistry. In steroid-insensitive asthma mice, bronchial epithelial cell pyroptosis was confirmed in morphology using transmission electron microscope. Compared with controls, the protein expressions of Caspase-1 p20, cleaved-GSDMD and HMGB1 in lung tissues were increased in mice with steroid-insensitive asthma, which could be attenuated by MCC950. Th17 cells precentage and proteins expressions of p-STAT3, IL-17A and IL-17F were also increased in lung of steroid-insensitive asthmatic mice, which were also attenuated by MCC950. Similarly, the counts of IL-17A + cell and p-STAT3 + cell were more in airway of steroid-insensitive asthmatic mice than controls, and was attenuated by MCC950. In conclusion, bronchial epithelial cell pyroptosis could promote Th17 inflammation in airway of steroid-insensitive asthma mouse, which will provide further understanding on the interaction between innate immunity and acquired immunity in the pathogenesis of steroid-insensitive asthma.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251372592"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histopathologic effect and immunomodulatory of <i>Indigofera oblongifolia</i> with silver nanoparticles against splenic injury by <i>Plasmodium chabaudi</i> infection in mice.","authors":"Mutee Murshed, Jameel Al-Tamimi, Hind Alzaylaee, Hani Ahmeda, Saleh Al-Quraishy","doi":"10.1177/17534259251396376","DOIUrl":"10.1177/17534259251396376","url":null,"abstract":"<p><p>Malaria, a globally prevalent disease caused by Plasmodium species, significantly impacts the immune system, particularly affecting splenic function. This study investigates the therapeutic potential of <i>Indigofera oblongifolia</i> leaf extracts (IOLE) with silver nanoparticles (AgNPs) against <i>Plasmodium chabaudi</i>-induced splenic damage in a female C57BL/6 mice model. Fifty female mice were infected with <i>P. chabaudi</i> and subsequently treated with IOLE AgNPs or chloroquine phosphate. Histopathological and immunohistochemical analyses revealed that IOLE AgNPs effectively restored splenic architecture, reduced inflammatory markers, and improved immune responses compared to the control and chloroquine-treated groups. These findings suggest that IOLE AgNPs may offer a novel therapeutic approach to mitigate splenic dysfunction associated with malaria and provide comparative analysis between established therapies like chloroquine and innovative combination of traditional medical plant and modern nano technology.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251396376"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12627400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145549157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}