Journal of Inflammation-London最新文献

{"title":"Mesenchymal stem cell-derived exosomal CBLB ameliorates infantile pneumonia progression probably by ubiquitinating MAPK14.","authors":"Fang Guo, Fuxing Song, Zhenjiang Chen, Na Niu, Lina Sun, Min Yan, Min Liu","doi":"10.1186/s12950-025-00450-0","DOIUrl":"10.1186/s12950-025-00450-0","url":null,"abstract":"<p><strong>Background: </strong>Infantile pneumonia (IP) is a significant cause of morbidity and mortality in young children. Mesenchymal stem cells (MSCs) have emerged as potential therapeutic agents in pneumonia due to their immunomodulatory properties. The study analyzed the role of MSCs from bone marrow in IP and the underlying mechanism.</p><p><strong>Methods: </strong>Human embryonic lung fibroblasts (WI-38) were stimulated using lipopolysaccharide (LPS) to mimic an IP cell model. This study employed flow cytometry to analyze the expression of hematopoietic markers and marker proteins on MSCs. The differentiation potential of MSCs was assessed through microscopy, oil red O staining, and alkaline phosphatase (ALP) assays. The localization of exosomes in WI-38 cells was observed using the cell membrane green fluorescent probe DIO. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting and immunohistochemistry assays were used to analyze the expression of mRNA or protein. Cell viability, proliferation, and apoptosis were evaluated using Cell counting kit-8, 5-Ethynyl-2'-deoxyuridine, and flow cytometry assays, respectively. Enzyme-linked immunosorbent assays were conducted to measure cytokine levels. A mouse model of pneumonia was utilized to assess the therapeutic potential of MSC-derived exosomes on lung injury. Co-immunoprecipitation (Co-IP) assay was performed to study the interaction between Cbl proto-oncogene B (CBLB) and mitogen-activated protein kinase 14 (MAPK14).</p><p><strong>Results: </strong>MSC-derived exosomes could be transferred into LPS-induced WI-38 cells, where they mitigated the inhibitory effects of LPS on CBLB mRNA expression. These exosomes improved WI-38 cell proliferation, reduced apoptosis, and decreased the production of pro-inflammatory cytokines including IL-6, IL-1β, and TNF-α by regulating CBLB after LPS treatment. Moreover, in a mouse model, MSC-derived exosomes protected against LPS-induced lung injury, whereas the effect was reversed after treatment with the exosomes isolated from CBLB-deficient MSCs. In addition, CBLB was found to destabilize MAPK14 protein expression in WI-38 cells. Further, overexpression of CBLB ameliorated LPS-induced inhibitory effect on cell proliferation and promoting effects on cell apoptosis and inflammation in WI-38 cells by regulating MAPK14.</p><p><strong>Conclusion: </strong>MSC-derived exosomal CBLB has therapeutic potential in ameliorating the progression of IP probably by ubiquitinating MAPK14, which could lead to novel clinical interventions for treating this condition.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"23"},"PeriodicalIF":4.4,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144334485","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":"Intermittent methionine restriction and selenium supplementation protect against inflammation and the development of dermatitis.","authors":"Jason D Plummer, Jay E Johnson","doi":"10.1186/s12950-025-00451-z","DOIUrl":"10.1186/s12950-025-00451-z","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"24"},"PeriodicalIF":4.4,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180218/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144334484","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":"Plasma surrogate markers of neutrophil extracellular traps correlate with disease severity in patients with moderate to severe acute respiratory distress syndrome.","authors":"Joni A Aoki, Frederik Denorme, Mark J Cody, David P Perry, John L Rustad, Samuel M Brown, Stephanie A Goldstein, Elizabeth A Middleton, Christian C Yost, Estelle S Harris","doi":"10.1186/s12950-025-00448-8","DOIUrl":"10.1186/s12950-025-00448-8","url":null,"abstract":"<p><strong>Background: </strong>Although studies have evaluated the presence of cell-free DNA and neutrophil extracellular traps (NETs) in acute respiratory distress syndrome (ARDS), the kinetics of NET formation during the early ICU admission and whether plasma NET markers correlate with clinical outcomes in patients with moderate-to-severe hypoxemia remain unknown. We sought to determine whether serial plasma NET marker levels in study participants collected over 48 h post enrollment predict disease severity and mortality in non-COVID-19 ARDS patients.</p><p><strong>Methods: </strong>We obtained previously collected plasma samples (trial enrollment, 24 h, 48 h) from 200 randomly selected ARDS participants in the completed Reevaluation of Systemic Early Neuromuscular Blockade (ROSE) Trial, as well as from 20 healthy control donors. We determined plasma levels of surrogate biomarkers for NETs using a cell-free DNA fluorescence assay and a plasma myeloperoxidase (MPO)-DNA complex ELISA. We correlated these surrogate biomarker levels with clinical outcomes from the ROSE trial study participants.</p><p><strong>Results: </strong>ROSE plasma samples demonstrated significantly higher NET levels compared to healthy donor controls. Individual study participant NET levels did not change over the forty-eight hours after trial enrollment. Higher levels of both surrogate markers correlated with fewer ventilator-free days, but only cell free-DNA correlated with mortality and higher illness severity scores.</p><p><strong>Conclusion: </strong>Surrogate markers for plasma NET levels measured in patients with moderate or severe ARDS correlate directly with adverse clinical outcomes and may serve as biomarkers for predicting severe disease. Further studies of surrogate biomarkers for NET formation in moderate-to-severe ARDS are warranted.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"22"},"PeriodicalIF":4.4,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295469","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":"RhIL-11 reverses liver damage in septic mice by STAT3-mediated M-MDSCs induction modulated by a parallel mTORC1 signaling branch.","authors":"Yuefang Liu, Shujun Gao, Zhanghui Li, Lei Yin, Shiyao Ge, Yangjing Zhao, Hui Wang, Bing Wan, Qixiang Shao","doi":"10.1186/s12950-025-00447-9","DOIUrl":"10.1186/s12950-025-00447-9","url":null,"abstract":"","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"21"},"PeriodicalIF":4.4,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144276821","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":"LL-37 and citrullinated-LL-37 modulate IL-17A/F-mediated responses and selectively suppress Lipocalin-2 in bronchial epithelial cells.","authors":"Anthony Altieri, Dylan Lloyd, Padmanie Ramotar, Anne M van der Does, Mahadevappa Hemshekhar, Neeloffer Mookherjee","doi":"10.1186/s12950-025-00446-w","DOIUrl":"10.1186/s12950-025-00446-w","url":null,"abstract":"<p><strong>Background: </strong>Levels of the human cationic antimicrobial host defence peptide LL-37 are enhanced in the lungs during neutrophilic airway inflammation. LL-37 drives Th17 differentiation, and Th17 cells produce IL-17A and IL-17F which form the biologically active heterodimer IL-17A/F. While IL-17 is a critical mediator of neutrophilic airway inflammation, LL-37 exhibits contradictory functions; LL-37 can both promote and mitigate neutrophil recruitment depending on the inflammatory milieu. The impact of LL-37 on IL-17-induced responses in the context of airway inflammation remains largely unknown. Therefore, we examined signaling intermediates and downstream responses mediated by the interplay of IL-17A/F and LL-37 in human bronchial epithelial cells (HBEC). As LL-37 can become citrullinated during airway inflammation, we also examined LL-37-mediated downstream responses compared to that with citrullinated LL-37 (citLL-37) in HBEC.</p><p><strong>Results: </strong>Using an aptamer-based proteomics approach, we identified proteins that are altered in response to IL-17A/F in HBEC. Proteins enhanced in response to IL-17A/F were primarily neutrophil chemoattractants, including chemokines and proteins associated with neutrophil migration such as lipocalin-2 (LCN-2). We showed that selective depletion of LCN-2 mitigates neutrophil migration, functionally demonstrating LCN-2 as a critical neutrophil chemoattractant. We further demonstrated that LL-37 and citLL-37 selectively suppress IL-17A/F-induced LCN-2 abundance in HBEC. Mechanistic studies revealed that LL-37 and citLL-37 suppresses IL-17 A/F-mediated enhancement of C/EBPβ, a transcription factor required for LCN-2 production. In contrast, LL-37 and citLL-37 enhance the abundance of ribonuclease Regnase-1, which is a negative regulator of IL-17 and LCN-2 in HBEC. In an animal model of allergen-challenged airway inflammation with elevated IL-17A/F and neutrophil elastase in the lungs, we demonstrated that CRAMP (mouse orthologue of LL-37) negatively correlates with LCN-2.</p><p><strong>Conclusions: </strong>Overall, our findings showed that LL-37 and citLL-37 can selectively suppress the abundance of IL-17A/F-mediated LCN-2, a protein that is critical for neutrophil migration in HBEC. These results suggest that LL-37, and its modified citrullinated form, have the potential to negatively regulate IL-17-mediated neutrophil migration during airway inflammation. To our knowledge, this is the first study to report that the immunomodulatory function of LL-37 enhances the RNA binding protein Regnase-1, suggesting that a post-transcriptional mechanism of action is mediated by the peptide.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"20"},"PeriodicalIF":4.4,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144133340","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":"Exosomes derived from M2 macrophages regulate airway inflammation by modulating epithelial cell proliferation and apoptosis.","authors":"Yinying Ren, Mi Zhou, Yuehan Li, Yan Li, JinYing Xiang, Fang Deng, Zhengxiu Luo, Enmei Liu, Jinyue Yu, Zhou Fu, Fengxia Ding, Bo Liu","doi":"10.1186/s12950-025-00444-y","DOIUrl":"10.1186/s12950-025-00444-y","url":null,"abstract":"<p><strong>Background: </strong>Asthma is a chronic inflammatory disease characterized by airway remodeling and immune dysregulation. This study aimed to explore the mechanisms by which M2 macrophage-derived exosomes (M2Φ-Exos) regulate airway inflammation in asthma by modulating epithelial cell proliferation and apoptosis.</p><p><strong>Methods: </strong>M2Φ-Exos were extracted and characterized by morphology, size, and marker protein expression. In vitro, the effects of M2Φ-Exos on House Dust Mites (HDM)-stimulated mouse lung epithelial cells (MLE-12s) were evaluated using western blotting to analyze Proliferating Cell Nuclear Antigen (PCNA), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), and cleaved caspase-3 expression. In vivo, M2Φ-Exos were administered to HDM-induced asthmatic mice to assess their impact on airway inflammation, epithelial remodeling, and proliferation-apoptosis balance using immunohistochemistry, immunofluorescence, and western blotting. Cytokine levels in lung tissue and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA.</p><p><strong>Results: </strong>M2Φ-Exos displayed typical cup-shaped morphology, an average diameter of 115.5 nm, and expressed marker proteins CD9, TSG101, and CD63. MLE-12 cells internalized M2Φ-Exos, leading to reduced abnormal proliferation and apoptosis in HDM-stimulated cells. In asthmatic mice, M2Φ-Exos alleviated airway inflammation and epithelial thickening while reducing PCNA, cleaved caspase-3, and Bax levels and increasing Bcl-2 expression. M2Φ-Exos suppressed pro-inflammatory cytokines (IL-4, IL-5, IL-13) and Transforming growth factor (TGF)-β, while enhancing anti-inflammatory cytokine IFN-γ and IL-10.</p><p><strong>Conclusion: </strong>These findings demonstrate that M2Φ-Exos regulate the imbalance in epithelial proliferation and apoptosis in asthma, reducing inflammation and mitigating tissue remodeling, and provide new insights into potential therapeutic strategies for asthma management.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"19"},"PeriodicalIF":4.4,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12090695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103331","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":"Exosomal non-coding RNAs: gatekeepers of inflammation in autoimmune disease.","authors":"Mohamed J Saadh, Omer Qutaiba B Allela, Ali Fawzi Al-Hussainy, Lalji Baldaniya, M M Rekha, Deepak Nathiya, Parjinder Kaur, Zafar Aminov, Hayder Naji Sameer, Huda Ghassan Hameed, Zainab H Athab, Mohaned Adil","doi":"10.1186/s12950-025-00443-z","DOIUrl":"https://doi.org/10.1186/s12950-025-00443-z","url":null,"abstract":"<p><p>Autoimmune diseases (AIDs) are marked by systemic inflammation and immune dysregulation, yet current therapies often fail to target their underlying causes. Emerging evidence positions exosomal non-coding RNAs (ncRNAs)-including miRNAs, lncRNAs, and circRNAs-as key regulators of inflammatory pathways, providing critical insights into AID pathogenesis. This review synthesizes recent advances in how these ncRNAs orchestrate immune cell communication, modulate inflammatory mediators, and drive microglial activation in neuroinflammatory AIDs. It evaluates their dual role as disease amplifiers (e.g., miR-155 in lupus, miR-326 in rheumatoid arthritis) and therapeutic targets, emphasizing their potential to reprogram immune responses or deliver anti-inflammatory agents. In this review, we first provide a glimpse into the pathogenesis of autoimmune diseases and delve into the structure and function of exosomes, emphasizing their role in cell-cell communication. We then discuss the regulatory roles of exosomal ncRNAs in immune modulation, detailing their types, functions, and mechanisms of action. Finally, we examine the implications of exosomes and exosomal ncRNAs in the context of autoimmune diseases, with a particular focus on microglial activation and its contribution to neuroinflammation.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"18"},"PeriodicalIF":4.4,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12079953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144082281","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":"Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.","authors":"Mohammad Chand Jamali, Asma'a H Mohamed, Azfar Jamal, Mohammad Azhar Kamal, Waleed Al Abdulmonem, Bashar Abdullah Saeed, Nasrin Mansuri, Fuzail Ahmad, Mustafa Mudhafar, Alaa Shafie, Haroonrashid M Hattiwale","doi":"10.1186/s12950-025-00438-w","DOIUrl":"10.1186/s12950-025-00438-w","url":null,"abstract":"<p><p>Allergic diseases significantly impact the quality of life of people around the world. Cytokines play a crucial role in regulating the immune system. Due to their importance in pro-inflammatory mechanisms, cytokines are used to understand pathogenesis and serve as biomarkers in many diseases. One such cytokine is interleukin-33, a member of the IL-1 family, including IL- 1α, IL-1β, and IL-18. The IL-33 receptor is a heterodimer of IL-1 receptor-like 1 and IL-1 receptor accessory protein. IL-33 plays a critical role in regulating innate and adaptive immune responses. The primary targets of IL-33 in vivo are tissue-resident immune cells, including mast cells, group 2 innate lymphoid cells, regulatory T cells, T helper 2 cells, eosinophils, basophils, dendritic cells, Th1 cells, CD8 + T cells, NK cells, iNKT cells, B cells, neutrophils, and macrophages. However, IL-33 appears to act as an alarm signal that is promptly released by producing cells under cellular damage or stress conditions. IL-33 regulates signaling and various biological functions, including induction of pro-inflammatory cytokines, regulation of cell proliferation, and involvement in tissue remodeling. IL-33 is fundamental in immune-related diseases and plays a critical role in the control of inflammation. Recently, IL-33 has been shown to significantly impact allergic diseases, primarily by inducing Th2 immune responses. IL-33 is a key regulator of mast cell function and a promising therapeutic target for treating allergic diseases. This review provides an overview of the current understanding of the role of IL-33 in allergy pathogenesis and potential clinical approaches.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"17"},"PeriodicalIF":4.4,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057449","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":"Comparison of the inflammatory biomarkers IL- 6, TNF-α, and CRP to predict the effect of nutritional therapy on mortality in medical patients at risk of malnutrition : A secondary analysis of the randomized clinical trial EFFORT.","authors":"Carla Wunderle, Elisabeth Martin, Alma Wittig, Pascal Tribolet, Thomas A Lutz, Christina Köster-Hegmann, Zeno Stanga, Beat Mueller, Philipp Schuetz","doi":"10.1186/s12950-025-00442-0","DOIUrl":"https://doi.org/10.1186/s12950-025-00442-0","url":null,"abstract":"<p><strong>Background: </strong>Inflammation is a key driver of disease-related malnutrition and patients with high inflammation may not show the same benefits from nutritional therapy as other patients. We compared in an exploratory manner the prognostic ability of interleukin- 6 (IL- 6), tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP) to predict outcome and response to nutritional therapy, respectively, within a large cohort of patients from a previous nutritional trial.</p><p><strong>Methods: </strong>This is a secondary analysis of the Swiss-wide, multicenter, randomized controlled Effect of early nutritional therapy on Frailty, Functional Outcomes, and Recovery of malnourished medical inpatients Trial (EFFORT) trial comparing individualized nutritional support with usual care nutrition in medical inpatients. The primary endpoint was 30-day all-cause mortality.</p><p><strong>Results: </strong>We included 996 patients with an overall mortality rate of 6% within 30 days. Compared to patients with low IL- 6 level < 11.2pg/mL, patients with high levels had a more than 3-fold increase in mortality at 30-days (adjusted HR 3.5, 95% CI 1.95-6.28, p < 0.001), but tended to have a less pronounced mortality benefit from individualized nutritional therapy as compared to usual nutritional care (hazard ratio 0.82 vs. 0.32). CRP and TNF-α were not associated with mortality, but patients with increased CRP levels > 100 mg/dl also showed a trend towards a diminished response to nutritional intervention (hazard ratio 1.25 vs. 0.47).</p><p><strong>Conclusion: </strong>Our findings support the thesis that a high inflammatory state is linked to reduced benefits from nutritional therapy. Apparently, CRP and IL- 6 effectively predict treatment response, but IL- 6 may additionally serve as a prognostic marker for increased mortality. This finding might help to develop improved treatment strategies for patients with elevated inflammatory profiles.</p><p><strong>Trial registration: </strong>Clinicaltrials.gov as NCT02517476 (registered 7 August 2015).</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"16"},"PeriodicalIF":4.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019905","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":"Mucosal immunotherapy targeting APC in lung disease.","authors":"Yangqi Liu, Zijian Chen, Hanchang Cheng, Runzhi Zheng, Weizhe Huang","doi":"10.1186/s12950-025-00432-2","DOIUrl":"https://doi.org/10.1186/s12950-025-00432-2","url":null,"abstract":"<p><p>Several studies have demonstrated that the pulmonary immune response is primarily facilitated by antigen-presenting cells (APCs), and that both professional and non-professional APCs contribute to overall pulmonary immunity. APCs play unique roles and mechanisms in pathogen elimination and immunomodulation. Mucosal immunity exhibits potential advantages over traditional parenteral immunity in that it stimulates immune defenses in mucosal and systemic tissues, which is important for reducing the burden of lung disease. However, obtaining a comprehensive understanding of the crosstalk between mucosal immunity and APC in the context of various lung diseases remains challenging. This mini-review aimed to elucidate the mechanisms of novel mucosal immunity, targeting APC action during lung infections, allergies, and malignant tumorigenesis. This minreview provides important insights into more effective therapeutic approaches for various lung diseases.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"22 1","pages":"15"},"PeriodicalIF":4.4,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11998460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019907","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}