FASEB bioAdvances最新文献

{"title":"Elevated LncRNA LINC00966 Suppresses PDE2A to Impair Sperm Motility in Asthenozoospermia","authors":"Bingrou Guo,&nbsp;Junyi Ke,&nbsp;Hanran Mai,&nbsp;Ting Zhang,&nbsp;Zhaojin Lu,&nbsp;Zilin Zheng,&nbsp;Jieyi Luo,&nbsp;Yifan Zhang,&nbsp;Mei Yan,&nbsp;Shuo Yang,&nbsp;Yanxia Qu,&nbsp;Fan Jiang,&nbsp;Xiaoping Liu,&nbsp;Hao Chen,&nbsp;Liandong Zuo","doi":"10.1096/fba.2026-00137","DOIUrl":"10.1096/fba.2026-00137","url":null,"abstract":"<p>Emerging evidence indicated that long non-coding RNAs (lncRNAs) play critical roles in mammalian reproductive physiology, yet their roles in asthenozoospermia (AS), a major contributor to male infertility, remain elusive. Here, we identify <i>LINC00966</i> as a candidate lncRNA associated with impaired sperm function. <i>LINC00966</i> expression was significantly elevated in semen from AS patients and negatively correlated with sperm concentration, total motility, and progressive motility. In mouse testes, <i>Linc00966</i> was detected in spermatogonia, spermatocytes and spermatids with predominant cytoplasmic localization as well as in GC-2spd cells. Furthermore, <i>Linc00966</i> overexpression reduced cell viability and migration and increased intracellular reactive oxygen species (ROS), whereas knockdown enhanced viability and migration and lowered ROS in GC-2spd cells. Bulk RNA-seq analysis revealed that the phosphodiesterase 2A (Pde2a), a key cGMP/cAMP-hydrolyzing enzyme, were upregulated when <i>Linc00966</i> was knockdown. The GO enrichment and KEGG analysis of differentially expressed genes suggested the cyclic guanosine monophosphate (cGMP) process were enriched. Further validation found that <i>Linc00966</i> suppressed <i>Pde2a</i>. In clinical semen samples, <i>LINC00966</i> and <i>PDE2A</i> expression levels were inversely correlated, and both were closely associated with semen quality parameters. Collectively, these findings implicated <i>LINC00966</i> and its downstream target <i>PDE2A</i> as potential pathogenic regulators of sperm motility in AS. By linking lncRNA-mediated modulation of cGMP signaling and oxidative stress to spermatogenic cell function, our results demonstrated a plausible signaling axis underlying AS and suggests <i>LINC00966/PDE2A</i> as promising candidates for biomarker development and therapeutic investigation in male infertility.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13450733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Origin of the COVID19 Pandemic Is Still Important","authors":"Jason D. Bannan","doi":"10.1096/fba.2026-00227","DOIUrl":"10.1096/fba.2026-00227","url":null,"abstract":"<p>The COVID19 pandemic, caused by the betacoronavirus SARS-CoV-2, now ranks among the world's deadliest plagues, and certainly one of the most significant public health crises in the last 100 years. Despite more than 6 years of investigating the pandemic, it has been difficult to assess the origin of the disease in the City of Wuhan, China. The Wuhan Municipal Public Security Bureau regretfully suppressed information exchanges between physicians early in the Wuhan outbreak, which interfered with the contact tracing necessary for epidemiological investigations. The scientific community and government agencies throughout the world have been divided in their assessments of the pandemic's origin in Wuhan China. In the 2021 intelligence assessment released by the U.S. Office of the Director of National Intelligence (ODNI), only the FBI assessed the possibility of a laboratory origin. By 2023 the U.S. Department of Energy (DOE) revised its assessment to acknowledge a lab origin was likely, and in 2025 the U.S. Central Intelligence Agency (CIA) acknowledged a similar view. There has been political polarization of views, condescension and accusations of conspiracies among scientists. The COVID19 pandemic is prompting policy changes to research guidelines and recommendations for research restrictions based upon the assessment that pandemic may have resulted from laboratory research. While some express this as politically motivated, as we approach the seventh year of the COVID19 pandemic, more evidence has emerged that supports the research origin theory and scant evidence supporting a zoonotic emergence. It is imperative that our policy makers understand the facts when considering legislation and policies that could affect infectious disease research.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13446652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemogenetic Activation of G12 Signaling Thickens the Epidermis With Enhanced Barrier Function","authors":"Nozomi Kamakura,&nbsp;Natsumi Hirai,&nbsp;Kaito Arai,&nbsp;Yaxin Du,&nbsp;Toshiaki Kogame,&nbsp;Yusuke Ohno,&nbsp;Akio Kihara,&nbsp;Kenji Kabashima,&nbsp;Asuka Inoue","doi":"10.1096/fba.2026-00042","DOIUrl":"https://doi.org/10.1096/fba.2026-00042","url":null,"abstract":"<p>The epidermis provides the body's outermost barrier, yet how G-protein-coupled receptor (GPCR) signaling via the G_12/13 family regulates epidermal homeostasis in vivo remains unclear. Here, we selectively activated G₁₂ signaling in keratinocytes using a chemogenetic strategy. Activation of a G₁₂-coupled designer receptor (G₁₂D) in mouse epithelial cells induced pronounced epidermal thickening while preserving stratified architecture and avoiding overt inflammatory skin changes. This thickening was accompanied by increased Ki67-positive cells, expansion of keratin 10- and filaggrin-positive layers, and transcriptomic upregulation of genes related to keratinocyte differentiation, keratinization, and epidermal barrier function. Functionally, G₁₂D activation strengthened barrier performance, as shown by blunted transepidermal water loss responses to mechanical barrier disruption. Although alarmin-related genes were upregulated, cytokine analyses indicated only modest inflammatory changes. Pharmacologic inhibition of TYK2 (deucravacitinib) partially reduced G₁₂D-driven epidermal thickening, whereas mTORC1 inhibition (rapamycin) produced a stronger suppressive effect, suggesting that the mTORC1-dependent keratinocyte response is a major driver of this phenotype, with a moderate TYK2-dependent component. Together, these findings identify epidermal G₁₂ signaling as a regulator that promotes “non-pathological” epidermal thickening coupled to enhanced barrier function, supporting G₁₂-coupled GPCRs as potential therapeutic entry points for barrier-compromised skin disorders.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2026-00042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148647680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simulated Microgravity Reprograms Host Cell Architecture and Mitochondrial Function, Altering Toxoplasma gondii Growth","authors":"Musfika Tasnim Shirin,&nbsp;Takafumi Yamada,&nbsp;Daisuke Kondoh,&nbsp;Hiroki Bochimoto,&nbsp;Kentaro Kato","doi":"10.1096/fba.2026-00146","DOIUrl":"10.1096/fba.2026-00146","url":null,"abstract":"<p>Simulated microgravity (SMG or μG) influences <i>Toxoplasma gondii</i> growth and modifies the cellular structure and function of the host cells. As an obligate intracellular parasite, <i>Toxoplasma gondii</i> depends on the metabolic activity and mitochondrial function of its host. However, the impact of SMG on host–pathogen interactions remains unclear. We investigated the effect of SMG on host cell structure and mitochondrial functions and its impact on <i>Toxoplasma gondii</i> infection. Cultured human foreskin fibroblasts (HFF) and Vero cells under SMG formed stratified cell layers and exhibited morphological mitochondrial abnormalities, such as outer membrane distortion and inner membrane distension. Functional analyses revealed altered mitochondrial membrane potential and intracellular ATP levels without substantial changes in reactive oxygen species. Upon infection, <i>T. gondii</i> showed cell-type-dependent growth, increasing in Vero cells but decreasing in HFF at 48 h post-infection. These findings indicate that SMG-induced mitochondrial remodeling is associated with altered host cell susceptibility to toxoplasmosis. Our study highlights the role of physical environmental changes in modulating host–pathogen interactions in the context of host cell mitochondrial function.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13386239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenging Patterns of Fine-Scale Genetic Structure in Galicia and East-to-West Genetic Divergence Across the Iberian Peninsula—When Technical Batches Rewrite History","authors":"Jacobo Pardo-Seco,&nbsp;Alberto Gómez-Carballa,&nbsp;Conrado Martínez-Cadenas,&nbsp;Federico Martinón-Torres,&nbsp;Antonio Salas","doi":"10.1096/fba.2026-00134","DOIUrl":"https://doi.org/10.1096/fba.2026-00134","url":null,"abstract":"<p>The influential 2019 study by Bycroft et al. reported remarkably pronounced ultrafine-scale genetic structure within a small region of Galicia (northwestern Iberia). Using <i>fineSTRUCTURE</i> clustering of <i>ChromoPainter</i> coancestry profiles, the authors identified multiple internally coherent clusters characterized by high levels of within-group haplotype sharing and reduced sharing with neighboring populations. On a broader national scale, they also reported a marked East–West genetic differentiation and North–South homogeneity across the Iberian Peninsula, patterns which they largely attributed to historical population movements associated with the gradual territorial expansion of Christian kingdoms between the 8th and 15th centuries following the initial Islamic conquest. Several subsequent studies have adopted similar interpretations, but all relied on the same genetic resource, the EPICOLON Phase I cohort. Following a detailed reexamination of Bycroft et al., we identify multiple methodological issues, most notably signals consistent with unaccounted batch effects in EPICOLON, some of which were recognized by the authors in earlier studies. In contrast, we highlight recent analyses based on independent genomic datasets that consistently report high levels of genetic homogeneity within Galicia and across central and southern Iberia, with no evidence supporting a pronounced East–West genetic divide across Iberia. In addition, recent studies have documented North African demographic influences in Iberia, particularly in Galicia, predating the period of Islamic rule and therefore challenging the historical interpretation proposed by Bycroft et al. We also show that while <i>fineSTRUCTURE</i> is a powerful tool for detecting subtle population stratification, it may be highly sensitive to technical confounders, which can magnify or distort inferred clustering patterns. This study demonstrates that technical artifacts can strongly affect fine-scale population structure inferred by <i>fineSTRUCTURE</i>, emphasizing the need for rigorous quality control and cautious interpretation of highly resolved genetic clusters.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2026-00134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essential Role for Telomeric Repeat-Binding Factor 2 in Cardiac Development and Function","authors":"Ali Hakim Shoushtari,&nbsp;Aysenure Danis,&nbsp;Michael Wayne Stoner,&nbsp;Jeffrey Baust,&nbsp;Andrea Sebastiani,&nbsp;Paramesha Bugga,&nbsp;Janet R. Manning,&nbsp;Bellina A. S. Mushala,&nbsp;Nisha Bhattarai,&nbsp;Imad Al Ghouleh,&nbsp;Iain Scott,&nbsp;Maryam Sharifi-Sanjani","doi":"10.1096/fba.2026-00129","DOIUrl":"https://doi.org/10.1096/fba.2026-00129","url":null,"abstract":"<p>Telomere repeat-binding factor 2 (Trf2) is essential for protecting our telomeres. While Trf2 global deletion is lethal, its role in organ-specific development, particularly in the heart, remains less understood. In this study, we investigated the role of Trf2 in cardiac development and function. Our studies reveal that cardiomyocyte (CM)-specific loss of Trf2 leads to profound defects in heart morphology, including impaired ventricular wall formation and compromised CM proliferation, concurrent with no CM telomere length attrition. Further, in vivo functional assessment and molecular analyses of CM-Trf2 deficient ventricles revealed severe cardiac dysfunction and, interestingly, altered nuclear envelope gene expression. Our work provides new insights into the essential role of Trf2 in heart development and function and potential avenues for therapeutic intervention targeting telomere biology.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2026-00129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148373301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of Spexin Effects on Insulin-Dependent Pathway Genes in High-Glucose-Induced Insulin-Resistant C2C12 Myotubes","authors":"Ann Sze Cheah,&nbsp;Ji Wei Tan,&nbsp;Faizul Jaafar,&nbsp;Wendy Wai Yeng Yeo","doi":"10.1096/fba.2026-00003","DOIUrl":"10.1096/fba.2026-00003","url":null,"abstract":"<p>Diabetes is a global health concern, with type 2 diabetes mellitus (T2DM) being the most common form. T2DM is characterized by insulin resistance and impaired glucose uptake in skeletal muscle. Spexin shows hypoglycaemic effects, but its mechanism of action, especially in skeletal muscles, remains elusive. This study aims to investigate the effects of spexin on key genes associated with the insulin-dependent pathway in C2C12 cells. The differentiation of C2C12 myoblasts to C2C12 myotubes was confirmed using the fusion index and gene expression of myogenic factor 5 (<i>Myf5</i>), myosin heavy chain (<i>MyHC</i>), and myogenic regulatory factor 4 (<i>MRF4</i>) analysis. Cytotoxicity of spexin at varying concentrations (100 nM, 200 nM, 400 nM, 800 nM, and 1000 nM) was assessed via MTS assay. Insulin resistance–like conditions were induced in C2C12 myotubes using a high-glucose medium and characterized at the mRNA level by quantitative reverse transcription PCR (RT-qPCR) of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (<i>PGC-1α</i>), glucose transporter 4 (<i>GLUT4</i>), and hexokinase II (<i>HKII</i>) genes. Fusion index analysis evaluated high-glucose effects on myogenesis. RT-qPCR examined spexin's effects on insulin receptor substrate 1 (<i>IRS-1</i>), phosphatidylinositol 3-kinase (<i>PI3K</i>), and <i>GLUT4</i> expression over different time points. Spexin concentrations at 1000 nM were not cytotoxic. High-glucose incubation did not affect myogenesis yet was associated with downregulation of <i>PGC-1α</i> and <i>GLUT4</i> genes, consistent with a transcriptional profile typically observed in insulin-resistant states. Spexin-treated C2C12 cells statistically significantly downregulated the expression of <i>IRS-1</i> after 2 h of incubation. The effects of spexin on <i>IRS-1</i>, <i>PI3K</i>, and <i>GLUT4</i> gene expression were comparable to metformin-treated in insulin resistance C2C12 myotubes.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288056/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “MicroRNA 15a and 16 Regulate Proteostasis in Non-Small Cell Lung Cancer”","authors":"","doi":"10.1096/fba.2026-00177","DOIUrl":"https://doi.org/10.1096/fba.2026-00177","url":null,"abstract":"<p>\u0000 <span>P. J. Ryan</span>, <span>B. C. Guerra</span>, <span>P. Nghiem</span>, <span>S. E. Riechman</span>, <span>M. Janini Gomes</span>, and <span>J. D. Fluckey</span>, “ <span>MicroRNA 15a and 16 Regulate Proteostasis in Non-Small Cell Lung Cancer</span>,” <i>FASEB BioAdvance</i> <span>8</span>, no. <span>5</span> (<span>2026</span>): e70111, https://doi.org/10.1096/fba.2026-00075.\u0000 </p><p>The original author list included Peter Nghiem. The author's name should have read: Peter P. Nghiem.</p><p>The Results and Discussion sections referred to the H446 lung cancer cell line, instead of the H460 lung cancer cell line that was used in the study. Each reference to “446” should have read “460,” in reference to the H460 cell line that was actually used in the study.</p><p>Figure 2 caption inaccurately expressed controls as models of NSCLC. This caption should have read: “<b>FIGURE 2</b> | MiR15a/16 Suppress Cellular Growth and Protein Anabolism in NSCLC. Overexpression of miR15a/16 in H460 and A549 cells slows cellular proliferation over 72 hours (A, B, <i>n</i> = 5) and blunts protein synthesis rates (C, D, <i>n</i> = 4). * indicates a difference of <i>p</i> &lt; 0.05, **** indicates a difference of <i>p</i> &lt; 0.0001.”</p><p>The authors apologize for these errors.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 6","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2026-00177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148237954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction of Risk of Unplanned Readmission or Death in Elderly Heart Failure Patients During the Vulnerable Phase: Machine Learning With SHAP Interpretation","authors":"Hao Luo,&nbsp;Qi Wu,&nbsp;Zaiyong Zheng,&nbsp;Xuefeng Wang,&nbsp;Na Lai,&nbsp;Yixuan Li,&nbsp;Xiang Zheng,&nbsp;Yihang Li,&nbsp;Deqiang Li,&nbsp;Kai Guo,&nbsp;Ji Li","doi":"10.1096/fba.2026-00164","DOIUrl":"https://doi.org/10.1096/fba.2026-00164","url":null,"abstract":"<p>Heart failure (HF) as the final stage of cardiovascular disease in the elderly leads to frequent readmissions and seriously affects their quality of life. This study aimed to develop a predictive model for hospital readmission or death during the vulnerable phase in elderly HF patients, and to identify the key associated risk factors. The dataset was randomly divided into 70% training sets and 30% validation sets. Three feature selection methods were applied to the training data, followed by the construction of 18 predictive models using six machine learning (ML) algorithms (XGBoost, LightGBM, AdaBoost, GBDT, GNB, and SVM). The performance of each model was assessed on the validation set using receiver operating characteristic (ROC) curves, sensitivity, accuracy, specificity, F1 score, and Brier score. SHapley Additive exPlanations (SHAP) were used to interpret the feature contributions both globally and locally. Eleven models achieved an area under the ROC curve (AUC) greater than 0.8, with the Boruta-XGBoost model performing best, showing an AUC of 0.873 in the validation set, along with a sensitivity of 0.839, accuracy of 0.769, specificity of 0.747, F1 score of 0.634, and Brier score of 0.130. SHAP analysis revealed that the top five important features were hemoglobin (HGB), serum free thyroxine (FT4), age, diabetes, and serum potassium (K). The Boruta-XGBoost based risk prediction model, combined with SHAP interpretation, demonstrated high predictive accuracy and robust interpretability for forecasting hospital readmission or death during the vulnerable phase in elderly HF patients.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 6","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1096/fba.2026-00164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148237692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Effects of Cigarette and Hookah Smoking on Oral Microbiota Composition and Blood Indices in Young Adult Males","authors":"Fayez Alghofaili,&nbsp;Hemin Mohamad Hussein,&nbsp;Hastyar Hama Rashid Najmuldeen,&nbsp;Soma Yasin Tahsin,&nbsp;Asia Hamasaeed Muhamad,&nbsp;Ara Jabbar Othman,&nbsp;Kashan Faraidun Karim,&nbsp;Aryan Omer Ali,&nbsp;Ala Salam Karim","doi":"10.1096/fba.2025-00296","DOIUrl":"10.1096/fba.2025-00296","url":null,"abstract":"<p>Cigarette and hookah smoking remain prevalent worldwide, yet their comparative effects on oral microbiota and hematological parameters are not fully understood. This cross-sectional study investigated these impacts among 87 healthy males (18–40 years) in Sulaymaniyah, Iraq, divided into cigarette smokers, hookah smokers, and non-smokers (<i>n</i> = 29 each). Oral rinses were analyzed for microbial load and species distribution using selective media and standard identification techniques, while venous blood samples were evaluated for complete blood counts using an automated analyzer. Cigarette smokers exhibited the highest oral bacterial load (5.96 ± 0.19 log₁₀ CFU/mL) compared with non-smokers (3.70 ± 0.10; <i>p</i> &lt; 0.001), followed by hookah smokers. Colonization by <i>Candida albicans</i> and Gram-positive cocci (Staphylococcaceae, Streptococcaceae) was more frequent in smokers. Both smoking methods significantly increased RBC count, hemoglobin, and hematocrit levels (<i>p</i> &lt; 0.01). Mean corpuscular volume increased significantly only in cigarette smokers, whereas red cell distribution width and mean platelet volume were significantly higher in hookah smokers (<i>p</i> &lt; 0.01). Exploratory correlation analysis revealed strong positive associations between oral bacterial load and erythrocyte-related parameters (RBC, HGB, HCT; <i>r</i> = 0.91–0.94), while weak correlations were observed with inflammatory and platelet indices (WBC, RDW, MPV). These findings indicate that cigarette and hookah smoking disrupt oral microbial balance and alter hematological parameters, with distinct patterns between smoking types. The observed correlations likely reflect parallel systemic effects of smoking-related toxicants rather than a direct causal link between oral dysbiosis and erythropoiesis. Overall, the results reinforce that hookah smoking is not a safer alternative to cigarette use and highlight the need for targeted public health interventions.</p>","PeriodicalId":12093,"journal":{"name":"FASEB bioAdvances","volume":"8 6","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}