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PubMed2026

Construction of molecular signatures based on the co-expression network of NECSO-related gene TRPM4 and its prognostic value in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) demonstrates significant prognostic variability that is not entirely accounted for by traditional staging systems. Necrosis by sodium overload (NECSO) is an emerging programmed cell death pathway, but its clinical relevance in HCC remains undefined. Therefore, this study aimed to identify TRPM4-associated core genes, develop and validate a prognostic signature, and investigate its relationship with the tumor immune microenvironment, tumor mutational burden, and single-cell expression patterns in HCC. METHODS: We integrated transcriptomic, clinical, and mutational datasets from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) (n=421) and Gene Expression Omnibus (GEO) cohorts (n=115) to identify genes co-expressed with TRPM4-a key NECSO mediator-and those differentially expressed in HCC. A prognostic signature was developed using least absolute shrinkage and selection operator (LASSO)-Cox regression and validated through survival analysis, time-dependent receiver operating characteristic (ROC) curves, and multivariate Cox regression analysis. The immune landscape was characterized using CIBERSORT, somatic mutation data were used to calculate tumor mutational burden (TMB) and assess its correlation with the risk score, and single-cell RNA sequencing (scRNA-seq) resolved cell-type-specific expression patterns. RESULTS: From 294 TRPM4-associated core genes, we identified an 11-gene signature (BRSK1, MMP1, GRIN2D, GP6, MYOM2, N4BP3, CCDC112, TSEN54, MAP3K9, SPP1, B3GNT4) that independently predicted overall survival (OS) (hazard ratio =5.419, P<0.001) with areas under the curve (AUCs) of 0.779, 0.693, and 0.701 at 1, 3, and 5 years. These values were superior or comparable to conventional clinicopathologic variables after direct comparison. High-risk patients exhibited an immunosuppressive microenvironment, characterized by enrichment of M0 macrophage, a higher M2/M1 ratio (P<0.001) and distinct immune checkpoint profiles. When integrated with TMB, the prognostic stratification was further refined: high-TMB/high-risk patients had poorest outcomes (median OS, 15.3 months), while low-TMB/low-risk patients had the most favorable survival (median OS, 68.7 months). Single-cell analysis revealed that MMP1 was induced in cancer-associated fibroblasts (CAFs) and SPP1 was downregulated in macrophages, single-cell risk scores confirmed TAFs and macrophages as the main contributors to the prognostic model. CONCLUSIONS: The TRPM4-centered 11-gene signature provides robust and independent prognostic stratification in HCC by integrating immune, mutational, and single-cell features. This signature serves as a potential tool for prognostic evaluation and may help inform immunotherapeutic strategies for HCC.

Hepatocellular carcinoma (HCC)↗

PubMed2006

Chemical interference of pathogen-associated molecular pattern-triggered immune responses in Arabidopsis reveals a potential role for fatty-acid synthase type II complex-derived lipid signals.

We describe an experimental setup using submerged cultures of Arabidopsis seedlings in 96-well microtiter plates that permits chemical intervention of rapid elicitor-mediated immune responses. Screening of a chemical library comprising 120 small molecules with known biological activities revealed four compounds reducing cellulysin- or flg22-activated gene expression of the early pathogen-associated molecular patterns (PAMP)-responsive ATL2 gene. One chemical, oxytriazine, was found to induce ATL2 gene expression in the absence of PAMP. By monitoring additional flg22-triggered immediate early plant responses, we present evidence that two compounds, triclosan and fluazinam, interfere with the accumulation of reactive oxygen species and internalization of the activated plasma membrane resident FLS2 immune receptor. Using triclosan structure types and enzyme activity inhibition assays, Arabidopsis MOD1 enoyl-acyl carrier protein reductase, a subunit of the fatty-acid synthase type II (FAS II) complex, was identified as a likely cellular target of triclosan. Inhibition of all tested elicitor-triggered early immune responses by triclosan indicates a potential role for signaling lipids in flg22-triggered immunity. Chemical profiling of eca mutants, each showing deregulated ATL2 gene expression, with the identified compounds revealed mutantspecific response patterns and allowed us to deduce tentative action sites of ECA genes relative to the compound targets.

Acetyltransferases↗

PubMed1996

Kinetics, localization and isotype profile of antibody responses to immune stimulating complexes (iscoms) containing human influenza virus envelope glycoproteins.

The immune stimulating complex (iscom) is a particulate adjuvant formulation combining multimeric presentation of antigen with a built-in adjuvant, Quillaja saponin. Iscoms induce strong serum antibody responses that are readily boosted. To further characterize this property of iscoms, the development and maturation of primary and secondary antibody responses to iscoms containing influenza virus antigen were investigated, in serum by ELISA and on single B-cell level by ELISPOT. After a single subcutaneous injection, B cells secreting antigen-specific IgG (IgG-SC) were primarily observed in the draining lymph nodes (LN), showing peak numbers at day 7 which then declined rapidly. Serum IgG levels, as well as IgG-SC in the spleen, persisted for several weeks and, with time, IgG-SC cells also appeared in the bone marrow (BM). These results suggest that the IgG response to iscoms initially is located to the LN but that IgG-SC are redistributed with time and may persist for a long time in other organs, including the spleen and BM. Moreover, a booster dramatically enhanced the frequency of IgG-SC in LN, spleen and BM suggesting that iscoms induce a potent B-cell memory. Comparisons of antibody responses to iscoms with those to influenza virus antigen in Freund's complete adjuvant, TiterMax or aluminium hydroxide suggest that the choice of adjuvant influences both the magnitude, kinetics, localization and isotype profile of antibody responses.

Adjuvants, Immunologic↗

PubMed2004

Basic immunological aspects of botulinum toxin therapy.

Previous studies in this laboratory had mapped the immune recognition profile of the regions recognized antibodies (Abs) and by T cells on the protective H(C) domain (C-terminal fragment corresponding to residues 855-1296 of the heavy chain) of botulinum neurotoxin serotype A (BoNT/A). The localization of these regions has several potential applications and has provided a basis for the understanding of immunoresistance to treatment. We briefly outline these localized regions and discuss the impact of these findings on the immunotherapeutic applications of BoNT/A. Immunoresistance to toxin therapy can appear in some patients after a few injections with the toxin. Our epitope mapping studies have shown that several factors can influence the immune response to the toxin. These factors include dose, duration of treatment, frequency of immunization, and quality of the toxin. The immune response to the whole toxin is under genetic control, and the response to each epitope is under separate genetic control. Therefore, the appearance of blocking Abs (i.e., immunoresistance) in patients might be controlled by the major histocompatability of the host. Once a patient becomes immunoresistant to one toxin then switching to another toxin will most often be of limited and short-lived benefit, because the patient becomes rapidly immunoresistant to the second toxin. Finally, because of the considerable structural homology between tetanus neurotoxin (TeNT) and BoNTs, it is possible, although not certain, that a prior active immune response to TeNT might play some role in the early appearance on anti-BoNT Abs in some patients.

Amino Acid Sequence↗

PubMed1993

Effects of fumonisin-contaminated corn screenings on growth and health of feeder calves.

Fumonisins are myocotoxins produced by Fusarium moniliforme and F. proliferatum, common molds of corn in North America. The toxin is at especially high concentrations in corn screenings. Fumonisins are toxic to swine and horses, but effects of these toxins in cattle have not been evaluated. This experiment was conducted to determine the effects in cattle of feeding fumonisins at levels known to be toxic to swine and horses. A total of 18 crossbred feeder calves were fed diets containing fumonisins at 15, 31, or 148 micrograms/g for 31 d. Feed consumption, weight gain, complete blood count, serum clinical chemistries, and an immune function profile were done on d -3, 4, 10, 17 and 31 relative to the start of fumonisin feeding. There was no treatment-related effect on feed intake or weight gain, but feed containing 148 micrograms/g of fumonisins seemed to be less palatable than other feeds. Significant increases in serum aspartate amino transferase, gamma glutamyl transpeptidase, lactate dehydrogenase, bilirubin, and cholesterol occurred from d 10 through 31. Mild microscopic liver lesions were present in two calves fed at the highest fumonisin level. Lymphocyte blastogenesis was significantly impaired at the end of the feeding period in the group given the highest dose. Other measures of immune function were not affected significantly. Fumonisins are capable of causing changes in liver function and in some measures of immune function. However, cattle seem to be relatively less susceptible to fumonisins present naturally in grains than either swine or horses.

Animal Feed↗

PubMed2026

Prognostic value of genes associated with metastasis and propionate metabolism in rectal cancer.

BACKGROUND: Research indicates that alterations in propionate metabolic pathways play a critical role in cancer development and invasion. Postoperative metastatic recurrence remains a major cause of mortality in patients with rectal cancer. However, propionate metabolism-related genes (PMRGs) in rectal cancer remain insufficiently characterized. Therefore, this study aimed to identify prognostic biomarkers associated with lymph node metastasis and propionate metabolism and construct a risk‑prediction model for rectal cancer via bioinformatic analyses. METHODS: The Cancer Genome Atlas-Rectum Adenocarcinoma (TCGA-READ) and GSE87211 datasets, together with a curated PMRGs gene set, were used in this study. Pearson correlation analysis was performed to assess associations between overlapping genes (differentially expressed genes between READ and normal tissues, as well as between N0 and N1-N2 stages) and PMRGs, leading to the identification of candidate genes. Functional enrichment analyses were subsequently conducted to characterize the biological roles of these candidates. Prognostic biomarkers were identified using univariate Cox regression combined with least absolute shrinkage and selection operator (LASSO) regression, and a prognostic model was constructed accordingly. Independent prognostic validation was then performed. In addition, immune checkpoint profiling and immunotherapy response analyses were conducted across risk subgroups. Single-gene Gene Set Enrichment Analysis (GSEA) was applied to elucidate the pathways associated with the identified biomarkers. Finally, drug sensitivity analyses were performed. RESULTS: A total of 157 candidate genes were identified through the analytical pipeline. Functional enrichment analysis indicated that these genes were primarily involved in inflammatory response regulation and tumor necrosis factor (TNF) signaling pathways. Five prognostic biomarkers were subsequently identified and incorporated into a predictive model. External validation using the GSE87211 cohort confirmed the robustness of the model. Risk score and disease status were identified as independent prognostic factors. Six immune checkpoint molecules exhibited differential expression between risk groups. Correlation analyses revealed that the risk score was positively associated with most immune checkpoint genes. Single-gene GSEA demonstrated that the biomarkers were mainly enriched in ribosomal biogenesis and cell adhesion molecule-related pathways. Furthermore, 51 therapeutic agents exhibited significantly different half-maximal inhibitory concentration (IC50) values between risk subgroups. CONCLUSIONS: This study identified five biomarkers (CCL24, IGFBP3, ODC1, PYGM, and VKORC1) associated with lymph node metastasis and propionate metabolism pathways, providing a potential foundation for prognostic prediction in patients with rectal cancer.

Rectal cancer↗

PubMed2026

Icaritin Sensitizes Hepatocellular Carcinoma to PD-L1 Therapy by NQO1-Dependent Ferroptosis Induction.

Hepatocellular carcinoma (HCC) remains challenging with limited immunotherapy response. Despite its clinical promise in advanced HCC, the mechanisms of icaritin, especially concerning ferroptosis induction and immune modulation, remain elusive. This study aims to determine if the antitumor effect of icaritin involves the induction of ferroptosis via NAD(P)H quinone oxidoreductase 1 (NQO1) and if it can augment the efficacy of programmed cell death 1 ligand 1 (PD-L1) therapy by potentiating natural killer (NK) cell activity. Using human HCC cell lines (Huh7, Hep3B, PLC/PRF/5, SNU-449, and MHCC97-H) and two synergistic mouse models (Hepa1-6 and SgPten/c-Met), we examined icaritin's inhibition of tumor growth and induction of ferroptosis via the NQO1 pathway, monitoring key markers (reactive oxygen species [ROS], glutathione peroxidase 4 [GPX4], ferritin heavy chain 1 [FTH1]). The NQO1 inhibitor dicoumarol was employed to validate the pathway. Tumor microenvironment (TME) remodeling was assessed through cancer-associated fibroblasts (CAFs) markers and immune cell profiling, focusing on NK cell infiltration. Combination therapy with anti-PD-L1 was tested in vivo. Icaritin significantly inhibited HCC growth in vitro and in vivo. Its antitumor effect was mediated by NQO1-mediated ferroptosis, via elevated ROS, diminished mitochondrial membrane potential, and downregulated GPX4 and FTH1. Analysis of The Cancer Genome Atlas (TCGA) data revealed that NQO1 is overexpressed in human HCC tissues. Icaritin enhanced NK cell infiltration while reducing CAF abundance and suppressing recombinant focal adhesion kinase (FAK) and discoidin domain receptor 1 (DDR1) signaling. Notably, icaritin synergized with anti-PD-L1 therapy to enhance tumor suppression without increasing toxicity, correlating with potentiated NK cell immunity. Our findings demonstrate that icaritin triggered NQO1-mediated ferroptosis and remodeled TME to enhance NK cell recruitment and PD-L1 therapy efficacy. This provides rationale for evaluating icaritin-based combination immunotherapy in HCC through dual action on ferroptosis and NK cell activation.

Ferroptosis↗

PubMed2003

Genetic control of the innate immune response.

BACKGROUND: Susceptibility to infectious diseases is directed, in part, by the interaction between the invading pathogen and host macrophages. This study examines the influence of genetic background on host-pathogen interactions, by assessing the transcriptional responses of macrophages from five inbred mouse strains to lipopolysaccharide (LPS), a major determinant of responses to gram-negative microorganisms. RESULTS: The mouse strains examined varied greatly in the number, amplitude and rate of induction of genes expressed in response to LPS. The response was attenuated in the C3H/HeJlpsd strain, which has a mutation in the LPS receptor Toll-like receptor 4 (TLR4). Variation between mouse strains allowed clustering into early (C57Bl/6J and DBA/2J) and delayed (BALB/c and C3H/ARC) transcriptional phenotypes. There was no clear correlation between gene induction patterns and variation at the Bcg locus (Slc11A1) or propensity to bias Th1 versus Th2 T cell activation responses. CONCLUSION: Macrophages from each strain responded to LPS with unique gene expression profiles. The variation apparent between genetic backgrounds provides insights into the breadth of possible inflammatory responses, and paradoxically, this divergence was used to identify a common transcriptional program that responds to TLR4 signalling, irrespective of genetic background. Our data indicates that many additional genetic loci control the nature and the extent of transcriptional responses promoted by a single pathogen-associated molecular pattern (PAMP), such as LPS.

Animals↗

PubMed2004

Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome.

Severe acute respiratory syndrome (SARS) has spread to a global pandemic, especially in Asia. The transmission route of SARS has been clarified, but the immunopathogenesis of SARS is unclear. In an age-matched case-control design, we studied immune parameters in 15 SARS patients who were previously healthy. Plasma was harvested for detection of virus load, cytokines, and nitrite/nitrate levels, and blood leukocytes were subjected to flow cytometric analysis of intracellular mitogen-activated protein kinases (MAPKs) in different leukocytes. Patients with SARS had significantly higher IL-8 levels (p = 0.016) in early stage, and higher IL-2 levels (p = 0.039) in late stage than normal controls. Blood TNF-alpha, IL-6, and IL-10, and nitrite/nitrate levels were not significantly elevated. In contrast, TGF-beta and PGE(2) levels were significantly elevated in SARS patients. Five of the 15 SARS patients had detectable coronaviruses in blood, but patients with detectable and undetectable viremia had no different profiles of immune mediators. Flow cytometric analysis of MAPKs activation by phospho-p38 and phospho-p44/42 (extracellular signal-regulated kinase) expression showed that augmented p38 activation (p = 0.044) of CD14 monocytes associated with suppressed p38 activation (p = 0.033) of CD8 lymphocytes was found in SARS patients. These results suggest that regulation of TGF-beta and PGE(2) production and MAPKs activation in different leukocytes may be considered while developing therapeutics for the SARS treatment.

Adjuvants, Immunologic↗

PubMed2007

Asbestos-induced peribronchiolar cell proliferation and cytokine production are attenuated in lungs of protein kinase C-delta knockout mice.

The signaling pathways leading to the development of asbestos-associated diseases are poorly understood. Here we used normal and protein kinase C (PKC)-delta knockout (PKCdelta-/-) mice to demonstrate multiple roles of PKC-delta in the development of cell proliferation and inflammation after inhalation of chrysotile asbestos. At 3 days, asbestos-induced peribronchiolar cell proliferation in wild-type mice was attenuated in PKCdelta-/- mice. Cytokine profiles in bronchoalveolar lavage fluids showed increases in interleukin (IL)-1beta, IL-4, IL-6, and IL-13 that were decreased in PKCdelta-/- mice. At 9 days, microarray and quantitative reverse transcriptase-polymerase chain reaction analysis of lung tissues revealed increased mRNA levels of the profibrotic cytokine, IL-4, in asbestos-exposed wild-type mice but not PKCdelta-/- mice. PKCdelta-/- mice also exhibited decreased lung infiltration of polymorphonuclear cells, natural killer cells, and macrophages in bronchoalveolar lavage fluid and lung, as well as increased numbers of B lymphocytes and plasma cells. These changes were accompanied by elevated mRNA levels of immunoglobulin chains. These data show that modulation of PKC-delta has multiple effects on peribronchiolar cell proliferation, proinflammatory and profibrotic cytokine expression, and immune cell profiles in lung. These results also implicate targeted interruption of PKC-delta as a potential therapeutic option in asbestos-induced lung diseases.

Animals↗

PubMed2001

Characterization of a novel hepatitis B virus mutant: demonstration of mutation-induced hepatitis B virus surface antigen group specific "a" determinant conformation change and its application in diagnostic assays.

We report and characterize a novel mutant of the hepatitis B virus surface antigen (HBsAg). The mutant was isolated from a symptomatic patient who was found to be persistently positive for both HBsAg and anti-hepatitis B surface antibody (anti-HBs) and a long-lasting anti-HBc (core) IgM. Due to the unusual immune serological profile, polymerase chain reaction and sequencing were performed and revealed a genotype D mutant HBV (LBN). Aligned with known HBsAg sequences from GenBank, the LBN variant matched to consensus subtype ayw2 and revealed five mutation positions. Interestingly, none of the mutations was found within the group-specific "a" determinant region (124-147) and, specifically, two of the five mutations, T118K and P120Q, were located only a few amino acids adjacent to the 124-147 region. Using a panel of six monoclonal antibodies and vaccine raised human neutralizing antibodies, the recombinant wild-type HBsAg and the novel variant LBN HBsAg were investigated for their immunological reactivity. Vaccine raised human anti-HBs showed less reactivity to the variant LBN HBsAg than to wild-type HBsAg in enzyme immune assays. Furthermore, our observations demonstrate the influence of adjacent residues on the group-specific "a" determinant structural configuration; this resulted in severe antigenic changes of the immunodominant region as well as in the subtype serology. The importance of the variant LBN lies in the observation that mutations close to the "a" determinant can change the immunodominant region structure and therefore alter the group specific determinant antigenicity even though no mutations are present within this region. Hence, the classical definition of the "a" determinant cluster may need to be extended to cover a broader region to include the requirement of adjacent amino acids to support its conformation. In conclusion, by understanding the HBsAg major immunodominant region structure and by using a combination of antibodies with specificity covering all key mutation locations, maximal anti-HBs-based protection, and highly sensitive diagnostic assays can be achieved.

Adult↗

PubMed2002

Might wasp venom desensitization induced Th2 to Th1 shift cause pregnancy failure?

The case of a 28-year-old woman under wasp venom desensitization having a premature birth in her 24th week of pregnancy 16 days after the last injection is described. To test the hypothesis that a special profile of immune cells in the decidua may trigger abortions, placental and decidual tissue sections were stained with antibodies against T cells (CD3), cytotoxic cells (CD8), natural killer cells (CD56), and mast cells, and an in-situ-hybridization was performed for tumor necrosis factor-alpha (TNF-alpha). CD56+ Natural killer cells were the dominating population. In earlier analyses of healthy first trimester decidua the percentage of NK cells and T cells was in a similar range, but the CD8:CD3 ratio was only 2.2% in contrast to 27% in the present case. Mast cells, which are known to be able to secrete abortogenic TNF-alpha, were only detectable in the decidua (10 cells/mm2) and decidua sections were TNF-alpha positive. Since SIT induces a shift of the interleukin and functional profile from a Th2 type towards a Th1 type, and pregnancy is dependent on a Th2 pronounced profile, SIT may trigger abortions or immature births. This is supported by the present results and might have happened in this case.

Abortion, Spontaneous↗

PubMed2004

Abnormal production of transforming growth factor beta and interferon gamma by peripheral blood cells of patients with multidrug-resistant pulmonary tuberculosis in Brazil.

OBJECTIVES: The aim of the present study was to determine the immune response profile that differentiates patients with newly diagnosed (non-treated) pulmonary tuberculosis from multidrug-resistant (MDR) ones, as well as from healthy, tuberculin positive individuals. METHODS: Lymphocytes proliferative response to non-specific mitogen (PHA) and PPD were evaluated by 3H thymidine incorporation and cytokines were quantified using an ELISA assay. RESULTS: Patients with active disease showed a diminished proliferative response to PHA and PPD, while multidrug-resistant patients showed a diminished proliferative response to PHA, but a normal response to PPD. The cytokine production of newly diagnosed patients was characterized by a diminished production of IFNgamma and normal production of transforming growth factor (TGFbeta), while MDR patients revealed a normal production of IFNgamma accompanied by an increase in TGFbeta. CONCLUSIONS: The production of significant amounts of TGFbeta in MDR patients leads to a poor immune response and may contribute to the resistance of tuberculosis patients to drugs.

Adult↗

PubMed2025

Gene behaviors-based network enrichment analysis and its application to reveal immune disease pathways enriched with COVID-19 severity-specific gene networks.

MOTIVATION: Gene network analysis is essential for understanding the complex mechanisms underlying diseases, which often involve disruptions in molecular networks rather than individual genes. Despite the availability of large-scale omics datasets and computational tools for gene network analysis, interpretation of the biological relevance of these extensive networks remains challenging. RESULTS: We propose a novel computational strategy, gene behaviors-based network enrichment analysis, which systematically identifies functional pathways enriched in phenotype-specific gene networks. Our novel method incorporates comprehensive network characteristics, i.e. gene expression levels, edge strengths, and structural patterns of edges, to rank genes based on activity and assess pathway enrichment, effectively identifying functional pathways enriched within these networks. Through simulation studies, our strategy demonstrated superior performance compared with that of existing methods in identifying enriched pathways. We applied this strategy to whole-blood RNA-seq data from 1102 COVID-19 samples provided by the Japan COVID-19 Task Force. The analysis revealed immune disease pathways enriched with COVID-19 severity-specific gene networks, including "Systemic lupus erythematosus" in asymptomatic and severe samples and "Inflammatory bowel disease," "Primary immunodeficiency," and "Rheumatoid arthritis" in mild samples. Key biomarkers of COVID-19, such as CXCL8, S100A9, and HLA class I genes, have been identified as critical hub genes and the main players within these networks. AVAILABILITY AND IMPLEMENTATION: Code is available in Figshare (https://doi.org/10.6084/m9.figshare.29093648.v3).

COVID-19↗

PubMed1988

Analysis, characterization, and diagnostic utility of filarial antigen fractions isolated from immune complexes in bancroftian filariasis.

Circulating immune complexes isolated from clinical filarial patients' sera by 3% polyethylene glycol precipitation were analyzed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) on vertical slab gel. Silver staining of the gel after electrophoresis revealed 20 and 30 protein bands without and with reduction of immune complexes, respectively, in the molecular weight range of 148-18K. Filarial antigen in protein eluates from gel slices was detected by sandwich enzyme-linked immunosorbent assay. The eluates from four gel slices, viz., IC-2, IC-4, IC-7, and IC-9, showed filarial antigenic activity. These antigen fractions were characterized and explored for their diagnostic use. IC-7 and IC-9 fractions and microfilariae excretory-secretory (mf ES) antigen share common antigenic determinants as revealed by the fact that saturation of immobilized antibodies with IC-7 or IC-9 inhibited the binding of mf ES antigen coupled to penicillinase. IC-9 fraction appears to be useful in serological differentiation of Wuchereria bancrofti infected persons from those with disease manifestations. Biochemical characterization of the IC-9 fraction revealed the protein nature of the antigen. Comparison of the electrophoretic profiles of immune complexes and W. bancrofti mf ES antigen revealed several common protein bands. The 55 K protein band with antigenic activity was observed in both preparations.

Animals↗

PubMed2003

In vitro cellular and humoral responses to Schistosoma mansoni vaccine candidate antigens.

Few studies comparing schistosomiasis vaccine candidate antigens between laboratories have been carried out and published. Generally, only the investigators who discovered the molecules have evaluated them in either experimental animal models or in human correlate studies. In an attempt to identify responses against specific antigens and investigate their association with resistance versus susceptibility to re-infection, we studied the serological reactions and the cytokine responses stimulated by a panel of 10 candidate vaccine molecules in 225 long-term residents of an area endemic for Schistosoma mansoni in Egypt. The panel consisted of four recombinant antigens (Sm62-Irv5, Sm37-G3PDH, Sm28-GST and Sm14-FABP), one full-length native protein (Sm97-paramyosin), two synthetic peptides (MAP3 and MAP4) and three unpublished antigens (PR52-filamin, PL45-phosphoglycerate kinase, PN18-cyclophilin). Two different study designs, one based on retrospective and the other on prospective parasitological data were applied in the evaluation of the immune responses. Using historical data collected over the previous 5 years, correlations between frequency of re-infection and antigen-specific immune responses were investigated. In the prospective arm of the study, the subjects were followed over time after treatment with praziquantel with periodic immunological tests and stool examinations. Thus, highly specific humoral and cellular immune reactions in response to the 10 antigens described above could be correlated, both prospectively and retrospectively, with detailed epidemiological data covering a 66-month period. The immune response profiles produced were unique to each antigen but no clear "winner" or "winners" were identified. However, markers for both resistance and susceptibility to re-infection were identified for each molecule indicating which types of responses to aim for in vaccination and which ones to avoid. The insights gained from this approach should be useful for antigen selection and ultimately for vaccine formulation prior to Phase I/II trials in humans.

Adolescent↗

PubMed2005

Aging.

Respiratory tract infections are a leading cause of morbidity and mortality in the elderly. Many factors, such as malnutrition and the presence of structural lung disease, increase the risk of respiratory infection in older individuals. Aging is also accompanied by a gradual decline in many aspects of immune function, and waning immunity is thought to be an important risk factor for pneumonia in the elderly. Although a generalized decline in both the cell-mediated and humoral aspects of acquired immunity have been described in otherwise normal elderly populations, relatively little is known about the effect of age on compartmentalized pulmonary immune surveillance and immune responses to a challenge with a respiratory pathogen. Changes in immune cell profiles and acellular components of bronchoalveolar secretions have been detected by bronchoalveolar lavage, but the impact of these changes on host defense against respiratory infections is unknown. An improved understanding of the age-associated changes in pulmonary host defense mechanisms and how these might be manipulated to reduce the susceptibility of the elderly to respiratory tract infections may reduce the possibility of severe debilitation and death and the considerable health care burden posed by the increased incidence of pneumonia in this at-risk population.

Age Factors↗

PubMed2026

Multi-omics analysis reveals stage-associated differences in gut immunity and microbiota between juvenile and adult common carp (Cyprinus carpio).

In vertebrates, the development of intestinal immunity is closely associated with dynamic changes in the gut microbiota. However, stage-associated differences in intestinal immunity and gut microbial communities remain poorly characterized in teleost fish. In this study, transcriptomic analysis combined with 16S rRNA gene sequencing was employed to characterize intestinal immunity and gut microbial communities in juvenile and adult common carp (Cyprinus carpio). Transcriptomic profiling revealed marked developmental differences in intestinal immune function. Juvenile carp exhibited a predominantly innate immune phenotype, characterized by elevated expression of pro-inflammatory cytokines, antimicrobial peptides, and lysozyme-related genes. This immune profile was accompanied by enhanced mucosal barrier function and a relatively pro-inflammatory intestinal environment. In contrast, adult carp displayed increased expression of genes associated with adaptive immunity, suggesting that adult common carp exhibit relatively stronger adaptive immune characteristics than juvenile fish. Gut microbiota analysis demonstrated significant stage-dependent differences in microbial diversity and community composition. Juvenile fish were enriched with bacterial taxa potentially associated with innate immune activation, whereas adult fish harbored distinct microbial communities linked to intestinal homeostasis and barrier maintenance. Furthermore, correlation analyses identified significant associations between specific microbial taxa and innate immune-related gene expression, suggesting a close association between gut microbiota composition and intestinal immune characteristics in juvenile and adult common carp. Collectively, these findings reveal stage-associated differences in intestinal immunity and gut microbial communities between juvenile and adult common carp, thereby providing insights into intestinal immune characteristics at different developmental stages in teleost fish.

Animals↗