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PubMed1994

Immunostimulating effects of protein A in immunosuppressed aflatoxin-intoxicated rats.

Aflatoxin B1, the potent carcinogenic compound produced by the Aspergillus flavus group of fungi on food and feed, induces immunosuppressive effects in rodents. In this communication, we report an immunomodulatory approach to abrogate aflatoxin B1-induced immunotoxicity in rats using protein A of Staphylococcus aureus Cowan 1. We have earlier demonstrated that protein A can protect the animals from toxicities induced by a number of drugs, chemicals and toxins. In the present study various combinations of aflatoxin B1 exposure and protein A treatment in animals were used. It was observed that protein A could provide protection to animals from aflatoxin B1-induced immunotoxicity, as measured by a battery of tests assessing cell-mediated immunity (CMI) profile of the host. Various parameters showing suppression of CMI following aflatoxin B1 exposure were reverted back towards normalcy in protein A-treated animals. It is concluded that protein A may prove to be a useful agent to protect the host from aflatoxin immunotoxicity, in view of its stimulatory effects on various immune functions even after their initial depression due to aflatoxin B1.

Adjuvants, Immunologic↗
PubMed2025

AI-driven multi-omics modeling of myalgic encephalomyelitis/chronic fatigue syndrome.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic illness with a multifactorial etiology and heterogeneous symptomatology, posing major challenges for diagnosis and treatment. Here we present BioMapAI, a supervised deep neural network trained on a 4-year, longitudinal, multi-omics dataset from 249 participants, which integrates gut metagenomics, plasma metabolomics, immune cell profiling, blood laboratory data and detailed clinical symptoms. By simultaneously modeling these diverse data types to predict clinical severity, BioMapAI identifies disease- and symptom-specific biomarkers and classifies ME/CFS in both held-out and independent external cohorts. Using an explainable AI approach, we construct a unique connectivity map spanning the microbiome, immune system and plasma metabolome in health and ME/CFS adjusted for age, gender and additional clinical factors. This map uncovers altered associations between microbial metabolism (for example, short-chain fatty acids, branched-chain amino acids, tryptophan, benzoate), plasma lipids and bile acids, and heightened inflammatory responses in mucosal and inflammatory T cell subsets (MAIT, γδT) secreting IFN-γ and GzA. Overall, BioMapAI provides unprecedented systems-level insights into ME/CFS, refining existing hypotheses and hypothesizing unique mechanisms-specifically, how multi-omics dynamics are associated to the disease's heterogeneous symptoms.

Humans↗
PubMed2026

A novel glutamine metabolism-based classification system for characterizing the heterogeneity of hepatocellular carcinoma.

BACKGROUND: Glutamine dependence is a hallmark of tumor cell metabolism, and further molecular classification based on glutamine metabolism in patients with hepatocellular carcinoma (HCC) may provide clinical value. This study thus comprehensively examined the patterns of HCC-specific alterations in glutamine metabolism. METHODS: Consensus clustering analysis was conducted on samples from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset based on glutamine metabolism-related genes, which was validated in the GSE76427, the Liver Cancer-France (LICA-FR) cohort, and the Liver Cancer-Japan (LIRI-JP) cohort from the ICGC. Somatic mutation features were evaluated with the Maftools package in R. The activity of oncogenic pathways was estimated via gene set enrichment analysis (GSEA) or single-sample GSEA (ssGSEA). The tumor microenvironment was analyzed using both the CIBERSORT algorithm (for immune cell infiltration estimation) and the ESTIMATE algorithm (for stromal and immune score calculation). Drug sensitivity and immune checkpoint blockade (ICB) response were also analyzed, for which a classifier was built via least absolute shrinkage and selection operator (LASSO). Immunohistochemistry (IHC) was performed to validate the protein expression levels of key differentially expressed genes (DEGs). Intracellular glutamine content under different glutamine concentrations was measured. The viability of HCC cell lines under varying glutamine concentrations was assessed via Cell Counting Kit-8 (CCK-8) assays. Cell migration and invasion were evaluated through Transwell assays, and protein expression was analyzed via Western blotting. RESULTS: HCC samples were classified into two glutamine metabolism-based clusters, with cluster 1 having a more advanced stage of disease and shorter survival than cluster 2. A higher frequency of genetic mutations and stronger activation of oncogenic pathways was found in cluster 1. There were substantial differences in immune cell infiltration and stromal scores between clusters 1 and 2. Cluster 1 exhibited significantly higher infiltration of immunosuppressive cells and lower stromal scores compared to cluster 2. Cluster 1 had a stronger response to ICB due as indicated by a higher tumor mutation burden (TMB) and T cell-inflamed gene expression profile score, immune checkpoints, and Tumor Immune Dysfunction and Exclusion (TIDE)-predicted data. Moreover, the LASSO classifier accurately differentiated the two clusters. The DEGs between the two clusters were validated in clinical samples. IHC confirmed the differential expression of glutamine metabolism-related genes in HCC samples. CCK-8 assays showed no significant effect of glutamine concentration on cell proliferation. However, Transwell assays revealed that glutamine deprivation (0.2 mM) reduced migration and invasion, while high-glutamine conditions (10 mM) promoted them. Western blotting showed increased expression of metabolism-related proteins under high-glutamine conditions and reduced expression under deprivation. CONCLUSIONS: Altogether, these findings indicate the involvement of glutamine metabolism in HCC and may help inform patient stratification and the formulation of precision therapeutics for this population.

Hepatocellular carcinoma (HCC)↗
PubMed2001

Considering genetic profiles in functional studies of immune responsiveness to HIV-1.

Over the last two decades HIV-1 has spread worldwide and has now surpassed malaria as the leading cause of infectious disease mortality in adults (http://www.who.int/infectious-disease-report/pages/ch1text.html). The clinical course and outcome of HIV-1 infection are highly variable among individuals. Most individuals infected with HIV develop AIDS within 10 years. However about 1-5% remain relatively healthy for 15 years or more (long-term nonprogressors), while others progress to AIDS within the first 2-3 years after infection (rapid progressors). A small number of individuals are resistant to infection, while some individuals appear to eliminate the virus. Factors that influence susceptibility to infection and rate of disease progression are a combination of viral, host, and environmental determinants. With few exceptions, genetic resistance to infectious diseases is likely to involve a complex array of host genetic effects involving variants that have very subtle, but significant consequences on gene expression or protein function. We have gained considerable insight into the genetic effects on HIV-1 disease, yet we likely have uncovered only a fraction of the total picture. The greater our knowledge of various effects on HIV disease, the more likely we will be able to predict disease outcome on an individual-by-individual basis. While this may seem obvious, there is no standard practice of taking into account the genetic profile (i.e. genotypes at loci known to associate with rate of AIDS progression) of subjects used in functional studies of immune responsiveness to HIV-1. Here, we propose an approach for assessing overall genetic risk on an individual basis, and suggest that this information be considered when selecting comparison groups in studies of immune responses to HIV and/or in the interpretation of data derived from such studies.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Kinetics and physiopathology of immune depression following severe burns. Experimental study. Benefits of early excision. Role of prostaglandins].

The data obtained in a rat model supports the following conclusions. There is a period of normal immune responsiveness surrounding day 6, in spite of peaks of immunosuppression before and after that time. The spleen in burned animals is hypertrophic. This is due to its role as a filter (necrotic particles seen in macrophages) and as a "germ reservoir" (spleen culture studies). Impairment of immune function in spleen cells is important since, before day 6, there is an inhibition of antibody production with no alteration in lymphocyte transformation. After day 6, both functions are impaired. Most important to the clinical treatment of burns, all of these phenomena are diminished or abolished by early removal of the burned tissue. The profile of immune depression in burned rats therefore seems to show two stages: before and after day 6. During the first stage, stress and prostaglandins from burned skin are probably the cause of immune depression: during the second stage burn toxins and prostaglandins from the spleen cells are probably the cause.

Animals↗
PubMed2003

Maternal milk regulation of cell infiltration and interleukin 18 in the intestine of suckling rat pups.

BACKGROUND: and aims: In neonates the gastrointestinal tract is exposed to food and bacterial antigens at a time when the gut mucosal immune system has not developed the ability to induce oral tolerance. This increases the risk for an inappropriate immune response to oral antigens. Transforming growth factor beta (TGF-beta) is an immunoregulatory cytokine present in high concentration in maternal milk. Interleukin 18 (IL-18) is a cytokine that mediates early immune events, and drives T cell development. We assessed the role of TGF-beta in mediating mucosal immune development and specifically the effect on endogenous IL-18. METHODS: Rat pups were randomly assigned to the following groups, naturally suckled, maternal milk via cannula, and formula fed with and without physiological levels of TGF-beta2. A comparison of the immune response profile was then carried out. Cytokine profiles, dendritic cell, intestinal mast cell, and eosinophil numbers were assessed. RESULTS: We show that feeding formula deficient in TGF-beta2 resulted in accumulated IL-18 protein release from intestinal epithelial cells and IL-18 mRNA up regulation. A proinflammatory cytokine profile resulted in the gut, along with increased numbers of activated dendritic cells, eosinophils, and mast cells. Supplementation of the formula with TGF-beta2 down regulated the proinflammatory cytokine mRNA as well as the number of activated lymphocytes, eosinophils, mast cells, CD80, and CD86 positive dendritic cells. CONCLUSION: The data suggests an important role for maternal milk, in regulating immune responses after exposure to food antigens, which might otherwise induce deleterious immune responses in the intestine of suckling neonates. This regulation is potentially mediated by milk TGF-beta2, as well as endogenous IL-18.

Animals↗
PubMedDate not supplied

Mucosal cytokine and antigen-specific responses to Cryptosporidium parvum in IL-12p40 KO mice.

Studies of cellular immune responses to Cryptosporidium parvum have been limited in part by lack of suitable animal models. IL-12p40(-/-)mice are susceptible to initial infection with C. parvum but recover within 2 weeks, rendering the animals resistant to reinfection. Because the host responses that determine duration and severity of primary infection are not yet understood, we studied the cellular immune response to primary infection with C. parvum in IL-12p40(-/-)mice and also explored possible mechanisms for this response. Female IL-12p40(-/-)mice were inoculated with 10,000 oocysts. Uninfected age-matched mice served as controls. At different time intervals following exposure to oocysts, mice were sacrificed and their intestine, spleen, and mesenteric lymph node tissues were harvested. Cellular immune responses to C. parvum were characterized. Infection of IL-12p40(-/-)mice induced changes in the gene expression of the cytokines IFN-gamma, IL-4, IL-15, IL-18, TNF-alpha and TGF-beta during primary infection. There was also a significant increase in total numbers of lymphocytes and CD19/CD62L-expressing cells in mesenteric lymph nodes. These MLN cells exhibited increased antigen-specific proliferation and cytokine production (IL-6 and IFN-gamma) levels when stimulated in vitro. These observations delineate the cellular immune responses during acute C. parvum infection of the IL-12p40(-/-)mouse model.

Animals↗
PubMed2004

Toll and Toll-9 in Drosophila innate immune response.

In both insects and mammals, members of the Toll receptor family play important roles in the initial events leading to the activation of immunity genes. The prototypic Toll in Drosophila appears to be activated by a host protein ligand after microbial stimulation. The cellular events and the biological response after Toll activation, however, require further investigation. We used transgenic Drosophila strains expressing NF-kappaB and Toll proteins to investigate innate immune response in whole larvae and dissected larval fat bodies. Substantial activation of antimicrobial peptide genes was observed after septic injury. To circumvent the contribution of injury-induced response, we used dissected larval fat bodies to show that commercially available microbial compounds were able to alter the cellular distribution of Toll. The results also demonstrate that complex cellular events, including receptor trafficking, likely take place after stimulation of the larval immune tissue. By genome-wide expression analysis, we further show that Toll and Toll-9 may utilize the same signaling pathway in activating many immunity genes. Thus, the innate immune response in Drosophila is regulated by complex mechanisms, which involve Toll and other Toll-related proteins.

Animals↗
PubMed2005

Expression profiles of inflammatory and immune-related genes in Atlantic salmon (Salmo salar L.) at early time post vaccination.

Vaccination of Atlantic salmon parr with oil-based vaccines will inevitably cause inflammation at the site of injection, albeit the underlying mechanisms are not very well understood or studied in any detail. Here, we report time-course changes in expression levels, assessed by real-time RT-PCR of IL-1 beta, Mx, two beta-2-microglobulin variants and MHC class II beta, from 2 to 19 days post vaccination with a multi-component oil-adjuvanted vaccine. Highly variable individual responses to vaccination make selection of high responders essential prior to subtractive analysis. Based on the above mentioned expression profiles, high-responding individuals at 2, 8 and 19 days post vaccination, were selected for subtractive analysis. Clustering of clones according to putative function, suggest an initial up-regulation of genes involved in metabolism and cell signalling, before onset of genes involved in inflammation. The lag-time for genes considered as inflammatory markers was more than 48 h, while they were found to constitute the major part of up-regulated transcripts by 8 days post vaccination. By day 19, immune-related genes like immunoglobulin and T cell-receptor genes, comprised a higher proportion of the up-regulated genes than at earlier time points.

Adjuvants, Immunologic↗
PubMed2005

Immunization with gp120-depleted whole killed HIV immunogen and a second-generation CpG DNA elicits strong HIV-specific responses in mice.

HIV-1 Immunogen is a gp120-depleted whole killed virus vaccine candidate formulated with Incomplete Freund's Adjuvant (HIV-IFA). We evaluated in a mouse model the immunogenicity of HIV-IFA by itself and when combined with HYB2055, an immunomodulatory oligonucleotide consisting of a novel DNA structure and synthetic CpR immunostimulatory motif, as an adjuvant. C57/BL6 mice were immunized with HIV-IFA alone or combined with HYB2055. Mice treated with HYB2055 or with PBS were used as controls. Compared to HIV-IFA alone, immunization with HIV-IFA and HYB2055 combination elicited strong production of HIV- and p24-specific IFNgamma, RANTES, MIP 1alpha, and MIP 1beta, as well as high titers of HIV- and p24-specific antibodies. Inclusion of HYB2055 also reduced levels of IL-5 produced by HIV-IFA alone. HYB2055 enhances the immunogenicity of HIV-IFA and shifts responses towards a type 1 cytokine profile. The immune enhancing effects of HYB2055 adjuvant were dose-dependent. These findings warrant clinical evaluation of the HIV-1 immunogen/HYB2055 candidate as a therapeutic vaccine for HIV-1 infected patients.

AIDS Vaccines↗
PubMed1983

Immunisation against East Coast fever: correlation between monoclonal antibody profiles of Theileria parva stocks and cross immunity in vivo.

Stocks of Theileria parva, which had been characterised by monoclonal antibody profiles, were used to challenge cattle previously immunised against East Coast fever (ECF). When cattle were subjected to homologous challenge, or heterologous challenge with a stock of identical profile to that which had initiated immunity, they showed mild or inapparent reactions. However, when cattle were challenged with a stock of a different profile many underwent severe or fatal ECF reactions. Thus, there appears to be good correlation between cross resistance patterns in vivo and parasite differences detected in vitro by monoclonal antibodies. The results indicate that monoclonal antibody profiles can be used to characterise strains of T parva in vitro, and thus provide valuable data for planning field immunisation programmes. Now that monoclonal antibodies offer the potential of characterising theilerial parasites so precisely, the need arises for more disciplined use of terms describing parasite populations and collections. It is proposed that the rules of nomenclature devised for trypanosomes be adopted for Theileria species.

Animals↗
PubMed2003

Tumour-induced polarization of tumour vaccine-draining lymph node T cells to a type 1 cytokine profile predicts inherent strong immunogenicity of the tumour and correlates with therapeutic efficacy in adoptive transfer studies.

Previously we have shown that vaccination with the poorly immunogenic B16BL6-D5 melanoma (D5) elicits a dominant type 2 (T2) cytokine response that fails to protect the host from a subsequent tumour challenge. Here we investigated whether the inherent immunogenicity of a tumour can be correlated with its ability to bias the anti-tumour cytokine response towards either a type 1 (T1) or a T2 profile. The immune response to six tumours of different inherent immunogenicity was assayed. By isolating l-selectinlow T cells from tumour vaccine draining lymph nodes (TVDLN), it was possible to detect tumour-specific cytokine responses from both immunogenic, poorly immunogenic and non-immunogenic tumours. Immunogenic tumours (MCA-304, MCA-309, MPR-4) induced a predominant tumour-specific T1 cytokine response. In contrast, weakly (MCA-310, MPR-3) and poorly/non-immunogenic tumours (MPR-5, D5) sensitized T cells with a predominant tumour-specific T2 cytokine response. A significant correlation (P < 0.025) between immunogenicity and the ratio of tumour-specific interferon-gamma : interleukin-4 (IL-4) secretion by TVDLN T cells was identified. We then documented that non-therapeutic T cells primed by the poorly immunogenic D5, recognized "tumour-rejection" antigens and that reprogramming their cytokine response, by in vitro culture with IL-12 and anti-IL-4, to a T1 profile uncovered therapeutic efficacy. In contrast, TVDLN T cells primed by a therapeutic vaccine lose therapeutic efficacy when cultured with IL-4. These results provide insights into the development of a protective anti-tumour immune response and strengthen the hypothesis that a T1 cytokine response is critical for T-cell-mediated tumour regression.

Animals↗
PubMedDate not supplied

[The clinico-metabolic characteristics of the course of a chlamydial infection in newborns].

A clinical and laboratory investigation was done in 68 full-term newborn babies, with clinical forms of Chlamydia infection having been identified. There have also been studied cellular and humoral links of immunity, hormonal profile, system of peroxidation, antioxidant defence. In Chlamydia infection in full-term newborns presenting with acute bronchopulmonary pathologies during the acute phase of the illness, signs are noted of activation of processes of free-radical lipid oxidation against the background of retardation of the antioxidant defense, with synthesis of hormones of the thyroidal, hypophyseal and adrenal systems being on the increase. Metabolic changes are directly related to immunologic responsiveness which is characterized by weakness of primary immune response. The degree the above changes make themselves known depend on the clinical form of Chlamydia-associated infection. The identified metabolic changes may be the basis of causative factors for change in capacity of newborn infants with chlamydial infection to adapt.

Acute Disease↗
PubMed2005

Bayesian coclustering of Anopheles gene expression time series: study of immune defense response to multiple experimental challenges.

We present a method for Bayesian model-based hierarchical coclustering of gene expression data and use it to study the temporal transcription responses of an Anopheles gambiae cell line upon challenge with multiple microbial elicitors. The method fits statistical regression models to the gene expression time series for each experiment and performs coclustering on the genes by optimizing a joint probability model, characterizing gene coregulation between multiple experiments. We compute the model using a two-stage Expectation-Maximization-type algorithm, first fixing the cross-experiment covariance structure and using efficient Bayesian hierarchical clustering to obtain a locally optimal clustering of the gene expression profiles and then, conditional on that clustering, carrying out Bayesian inference on the cross-experiment covariance using Markov chain Monte Carlo simulation to obtain an expectation. For the problem of model choice, we use a cross-validatory approach to decide between individual experiment modeling and varying levels of coclustering. Our method successfully generates tightly coregulated clusters of genes that are implicated in related processes and therefore can be used for analysis of global transcript responses to various stimuli and prediction of gene functions.

Algorithms↗
PubMedDate not supplied

[Variants of immune response in children with acute respiratory viral infections].

Four patterns of changes in the proliferative activity of T-lymphocytes in the lymphocyte blastogenesis test with phytohemagglutinin (PHA) are distinguished in children with acute respiratory viral infections (ARVI). The differences between these patterns are due to aggravated clinical severity of the infection process and enhancement of the cytokine reaction of macrophage monocytes. Comparison of immunological characteristics of response to ARVI in 4 groups of children showed that high reactivity of T-lymphocytes during the acute phase of disease (first and third variants) correlated with a relatively weak production of immunoglobulins and antiviral antibodies, while the suppression of T-lymphocyte response to PHA (second and fourth variants) is associated with expressed humoral profile of immune response by the level of immunoglobulin and antiviral antibody production. These data permit a hypothesis about the predominant generation of T x 1-like clones in children with the first and third variants of immune response and of T x 2-like clones in children with the second and fourth variants.

Adenovirus Infections, Human↗
PubMed2006

Transcriptional analysis of protective antigen-stimulated PBMC from non-human primates vaccinated with the anthrax vaccine absorbed.

The transcriptional responses in recombinant protective antigen (PA)-stimulated peripheral blood mononuclear cells (PBMCs) from Anthrax Vaccine Absorbed (AVA)-vaccinated rhesus macaques were evaluated using Affymetrix HGU133 Plus 2.0 GeneChips. PBMCs from animals vaccinated at 0, 4, and 26 weeks were harvested at week 30, stimulated with PA, and RNA isolated. The expression of 295 unigenes was significantly increased in PA-stimulated compared to non-stimulated PBMCs; no significant decrease in gene expression was observed. These upregulated transcripts encoded for proteins functioning in both innate and adaptive immunity. Results were corroborated for several genes by real-time RT-PCR. This study provides information on the potential underlying transcriptional mechanisms in the immune response to PA in AVA-vaccinated rhesus macaques.

Animals↗
PubMed2004

Effect of dietary ribonucleotides on infant immune status. Part 2: Immune cell development.

The objective of this study was to determine whether dietary ribonucleotides alter immune cell phenotypes or function in the first year of life. Newborn term infants in a double-blind, 12-mo, multicenter trial were randomized to cow milk formula groups with (FN, n = 138) or without (F, n = 147) 72 mg/L supplemental ribonucleotides. A nonrandomized HMF cohort (n = 192) was concurrently enrolled. Eighty-eight immune blood cell types were characterized by flow cytometry. Data were analyzed by multivariate ANOVA (MANOVA), ANOVA, and repeated measures analysis (RMA), with adjustments made for multiple comparisons. Ribonucleotide feeding changed subpopulations of T and natural killer (NK) cells. FN had higher numbers and percentages of memory/effector (M/E) cytotoxic/suppressor (CD45R0(+)CD8(+), RMA) T, Fas(+) M/E (CD45R0(+)CD95(+)CD3(+), 6 mo) T, and CD56(+)CD16(-) NK cells (CD56(+)CD16(-)CD3(-)CD8(-), 12 mo), and higher percentages of M/E helper (CD45R0(+)CD4(+), RMA) T, Tc1 (IFN gamma(+)CD4(-)CD3(+), RMA), total interferon (IFN)gamma T (IFN gamma(+)CD4(+/-)CD3(+), RMA), Th2 (IL-4(+)CD4(+)CD3(+), 7 mo), and CD57(+) NK-T cells (CD57(+)CD56(-)CD3(+), 6 mo, 7 mo) compared with F. Percentages of naive helper T (CD45RA(+)CD4(+), 12 mo) and numbers and percentages of CD56(+) NK-T cells (CD56(+)CD16(-)CD3(+)CD8(-), 2 mo, 6 mo) were lower in FN than F. Percentages of M/E cytotoxic/suppressor, Th2, and CD56(+)CD16(-) NK cells in FN were significantly higher than F but were not different from HMF, whereas F was significantly lower than HMF. Ribonucleotide supplementation of infant formula supported increased T-cell maturation and affected immunoregulatory NK cell subsets. These FN-associated immune cell profiles either did not differ from those infants fed HMF or tended to be more like those fed HMF than those fed F.

Analysis of Variance↗
PubMed1990

An immunologic and genetic study of asthma in workers in an aluminum smelter.

The cause or causes of asthma among employees in aluminum smelters is unknown. We attempted to ascertain whether such workers who developed asthma differed in respect to indices of immunological function and certain genetic markers. Data were collected from 33 asthmatic and 127 nonasthmatic potroom workers. Asthmatic workers had significantly lower mean serum levels of immunoglobulin (Ig)M; however, mean levels of IgG and IgA, median levels of IgE, the capacity for recall of delayed type hypersensitivity, levels of immune complexes, and frequency of antinuclear or other autoantibodies did not differ from values for nonasthmatic workers. Asthma was found to develop on a background of atopy in 21 workers (64%), whereas there were no features of atopy in 12 workers (36%). Cigarette smoking had independent effects on immunological function. In respect to genetic markers, there was a higher frequency among asthmatic workers of the alpha-1-anti-trypsin deficiency phenotype MS, but the frequency of blood groups, Gm allotypes, or human leucocyte antigen types was similar. The study established that the profile of immune function, or genetic markers tested, did not differ essentially for workers in an aluminum smelter who did or did not develop asthma; however, there was an indication of heterogeneity in causation, as judged by "atopy-related" and "non-atopy-related" groups in the asthma population.

Adult↗