Biomedical subjects

Eduardo Arranz

Publications and source records attributed to Eduardo Arranz.

9 recordsLinked to original sources

PubMed2025

High-Dimensional Immunophenotyping of Post-COVID-19 and Post-Influenza Patients Reveals Persistent and Specific Immune Signatures After Acute Respiratory Infection.

Long-term consequences of SARS-CoV-2 infection are unknown since recovered individuals can experience symptoms and latent viral reactivation for months. Indeed, acute post-infection sequelae have also been observed in other respiratory viral infections, including influenza. To characterize post-COVID-19 and post-influenza induced alterations to the cellular immunome, peripheral blood mononuclear cells (PBMCs) were obtained from patients 3 months after recovery from COVID-19 (n = 93) or influenza (n = 25), and from pre-pandemic healthy controls (n = 25). PBMCs were characterized using a 40-plex mass cytometry panel. Principal component analysis (PCA), classification models, and K-means clustering were subsequently applied. PCA identified distinct immune profiles between cohorts, with both post-COVID and post-flu patients displaying an altered chemokine receptor expression compared to pre-pandemic healthy controls. These alterations were more prominent in post-COVID patients since they exhibited highly increased expression of chemokine receptors CXCR3 and CCR6 by various lymphoid populations, while post-influenza patients mainly showed a decrease in CCR4 expression by naïve T cells, monocytes, and conventional dendritic cells. Classification models using immunophenotyping data confirm the three groups, while K-means clustering revealed two subgroups among post-COVID patients, with younger patients showing more pronounced immune alterations in the chemokine receptor profile, independently of long COVID symptoms. In conclusion, post-COVID and post-influenza patients exhibit distinct and unique persistent immune alterations. Understanding these altered immune profiles can guide targeted therapies for post-COVID syndrome and highlight differences in immune recovery from various respiratory infections.

Humans↗

PubMed2006

[Cytokines in the pathogenesis of inflammatory bowel diseases].

Inflammatory bowel disease (IBD) is produced by an exaggerated response to bacterial flora within the intestinal mucous, in which both environmental and genetic factors are involved. T lymphocytes are involved during the genesis and maintenance of IBD, and their cytokine profile in Crohn's disease (mostly Th1 cytokines) is different from that in ulcerative colitis (mainly Th2 cytokines). After the inflammatory response has been established, the balance between proinflammatory and regulatory cytokines determines the degree of mucosal damage and the form of presentation. A deeper knowledge of the immunological mechanisms involved in IBD has opened new research lines aimed to the development of new therapies such as the neutralization of proinflammatory cytokines with antibodies and the administration of antiinflammatory cytokines, which are currently at different stages of research.

Animals↗

PubMed2005

Tachyphylaxis to beta2-agonists in Spanish asthmatic patients could be modulated by beta2-adrenoceptor gene polymorphisms.

BACKGROUND: The study of determinants of asthma is a subject of much interest currently, especially the pharmacogenetic aspects of asthma management. Genetic polymorphisms affecting amino-acids at positions 16 and 27 within beta(2)-adrenoceptor (beta(2)AR) gene have been implicated in the asthma phenotypes and influence on the variability observed in response to use of bronchodilator agents used in the treatment of asthma. Whether these polymorphisms alter the bronchoprotection response to beta(2)-agonist treatment in Spanish asthmatic population is unknown. The aim of this study was to investigate whether genetic polymorphisms within beta(2)AR gene modulate the clinical outcomes of the individual response to beta(2)-agonist therapy and the development of desensitization in Spanish asthmatic patients. METHODS: In a prospective, case-control study were included 80 asthmatic patients. Based on the standard criteria, patients were classified into two groups: patients with tachyphylaxis and good responders to beta(2)-agonist therapy. DNA samples were genotyped for the Arg(16)Gly and Glu(27)Gln alleles within the beta(2)AR gene as well as in 64 control samples from blood donors. RESULTS: Arg(16) allele was slightly more frequent within the group with tachyphylaxis (P=0.039), whereas Gly(16) allele carriers were overrepresented within the group of good responders (59.7%, P=0.028). On the other hand, the allele frequency of Gln(27) and the proportion of Gln(27) carriers was higher within the group with tachyphylaxis (P=0.010 and 0.049, respectively) and Glu(27) allele carriers were overrepresented within the group of good responders (P=0.026). The Arg(16) and Gln(27) alleles were in strong linkage disequilibrium across this locus, resulting in the occurrence of disease haplotype. CONCLUSIONS: The predisposition to develop tachyphylaxis in our population seems to be linked to the Arg(16) and Gln(27) alleles and to the Arg(16)/Gln(27) risk haplotype (positive association between the presence of the Arg(16) and Gln(27) alleles and tachyphylaxis). The Arg(16) allele is perhaps overrepresented due to the strong linkage disequilibrium between both polymorphisms. The presence of the Glu(27) allele seems to be a protective factor against tachyphylaxis in this cohort study.

Adolescent↗

PubMed2005

[Cytokines in the pathogeny of celiac disease].

Celiac disease is manifested by an enteropathy caused by intolerance to gluten, a family of proteins found in wheat and other cereals. Following intestinal T-cell activation in predisposed individuals, different inflammatory mechanisms are triggered under the control of the cytokine balance including those with a pro-inflammatory Th1 pattern such as IFNgamma, TNFalpha, IL-15 and IL-18; and regulatory cytokines such as TGFbeta and IL-10. These cytokines, besides increasing the intensity of the activation and the number of immune cells within the intestinal mucosa, regulate the activity of epithelial growth factors and metalloproteinases, a group of molecules involved in the maintenance and turnover of the intestinal mucosa structure; in inflammatory conditions, they also induce the intestinal lesion responsible for malabsorption syndrome.

Celiac Disease↗

PubMed2005

[Celiac disease. New therapeutic alternatives based on a better knowledge of molecular pathogenesis].

Coeliac disease is a chronic autoimmune-like gastrointestinal disorder triggered by a known exogenous antigen (gluten). The disease is strongly linked to the HLA system, though other genetic, environmental and immunologic factors, may determine the type and timing of presentation. The immune response within the intestinal mucosa is characterized by a well defined TH1 response, where IFNgamma secreted by specific T cells is the predominant cytokine, as well as an innate immune response to certain gluten-derived peptides, mediated by IL-15. The strict gluten-exclusion diet is the best way of reversing both the symptoms and the histological changes in the intestinal mucosa. However, the frequency of transgressions and a low dietary compliance had led to the description of new therapeutic alternatives discussed in this review.

Celiac Disease↗

PubMed2004

Celiac disease diagnosis in patients with giardiasis: high value of antitransglutaminase antibodies.

OBJECTIVES: The main objective of this study is to assess the presence of celiac disease (CD) in patients with giardiasis and to evaluate the tools for diagnosis of CD in these patients. METHODS: A total of 40 patients with giardiasis were evaluated. Celiac disease was confirmed or discarded by intestinal biopsy and serological markers. Antigliadin antibodies were determined by ELISA and antitransglutaminase antibodies by one-step immunochromatographic assay and ELISA. RESULTS: Out of the 40 patients with giardiasis 37 showed normal intestinal mucosa. In this group, IgA antibodies to gliadin were positive in 7 patients, yielding a specificity of 82%. All of them were negative for transglutaminase antibodies by the immunochromatographic assay and by ELISA (specificity of 100%). The remaining 3 patients showed a subtotal intestinal villous atrophy consistent with CD, however, only two presented IgA antibodies to transglutaminase and gliadin. CONCLUSIONS: Due to its low specificity antigliadin antibodies are not useful for the screening of CD in patients with giardiasis. On the other hand, antitransglutaminase antibodies are highly specific and sensitive. One-step immunochromatographic assay is an easy and economic alternative. The findings of villous atrophy must be supported by other markers of CD to achieve the diagnosis of CD in these patients.

Adolescent↗

PubMed2003

Serum procalcitonin in children with suspected sepsis: a comparison with C-reactive protein and neutrophil count.

OBJECTIVES: To investigate the specific characteristics of serum procalcitonin in children with severe infection, to identify relevant factors influencing procalcitonin increase, to assess its prognostic value, and to compare it with C-reactive protein and neutrophil count DESIGN: A prospective observational study and 48 hrs of follow-up of a cohort of cases. SETTING: A pediatric intensive care unit within a children's university hospital in collaboration with a laboratory mainly involved in research in pediatric clinical immunology. PATIENTS: A total of 80 children (median age, 3.1 yrs; range, 1 month to 16 yrs) admitted to a pediatric intensive care unit by suspicion of sepsis. INTERVENTIONS: All patients were treated according to a protocol using antibiotics, fluid resuscitation, inotropic drugs, and mechanical ventilation when they presented with shock or respiratory failure. MEASUREMENTS AND MAIN RESULTS: Serum procalcitonin and C-reactive protein were measured at admission in all patients and, when possible, repeated 6,12, 24, and 48 hrs later. In most cases, serum procalcitonin was already very high at onset (range, 1.0-722 ng/mL), and it did not increase significantly afterward. Contrary to C-reactive protein, serum procalcitonin did not vary according to the age of patients. The increase of procalcitonin was higher in patients with shock or multiple organ dysfunction syndrome, having a high severity score (Pediatric Risk of Mortality) or in patients who later died. CONCLUSIONS: Serum procalcitonin levels show a rapid increase in children with sepsis, even in infants < 12 month old, and they have a better prognostic value than C-reactive protein or neutrophil count.

Adolescent↗

PubMed2002

TNF alpha and LT alpha gene polymorphisms as additional markers of celiac disease susceptibility in a DQ2-positive population.

TNFalpha and TNFbeta, or linfotoxin (LTalpha), are two molecules playing an important role in inflammation. Their genes map on Chromosome 6, between the HLA class II and class I loci. Polymorphisms in, or near, TNF genes have been associated with susceptibility to several autoimmune diseases. Studies of TNF genes in celiac disease (CD) have presented contradictory results. We have assessed the role of TNFalpha and linfotoxin alpha (TNFbeta) in CD and their relative value as CD markers in addition to the presence of DQ2. The TNFA -308 polymorphism and the polymorphism at the first intron of the LTA gene were typed in CD patients and healthy controls and the results were correlated with the presence of DQ2. Significant differences were found in genotype and allele frequencies for the TNFA and LTA genes between CD patients and controls, with an increase in the presence of the TNFA*2 and LTA*1 alleles in CD patients. These differences increase when DQ2-positive CD patients and DQ2-positive controls are compared. In DQ2-positive individuals, allele 2 (A) in position -308 of the promoter of TNFA and allele 1 (G) of the NcoI RFLP in the first intron of LTA are additional risk markers for CD.

Celiac Disease↗

PubMed2002

One-step immunochromatographic assay for screening of coeliac disease.

Tissue transglutaminase is the autoantigen that elicits endomysial antibodies, which are the serological hallmarks of coeliac disease. We describe a simple, rapid immunochromatographic assay for IgA and IgG antibodies to transglutaminase, which is highly accurate for diagnosis of this disease. Results were positive for all samples from 50 untreated coeliac patients, and negative for 40 non-coeliac patients with gastrointestinal disorders. The assay seems to be a useful alternative to biopsy for mass screening for coeliac disease.

Antibodies, Monoclonal↗