Biomedical subjects

Calogero Caruso

Publications and source records attributed to Calogero Caruso.

62 records · Page 4Linked to original sources

PubMed2002

Measurement of inflammatory mediators of eosinophils and lymphocytes in blood in acute asthma: serum levels of ECP influence the bronchodilator response.

The aim of this study was to assess the relevance of immunoinflammatory markers on the response to short acting beta(2)-agonist in acute asthma exacerbation. Thus, we measured serum eosinophil cationic protein (ECP) levels and sIL-2R at acute exacerbation in 52 adult patients with atopic asthma, and assessed forced expiratory volume in 1 s (FEV(1)) before and after the administration of aerosolized salbutamol. After a cumulative dose of salbutamol causing a 10% improvement in FEV(1) from baseline [CD10, i.e. cumulative doses of salbutamol (800 microg) causing an improvement in FEV(1) from baseline to 10%] the patients were divided into two groups: group A with CD <10 and group B with CD >10. The bronchodilator response, as defined by a DeltaFEV(1) (percentage of predictive value of FEV(1)) of > or =10 predictive value, was shown by 40% of the patients. After 200, 400 and 800 microg of salbutamol, significant differences of FEV(1) with respect to baseline values were, respectively, p = 0.049, 0.0039 and 0.0014. In contrast, no significant difference of the means of FEV(1) between the doses of salbutamol was observed. Significant differences of DeltaFEV(1) between 200 and 400 microg (p = 0.0002) and between 200 and 800 microg (p < 0.0001) were observed, but not between 400 and 800 microg of salbutamol. There were significant correlations between baseline values of predictive FEV(1) and serum ECP levels (rho = -0.60, p < 0.0001) and sIL-2R levels (rho = -0.35, p = 0.01) respectively. Besides, a correlation between DeltaFEV(1) and serum ECP levels (rho = -0.53, p < 0.0001) was observed, whereas no correlation was found between DeltaFEV(1) and sIL-2R. By analyzing differences between the two groups (A and B) for serum ECP levels, sIL-2R and blood eosinophil count, a significant difference was found for serum ECP levels. We conclude that subjects with acute exacerbation of asthma show high serum levels of ECP and sIL-2R and, more interestingly, that the response to brochodilator was higher in patients with lower serum ECP levels.

Adolescent↗

PubMed2002

Prevalence of latex sensitization in health care workers of a general hospital in Palermo, Sicily.

STUDY OBJECTIVE: To assess the prevalence of latex sensitization in a group of hospital employees in a general hospital. DESIGN: Cross-sectional study on hypersensitivity to latex gloves among health-care workers. SETTING: A general hospital in Palermo, Sicily. PATIENTS: 196 health-care workers answered a questionnaire about their case history of allergic diseases (i. e., rhinitis and/or asthma) and about symptoms after wearing latex gloves. All subjects were tested by skin prick test (SPT) with commercial latex extract and aeroallergens and had blood draw for total serum IgE and latex-specific IgE testing and glove-use test. MAIN RESULTS: 42% of the subjects who answered the questionnaire reported at least one symptom after wearing latex gloves. All symptoms were local, and none of the subjects reported systemic reactions. The most common symptom was itching, but none of subjects with only itching presented a positive SPT or specific serum IgE to latex. The SPT to latex was positive in 19 of 196 subjects (9.7%). Specific IgE to latex were found in 15/196 subjects (7.6%). Glove-use test was positive in 14/196 (7.1%). CONCLUSIONS: The overall prevalence of latex sensitivity in health-care workers in our epidemiological setting is 7.1%. An accurate diagnosis must take in account the integration of in vivo and in vitro tests with previous history of allergic disease.

Adult↗

PubMedDate not supplied

Frequency of the HFE gene mutations in five Italian populations.

Genetic hemochromatosis is an autosomal recessive disorder characterized by iron overload and a variety of clinical manifestations such as liver cirrhosis and arthropathy. It is the most common genetic disease of northern European populations. The principal gene responsible for hereditary hemochromatosis, designated HFE, is located on chromosome 6 in the HLA region. The single point mutation 845A, changing cysteine at position 282 to tyrosine (C282Y), in this gene has been identified as the main genetic basis of hereditary hemochromatosis. Two other mutations, 187G, a histidine to aspartate at amino acid 63 (H63D), and 193T, a serine to cysteine at amino acid 65 (S65C), appear to be associated with milder forms of hereditary hemochromatosis. There is a high prevalence of the C282Y mutation in northern European populations, whereas in those of the Mediterranean basin the prevalence seems low and almost absent in Far East countries. This mutation seems usually to occur on the ancestral haplotype 7.1. Accordingly, a Celtic origin of this mutation has been suggested. The aim of this study was to determine the frequency of HFE gene mutations in five geographic regions in Italy. Samples were tested for C282Y, H63D, and S65C mutations of the HFE gene according to methods of each laboratory and the results were standardized with the exchange of typed samples between the different laboratories. In addition, C282Y-positive DNA samples were typed for D6S105 allele 8 and HLA-A3 by ARMS-PCR. We have found that the allele frequency of the C282Y mutation decreases from northeast Italy (Friuli, 6%) to northwest Italy (Piedmont, 4.8%) and to central Italy (Emilia-Romagna, 1.7%). However, this mutation is lacking in the two regions of the Mediterranean basin's center (Sicily and Sardinia). Accordingly, a significant difference in the frequency of the mutation was observed between these Italian regions (P = 0.07 x 10(-3)). In contrast, no difference was observed in allele frequency of H63D in the five Italian regions. Finally, as regards the S65C mutation a very low frequency was observed in Friuli, Emilia-Romagna, and Sardinia, whereas in Sicily and Piedmont we have not found this mutation. In conclusion, these data are consistent with the hypothesis that the C282Y mutation occurred in Caucasian populations of Celtic origin, whereas the H63D mutation is more ancient as demonstrated by the ubiquitous distribution.

Amino Acid Substitution↗

PubMedDate not supplied

Inflammation, genes and zinc in ageing and age-related diseases.

Lifelong antigenic burden determines a condition of chronic inflammation, with increased lymphocyte activation and pro-inflammatory cytokine production. A large number of studies have documented changes in Zn metabolism in experimental animal models of acute and chronic inflammation and in human chronic inflammatory diseases. In particular, modification of zinc plasma concentration as well as intracellular disturbance of antioxidant intracellular pathways have been found associated to age-related inflammatory diseases, like atherosclerosis. Zinc deficiency is extremely diffused in aged people that are educated to avoid meat and other high Zn-content foods due to fear of cholesterol. Rather, they increase consumption of refined wheat products that lack of Zn, magnesium and other critical nutrients in consequence of refining process. On the other hand, plasma concentration of metallic ions like Zn is influenced by pro-inflammatory cytokines production. A major target of Zn may be NF-kB, a transcription factor critical for the expression of many pro-inflammatory cytokines whose production is finely regulated by extra- and intracellular activating and inhibiting factors interacting with regulatory elements on cytokine genes. Moreover, this factor is regulated by the expression of specific cellular genes involved in inflammation. So it is not surprising that Zn deficiency is constantly observed in aged patients affected by infectious diseases. On the other hand, cytokine genes are highly polymorphic and some of these polymorphisms have been found associated to age-related diseases as atherosclerosis. Therefore, Zn deficiency in individuals genetically predisposed to a dis-regulation of inflammation response, may play a crucial role, in causing adverse events and in reducing the probability of a successful aging.

Aging↗

PubMedDate not supplied

Involvement of -308 TNF-alpha and 1267 Hsp70-2 polymorphisms and zinc status in the susceptibility of coronary artery disease (CAD) in old patients.

Coronary artery disease (CAD) is characterized by an inflammatory status and it represents the major cause of death in elderly. Zinc deficiency and inflammatory genes within major histocompatibility complex (MHC) region are implicated in ischaemic heart diseases. TNF-alpha is present in coronary artery plaques and may provoke plaque instability. Hsp70 plays instead a pro-atherogenic role, via proinflammatory cytokine production, in atherosclerotic lesions contributing to plaque rupture. Contradictory data report the association between -308 TNF-alpha polymorphism and CAD, while no investigations exist on Hsp70-2 gene in CAD. In the current study, we analysed -308 TNF-alpha and 1267 Hsp70-2 polymorphisms and zinc status in 190 healthy old controls and 216 old patients with carotid stenosis subdivided in two groups: the first one 105 patients with CAD (C group), and the second one 111 patients without cardiovascular events (D group). We found a lack of association between -308 TNF-alpha polymorphism and CAD. Conversely, 1267 Hsp70-2 polymorphism was associated with CAD. In particular, significant higher frequency of AB + BB genotypes (B + genotype) was observed in C patients than controls (71.4 vs.56.9%, P = 0.017, odds ratio = 1.898). However, when C patients were subdivided into four subgroups on the basis of presence/absence of 1267B Hsp70-2 and -308A TNF-alpha alleles, B + A + patients showed higher prothrombin activity as well as Hsp70-2, TNF-alpha, IL-6 gene expressions in carotid atheroma when compared to B - A - genotypes. The zinc status (plasma and Zn/Fe ratio in erythrocytes) is not affected by these polymorphisms. However, zinc deficiency is present in CAD condition. In conclusion, 1267 HSP70-2 polymorphism and zinc deficiency, rather than -308 TNF-alpha, are independently associated with CAD. B + A+ and B + A- carriers seem more predisposed to ischaemic events; conversely, B - A- genotype may be considered a protective marker against CAD.

Aged↗

PubMedDate not supplied

Gamma/delta T lymphocytes are affected in the elderly.

gammadelta T lymphocytes are considered to represent a link between the inflammatory response and adaptive immunity. In the present paper we investigated whether these cells play any role in the remodeling of the immune system described in the elderly. We show that the absolute number of gammadelta T cells in peripheral blood of old and very old subjects is reduced. Moreover, gammadelta T cells from old people and centenarians show enhanced levels of the early activation marker CD69 both after culture in medium alone and in LPS-stimulated cells. Furthermore, they show a basal increased production of tumor necrosis factor (TNF)-alpha as evaluated at the single cell level. Additionally, the response of these cells to IPP in "in vitro" cultures is in part impaired. These results suggest that the high level of basal activation of gammadelta T cells is due to the "inflamed" environment. However, the changes in number and function of gammadelta T lymphocytes might influence the resolution of inflammatory immune responses in the elderly.

Adult↗

PubMedDate not supplied

Allele frequencies of +874T-->A single nucleotide polymorphism at the first intron of interferon-gamma gene in a group of Italian centenarians.

Ageing is characterized by a pro-inflammatory status which could contribute to the onset of major age-related diseases such as cardiovascular diseases, neurodegeneration, osteoarthritis and osteoporosis, and diabetes. Thus, it can be hypothesized that genetic variations in pro- or anti-inflammatory cytokines might influence successful ageing and longevity. We have studied the distribution of +874T-->A interferon-gamma (IFN-gamma) polymorphisms in a large number of Italian centenarians to evaluate if the two alleles might be differently represented in people selected for longevity. DNA samples were obtained from 174 Italian centenarians (>99 years old, 142 women and 32 men) and from 248 <60-year-old control subjects (90 women and 158 men) matched for geographical distribution. Polymorphisms at +874 were identified by using amplification refractory mutational system methodology. The +874T allele was found less frequently in centenarian women than in centenarian men or in control women whereas no significant differences were observed in the distribution of the two alleles between male or female controls. Allele frequencies in centenarian men were not found significantly different from male controls. Possession of the +874A allele, known to be associated with low IFN-gamma production, significantly increases the possibility to achieve extended longevity, suggesting that the pro-inflammatory status characteristic of ageing may be detrimental for successful ageing. The datum that the allele was significantly increased in female but not male centenarians seems to strengthen the idea that gender may be a major variable in the biology of the ageing process. However, the present data add another piece of evidence to the complex puzzle of genetic and environmental factors involved in controlling life span expectancy in humans. Thus, studies on cytokine gene polymorphisms may promise to individuate a complex network of trans-interactive genes able to influence the type and strength of responses to environmental stressors and as a final result, thereby conditioning individual life expectancy.

Adult↗

PubMedDate not supplied

Association between HFE mutations and acute myocardial infarction: a study in patients from Northern and Southern Italy.

There is interest in the role of iron in age-related diseases such as atherosclerosis. Tissue iron deposition could be harmful, because Fe(2+) can react with H(2)O(2) to form OH(-) radicals and Fe(2+) can react with O(2) to form reactive oxygen species. Free radicals react with cell membranes and cell organelles and could lead to the development of atherosclerosis by initiating lipid peroxidation. Hereditary hemochromatosis provides an opportunity for studying the effects of iron on cardiovascular disease. Some studies have shown that individuals who carried HFE mutations may be at greater risk of developing coronary heart disease than those without the mutations. In contrast, a large number of studies have reported no association between HFE mutations and coronary heart disease. These studies have possible confounding factors, such as the homogeneity of the population in term of geographical origin among others. We studied the relation between HFE mutations and acute myocardial infarction in two case-control studies involving two sets of subjects representing different age groups from different geographic regions in Italy. The first one was composed of 172 older patients (139 males and 33 females; mean age 67) and 207 healthy controls (91 males and 116 females; mean age 46) from Emilia-Romagna. The second one was composed of younger 77 patients (75 males and 2 females; mean age 41) and 172 healthy controls (75 males and 97 females, mean age: 38) from Sicily. All patients were genotyped for ApoE alleles, since the ApoE- epsilon 4 allele is considered a risk factor for cardiovascular diseases and can interfere with other genetic and environmental factors by modifying susceptibility to this disease. DNA typing for C282Y and H63D HFE alleles was performed also. There were no significant differences in frequencies of the different HFE alleles between acute myocardial infarction patients and controls in cohorts of both old and young patients. Also taking into account the presence or absence of the ApoE- epsilon 4 allele, no significant differences in H63D allele frequencies were observed. Thus, our study, performed in two samples of genetically homogeneous patients and controls, does not support the suggestion that HFE mutations may be associated with acute myocardial infarction in susceptible individuals.

Adult↗