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At least 289 records · Page 16Linked to original sources
PubMed1998

Comparative study of transfer factor and acyclovir in the treatment of herpes zoster.

Reactivation of varicella herpes virus (VHV), latent in individuals who have previously suffered varicella, gives rise to herpes zoster and in some cases leads to a sequela of post herpetic neuritis with severe pain which is refractory to analgesics. Many different antiviral agents have been tried without achieving satisfactory results. Of all the antiviral agents employed, acyclovir has been the most successful in reducing post herpetic pain. However acyclovir has not been as reliable as interferon alpha (IFN-alpha). We have previously looked into the use of transfer factor (TF) as a modulator of the immune system, specifically with respect to its effectiveness in the treatment of herpes zoster. In this work findings from a comparative clinical evaluation are presented. A double blind clinical trial of TF vs acyclovir was carried out in which 28 patients, presenting acute stage herpes zoster, were randomly assigned to either treatment group. Treatment was administered for seven days and the patients were subsequently submitted to daily clinical observation for an additional 14 days. An analogue visual scale was implemented in order to record pain and thereby served as the clinical parameter for scoring results. The group treated with TF was found to have a more favorable clinical course, P < or = 0.015. Laboratory tests to assess the immune profile of the patients were performed two days prior and 14 days after initial treatment. The results of these tests showed an increase in IFN-gamma levels, augmentation in the CD4+ cell population but not the percentage of T rosettes in the TF treated group. These parameters were however insignificantly modified in patients receiving acyclovir. Although TF treated patients showed an increase in CD4+ counts these cells remained below the levels for healthy individuals. The fact that IFN-gamma levels as well as the counts for CD4+ cells rose in the TF treated group and not in the acyclovir one is very significant and confirms the immunomodulating properties of TF.

Acyclovir↗
PubMed2003

Peripheral cytokine release in Alzheimer patients: correlation with disease severity.

Various studies suggested that inflammation is involved in the pathogenesis of Alzheimer's disease (AD). We investigated cytokine release from LPS-stimulated blood cells of 32 AD patients, with different disease severity, compared to 16 age-related controls. A significant decrease of IL-1beta and IL-6 secretion was observed in severely demented patients; TNF-alpha release was also decreased, but not significantly. By contrast, mild and moderate patients showed a cytokine release similar to controls. IL-1beta, IL-6 and TNF-alpha secretion was negatively correlated with the severity of dementia, quantified by the MMSE. Our data suggest that alterations of the immune profile are associated with AD progression.

Aged↗
PubMed1999

Analysis of post-transplant immune status in recipients of liver/bone marrow allografts.

The aims of this study were to assess the effect of donor bone marrow infusion on the reactivity of recipient peripheral blood lymphocytes (PBL) to mitogen and to donor and third-party cells after primary liver allotransplantation and to identify any correlation between altered immunoreactivity and HLA mismatches, occurrence of rejection, and immunosuppression. The immunoreactivity of recipient PBL toward frozen donor splenocytes was evaluated in mixed lymphocyte culture (MLC) (n = 29) and cell-mediated lympholysis (CML) (n = 27) assays in time intervals ranging from 0.7 to 27 months after transplant. Overall, the mean anti-donor MLC stimulation index (SI) fell from 25.6 +/- 5.2 preoperatively to 4.8 +/- 1.7 after transplantation (p < 0.002), with 14 out of 29 (48.3%) patients developing donor-specific MLC hyporeactivity. HLA class II mismatches were significantly associated with recipient post-transplant immune profile (p < 0.05): MLC donor specific hyporesponsiveness was observed in 70%, versus 37% of patients who shared a class II antigen, versus those that did not. Of the control group, 61.1% developed donor-specific nonreactivity versus 27.2% in the donor bone marrow cells (DBMC) group (p = 0.02). Donor-specific CML hyporeactivity was observed after transplantation, independent of DBMC infusion, with mean percentage values of pre- and post-transplant donor-specific lysis of 22.4% +/- 4.1% versus 3.1% +/- 1.6%, p = 0.0004, respectively. Our results suggest that DBMC infusion favors development of nonspecific MLC hyporesponsiveness to donor and third-party alloantigen, with maintenance of reactivity to mitogen and no additional effect on T-cell cytotoxicity.

Bone Marrow Cells↗
PubMed2003

Evaluation of novel aerosol formulations designed for mucosal vaccination against influenza virus.

Influenza viruses are among the most significant human pathogens, responsible for increased seasonal morbidity and mortality particularly in immunodepressed and chronically ill. Conventional vaccination with non-replicative vaccine is currently performed by injection. In the present study, we explore simple spray-dried lipid formulations containing whole inactivated virus or split-subunit vaccine that allow aerosolization and thus, mucosal vaccination of the pulmonary tract. We show that by using biocompatible excipients already approved for human use, one could engineer microparticles that induce substantial local and systemic immunity subsequent to pulmonary administration. Exposure of the bronchial-associated lymphoid tissue (BALT) to vaccine was more effective than parenteral or nasal administration in triggering specific immunity. Co-formulation of a biocompatible surfactant detergent greatly ameliorated the immune profile of microparticles containing a whole inactivated virus vaccine. In addition, mere formulation of a licensed split-subunit vaccine significantly enhanced its immunogenicity. Together, our data underline a simple strategy to convert conventional parenteral vaccination of currently available non-replicative vaccines against influenza virus, into one that is more effective and practical upon respiratory administration.

Aerosols↗
PubMed1998

Safety and tolerance of Lactobacillus reuteri supplementation to a population infected with the human immunodeficiency virus.

Probiotic supplementation may provide health benefits, especially for individuals with an underlying disease state that makes them more susceptible to infections. The purpose of this experiment was to evaluate the safety and tolerance of Lactobacillus reuteri ingestion by subjects infected with the human immunodeficiency virus (HIV). Thirty-nine subjects consumed a freeze-dried preparation of L. reuteri or a placebo for 21 days in a double-masked, parallel design experiment. Serum chemistry, haematology, immune profile, urinalysis, physical examination, gastrointestinal tolerance and faecal microbiota data were collected. No clinically significant changes were noted in any of the safety parameters measured. Overall, tolerance was good in both groups. Consumption of L. reuteri tended to increase faecal levels of L. reuteri on days 7, 14 and 21 of treatment feeding (P < 0.06, P < 0.11 and P = 0.05, respectively). However, faecal levels of L. reuteri and total Lactobacillus species were lower than levels previously observed in healthy male adults. Overall, this study documents that L. reuteri may be fed to HIV-positive individuals at 1 x 10(10) colony forming units/day without any clinically significant safety or tolerance problems.

Adult↗
PubMedDate not supplied

IgG subclasses serum concentrations in a population of children with Down syndrome: comparative study with siblings and general population.

Serum total IgG and subclasses were determined in three different groups of children: with Down syndrome, their siblings and general pediatric population. Several cases of IgG2 and IgG4 deficiency were identified, predominantly in children with Down syndrome. The differences, considering three age groups, were statistically significant for both groups in relation to the general population group, with an increase of IgG1 and IgG3 and a decrease in serum concentrations of IgG2 and IgG4. Down syndrome children and their siblings tend o have a similar variation of the IgG4 serum concentration levels (P < 0.05). The mechanisms of this concordance are not well understood. The results point out that an adequate strategy to improve the immune status of Down syndrome children could have a positive manifestation in the immune profile of their brothers.

Adolescent↗
PubMed1997

Home parenteral lipids in AIDS: a three-month study.

Parenteral nutrition is a part of the nutritional support regimen of patients with AIDS-associated wasting syndrome and gastrointestinal dysfunction. The cholesterol (CHOL) level in human immunodeficiency virus (HIV) membrane is very high, and recent lipid formulations with high phospholipid (PL) content have demonstrated the ability to trap CHOL from endogenous sources, modifying the composition of cell membranes. We administered lipid-based home parenteral nutrition for 3 mo to malnourished AIDS patients. The patients were randomly divided into two groups: 23 received the regular 20% fat emulsion formulation, and 27 received a 2% formulation enriched 10-fold with PLs but containing the same amount of triglycerides. All patients gained weight and improved their activity level. Those receiving the high-PL composition showed increased serum CHOL concentrations (from 147 to 241 mg/dL; P < 0.01), but no increase was seen in the number of CD4 cells or improvement in immune function. HIV infectivity was not modified. Patients receiving regular PLs had significantly decreased (P < 0.02) IgA concentrations (from 776 to 300 mg/dL) and improved mitogen response to phytohemagglutinin and to concanavalin A. This formula, too, had no effect on HIV infectivity. We conclude that standard parenteral nutritional influences the nutritional and immune status of malnourished AIDS patients. A PL-enriched parenteral formulation can trap CHOL, but it does not affect the immune profile or HIV infectivity in patients with advanced disease.

Acquired Immunodeficiency Syndrome↗
PubMed1999

A time course study for the development of an immunocompromised wound model, using hydrocortisone.

Although wound healing is essentially a physiologic process, some chronic wounds exhibit considerable delay in healing. Often these do not heal perfectly in individuals with low immune profiles. Thus, the present study was undertaken to develop an excision wound model in the immunocompromised state induced by pretreatment with hydrocortisone (HC) 40 mg/kg intramuscularly in male rats. Wounds of 8-mm diameter were made on the preshaved dorsal surface of rats using an Acuderm biopsy punch, following pretreatment with HC. After 14 days HC-treated animals exhibited atrophy of spleen and adrenal glands and a significant reduction of circulating lymphocytes and increase in neutrophils; these changes are indicative of immunosuppressive state of animals. The cell proliferation was significantly affected as shown by decreases in DNA (23%) and protein (11%). Furthermore, there were also significant reductions in tensile strength (37%) and hydroxyproline (33%) contents. These results were further supported by lack of contraction of wound edges. It is concluded that animals primed with HC 1 week prior to wounding developed prolonged immunosuppression, which significantly impaired the wound healing as compared with other groups. Thus, this can be experimentally employed as an immunocompromised wound model for evaluating compounds as novel wound healers suitable for immunocompromised subjects.

Adrenal Glands↗
PubMed2025

Immune dysfunction in Alzheimer disease.

Emerging evidence highlights the crucial role of peripheral immune cells in maintaining brain homeostasis and their influence on the pathology of Alzheimer disease (AD). Genome-wide association studies have identified numerous AD risk variants in genes expressed by immune cells, implicating innate and adaptive immune pathways in disease progression. Advances in neuroimmunology have revealed that immune cell crosstalk involving T cells, B cells, monocytes&#xa0;and/or&#xa0;macrophages and neutrophils can modulate the hallmark features of AD, including amyloid plaque accumulation, tau pathology and chronic neuroinflammation. Mechanistic insights suggest that chronic peripheral inflammation, immune exhaustion, metabolic dysfunction and epigenetic reprogramming exacerbate neurodegeneration in AD by promoting toxic inflammation and impairing protein clearance in the brain. These findings may catalyse the development of novel immunomodulatory strategies, such as immune checkpoint inhibition and cytokine targeting, among others, for AD. This Review examines peripheral immune alterations in AD, evaluates related therapeutic opportunities and highlights key knowledge gaps, particularly the need for human-derived data to advance translational progress. Future research should prioritize personalized approaches that integrate genetic risk, immune profiling and ageing to inform next-generation therapies for AD.

Humans↗
PubMed2003

Genetic interactions between susceptibility loci reveal epistatic pathogenic networks in murine lupus.

Interactions between Sle1 and other susceptibility loci were required for disease development in the NZM2410 model of lupus. Sle1 corresponds to at least three subloci, Sle1a, Sle1b, and Sle1c, each of which independently causes loss of tolerance to chromatin, but displays a distinctive immune profile. We have used congenic strains to analyze the interactions between the Sle1 subloci and other lupus susceptibility loci using Y autoimmunity accelerator (Yaa) and Faslpr as sensitizing mutations. Sle1 coexpressed with either one of these single susceptibility alleles resulted in a highly penetrant nephritis, splenomegaly, production of nephrophilic antibodies, and increased expression of B- and T-cell activation markers. Here, we show that only Sle1b interacted with Yaa to produce these phenotypes, suggesting that Sle1b and Yaa belong to the same functional pathway. Interactions between the three Sle1 loci and lpr resulted in lymphocyte activation and lupus nephritis, but a significant mortality was observed only for the Sle1a.lpr combination. This suggests a major role for the FAS pathway in keeping in check the loss of tolerance mediated by the Sle1 loci, especially for Sle1a. Our results illustrate the complexity of interactions between susceptibility loci in polygenic diseases such as lupus and may explain the clinical heterogeneity of the disease.

Alleles↗
PubMed1999

High mitotic index associated with poor prognosis in gastrointestinal autonomic nerve tumour.

AIMS: Three gastrointestinal autonomic nerve tumours (GANT) were characterized by immunohistochemistry and flow cytometry. Two of the three cases occurred in the small intestine, while the third was found in the stomach. Besides the immunohistochemical and ultrastructural description, the aim of this study was to examine the relation between the known and accepted predictive factors (ploidy data, the S-phase fraction, the mitotic and MIB-1 index and the size of the tumour) and the survival of the patients. METHODS AND RESULTS: The immune profile showed that 3/3 cases were vimentin and NSE, 2/3 were synaptophysin and PGP 9.5 positive, while 1/3 also showed S100 positivity. Ultrastructurally, all the cases had dense core granules, one of them contained skenoid fibres. The flow cytometry revealed diploid DNA in all cases, however, significant differences could be seen in the proliferative activity of the individual neoplasms. CONCLUSIONS: In spite of the published data of gastrointestinal stromal tumours (GIST) generally, neither the MIB-1 index and the ploidy data nor the size of the primary tumour helped to predict the clinical progression of the examined GANTs. However, the high proliferative activity (57 mitoses/10 HPF) and the elevated S-phase fraction (24%) was associated with advanced, metastatic and recurring disease in case 3. On the basis of these three cases, high mitotic activity is the most reliable factor in predicting aggressive clinical behaviour.

Adult↗
PubMed2001

Are poor responses to praziquantel for the treatment of Schistosoma mansoni infections in Senegal due to resistance? An overview of the evidence.

This paper summarizes and concludes in-depth field investigations on suspected resistance of Schistosoma mansoni to praziquantel in northern Senegal. Praziquantel at 40 mg/kg usually cures 70-90% of S. mansoni infections. In an initial trial in an epidemic S. mansoni focus in northern Senegal, only 18% of the cases became parasitologically negative 12 weeks after treatment, although the reduction in mean egg counts was within normal ranges (86%). Among other hypotheses to explain the observed low cure rate in this focus, the possibility of drug resistance or tolerance had to be considered. Subsequent field trials with a shorter follow-up period (6-8 weeks) yielded cure rates of 31-36%. Increasing the dose to 2 x 30 mg/kg did not significantly improve cure rates, whereas treatment with oxamniquine at 20 mg/kg resulted in a normal cure rate of 79%. The efficacy of praziquantel in this focus could be related to age and pre-treatment intensity but not to other host factors, including immune profiles and water contact patterns. Treatment with praziquantel of individuals from the area residing temporarily in an urban region with no transmission, and re-treatment after 3 weeks of non-cured individuals within the area resulted in normal cure rates (78-88%). The application of an epidemiological model taking into account the relation between egg counts and actual worm numbers indicated that the low cure rates in this Senegalese focus could be explained by assuming a 90% worm reduction after treatment with praziquantel; in average endemic situations, such a drug efficacy would result in normal cure rates. Laboratory studies by others on the presence or absence of praziquantel resistance in Senegalese schistosome strains have so far been inconclusive. We conclude that there is no convincing evidence for praziquantel-resistant S. mansoni in Senegal, and that the low cure rates can be attributed to high initial worm loads and intense transmission in this area.

Animals↗
PubMed1999

Phenotyping analysis of peripheral blood leukocytes in patients with multiple sclerosis.

Multiple sclerosis (MS) is a central nervous disease thought to be elicited by an autoimmune process. Many studies in recent years have concentrated on finding the alterations in the peripheral blood immune profile in MS patients that would reflect disease activity. In the present study, we investigated surface antigen expression on lymphocytes and granulocytes from MS patients and control subjects. We have studied 29 patients suffering from relapsing-remitting or relapsing-progressive forms of MS. The disease was diagnosed in all patients at least 12 months before inclusion into the study. All patients had no attack at the study entry date or within a previous month. The control group included 29 age-matched subjects. Phenotyping of peripheral blood leukocytes was carried out with different fluorescence-conjugated murine monoclonal antibodies. The analysis was performed with three-color flow cytometry. The following antigens were determined [cluster of definition (CD)]: leukocyte common antigen (LCA) (B220, T 200, Ly-5), CD45; LPS-R (lipopolysaccharide receptor), CD14; found on all T cells, CD3; LFA-2 (lymphocyte function associated antigen, T 11), CD2; coreceptor for MHC class II molecules, found on helper T cells, CD4; coreceptor for MHC class I molecules, found on suppressor/cytotoxic T cells, CD8; B4, found on all human B cells, CD19; NCAM (neural cell adhesion molecule), CD56; integrin beta2 subunit, associated with CD11a (CD11a/CD18, LFA-1, alphaLbeta2) and CD11b (CD11b/CD18, Mac-1,CR3, alphaMbeta2), CD18; alphaL, alpha subunit of integrin LFA-1 (alphaLbeta2, CD11a/CD18), CD11a; alphaM, alpha subunit of integrin Mac-1 (CR3, alphaMbeta2, CD11b/CD18), CD11b; ICAM-1 (intercellular adhesion molecule), CD54; H-CAM, Hermes antigen, Pgp-1, CD44; AIM (activation inducer molecule), early activation antigen, CD69; T-cell receptor gammadelta, TCR gammadelta. In the MS group, we have found a significant increased expression of CD54 and CD44 antigens on lymphocytes, and higher percentage CD54(+) and CD11a+CD54(+) lymphocytes out of all lymphocytes compared with the control group. We have also found a significant increased expression of CD11a, CD18 and CD54 antigens on granulocytes, and higher percentage CD11b+CD18(+) granulocytes out of all granulocytes in MS patients compared with control. Higher levels of expression of the adhesion molecules may reflect the activation state of leukocytes in MS patients.

Adult↗
PubMed2002

Siblings and the risk of inflammatory bowel disease.

BACKGROUND: Environmental exposures in early life have been implicated in the aetiology of inflammatory bowel disease (IBD). Siblings are used as proxy markers to characterize patterns of exposure relevant to the risk of IBD. METHODS: Some 15,823 patients with ulcerative colitis and 12,668 with Crohn disease from the Swedish In-patient Register were compared with 79,546 and 63,035 controls, respectively, in a case-control study. Multiple logistic regression was used to investigate associations with older and younger siblings, and adjustment was made for sex, year of birth, mother's age, region and, additionally, father's social class. RESULTS: Older siblings are associated with a graded increased risk for ulcerative colitis (P for trend <0.001) and an adjusted odds ratio of 1.15 (95% CI 1.07-1.24) for three or more older siblings. Younger siblings are associated with a graded decreased risk for Crohn disease (P for trend <0.001) with an adjusted odds ratio of 0.83 (0.76-0.90) for three or more younger siblings. The greatest protective association with Crohn disease was seen for younger siblings born within 2 years of the subject. Older maternal age is independently associated with a decreased risk of Crohn disease, with P for trend <0.001. Additional adjustment for social class did not substantially alter the results. CONCLUSIONS: Having siblings is associated with the risk and phenotype of developing IBD, possibly through their influence on patterns of antigenic exposure in early life. The association of maternal age with Crohn disease may reflect age-related changes in maternal immune profile.

Adult↗
PubMedDate not supplied

Determinants of vessel targeting in vasculitis.

Studies of autoimmune diseases have not yet elucidated why certain organs or vessels become the objects of injury while others are spared. This paper will explore the hypothesis that important differences exist in regions of the aorta that determine vulnerability to diseases, such as atherosclerosis, aortitis, giant cell arteritis and Takayasu's disease. The reader is invited to reassess; (1) whether the aorta is indeed a single homogeneous structure, and (2) whether the initial stage of aortitis (and indeed other diseases considered "autoimmune") may be primarily due to acquired alterations of substrate, that influence unique immune profiles, which by themselves may not be pathogenic. Disease susceptibility and patterns are influenced by many factors that are inborn and acquired. Examples include genetic background, gender, ethnicity, aging, prior and concomitant illnesses, habits, diet, toxin and environmental exposures. Studies of vascular diseases must assess how such variables may affect regional differences in endothelial cells, subendothelial matrix, vascular smooth muscle and the response of each to a variety of stimuli.

Aging↗
PubMed2003

Bartonella quintana bacteremia and overproduction of interleukin-10: model of bacterial persistence in homeless people.

Chronic asymptomatic bacteremia caused by Bartonella quintana occurs in homeless people, but its pathophysiology is unknown. We investigated homeless people with bacteremia to determine whether the persistence of B. quintana is associated with a specific immune profile. Homeless people without B. quintana infection exhibited an inflammatory profile--levels of circulating markers of leukocyte activation (soluble interleukin [IL]-2 receptor and neopterin) and cytokines released by mononuclear cells (tumor necrosis factor, IL-1beta, IL-6, and IL-10) were significantly higher than levels in healthy control subjects. In contrast, homeless people with B. quintana bacteremia exhibited specific increases in IL-10 secretion by mononuclear cells. This overproduction of IL-10 was associated with an attenuated inflammatory profile. The depressed inflammatory response was specific of bacteremia, because patients with specific antibodies and without bacteremia had responses similar to those of homeless people. The overproduction of IL-10 and attenuated inflammatory response may account for the persistence of B. quintana in homeless people.

Adult↗
PubMed2004

Interferon-alpha-associated sarcoidosis responsive to infliximab therapy.

Sarcoidosis, a multisystem disease characterized by noncaseating granulomas, has been reported to be associated with interferon alpha (IFN-alpha) therapy for hepatitis C infection. INF-alpha is known to stimulate T helper cells with a Th1 profile immune response, which is the key immunologic event of a sarcoid granuloma formation. We report a patient treated with IFN-alpha who developed hypercalcemia and renal insufficiency as presenting clinical manifestation of sarcoidosis. Prednisone therapy was effective in controlling hypercalcemia but had to be discontinued due to an increase in hepatitis C viral RNA count. Infliximab, a chimeric monoclonal antibody directed against tumor necrosis factor alpha was used as therapy in our patient for its known potent anti-inflammatory effects. The patient received three doses of infliximab (5 mg/kg) and achieved a rapid decline in serum calcium to normal levels in 7 days; the serum calcium level has remained normal 3 months after the last infusion.

Antibodies, Monoclonal↗
PubMed1995

Prospective clinical trial of high-purity factor VIII preparations in haemophiliacs.

An assessment of the immune status of both HIV-positive and HIV-negative haemophiliacs showed hypo-responsive and anergic patients in both groups. In HIV-positive patients, the immune suppression, in addition to HIV itself, may be caused by other viral infections such as all types of hepatitis as well as by factor VIII concentrates. The introduction of new technologies for preparing factor VIII concentrates led to the question of whether higher purity is associated with a protective effect on the immune system, which might improve the clinical course of HIV-positive patients. Factor VIII from two manufacturing processes was investigated, one prepared using an ion-exchange S/D step, and the other utilizing a monoclonal antibody step. It is concluded that changing the product, from the monoclonal antibody to the ion-exchange and vice versa in the HIV-negative patients does not cause a change in the immune profiles.

Chromatography, Ion Exchange↗