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Med Pregl. 2002 Nov-Dec;55(11-12):532-4.
[Case report: celiac disease]

[Article in Serbo-Croatian (Roman)]

Bojkovic G, Caparevic Z, Ilic V, Stojanovic D, Lalosevic D, Stojanovic M.

KBC Dr Dragisa Misovic-Dedinje, 11000 Beograd, Heroja Milana Tepica 1.

INTRODUCTION: Celiac disease (nontropical sprue, gluten-sensitive enteropathy, chronic intestinal malabsorption disorder) is caused by gluten intolerance. This hereditary disorder is caused by sensitivity to gliadin. Because the body's own immune system causes the damage, celiac disease is considered to be an autoimmune disorder. However, it is also classified as a disease of malabsorption because nutrients are not absorbed. When people with celiac disease eat foods containing gluten, their immune system responds by damaging the small intestine. Specifically, tiny finger-like protrusions, called villi, on the lining of the small intestine are lost. The diagnosis is suspected on the basis of symptoms and signs, enhanced by laboratory and x-ray studies, and confirmed by biopsy revealing flat mucosa and subsequent clinical and histologic improvement on a gluten-free diet. Gluten must be excluded from diet. Supplementary vitamins, minerals and hematinics may be given depending on deficiency. CASE REPORT: This is a case report of a 23-year old female patient with a mineralization defect (osteomalacia) and secondary osteoporosis caused by long-time unrecognized celiac disease. The patient had many symptoms: short stature, steatorrhea, anemia, weight loss and chronic bone pain. Laboratory and x-ray studies and jejunal biopsy revealed a chronic intestinal malabsorption disorder caused by gluten intolerance. Gluten-free diet and supplementary vitamins, minerals and hematinics were included with apparent clinical remission. DISCUSSION AND CONCLUSION: Some people with celiac disease may not have symptoms. The undamaged part of their small intestine is able to absorb enough nutrients to prevent symptoms. However, people without symptoms are still at risk for complications of celiac disease. Biopsy of the small intestine is the best way to diagnose celiac disease. Decreased bone density (osteoporosis and osteomalacia) is a serious problem for celiacs. If calcium is not absorbed, due to small intestinal damage caused by untreated celiac disease, bones are not as dense. The only treatment for celiac disease is gluten-free diet, that is, avoiding all foods that contain gluten. For most people, this diet stops symptoms, heals the existing intestinal damage, and prevents further damage.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12712900&dopt=Abstract



Hybrid Hybridomics. 2003 Feb;22(1):23-31.
Rapid monoclonal antibody generation via dendritic cell targeting in vivo.

Berry JD, Licea A, Popkov M, Cortez X, Fuller R, Elia M, Kerwin L, Kubitz D, Barbas CF 3rd.

The Skaggs Institute for Chemical Biology and the Department of Molecular Biology, The Scripps Research Institute, BCC-515, 10550 North Torrey Pines Road, La Jolla, CA 92126.

Dendritic cells (DC) are the professional antigen-presenting cells of the immune system. Previous studies have demonstrated that targeting foreign antigens to DC leads to enhanced antigen (Ag)-specific responses in vivo. However, the utility of this strategy for the generation of MAbs has not been investigated. To address this question we immunized mice with IgG-peptide conjugates prepared with the hamster anti-murine CD11c MAb N418. Synthetic peptides corresponding to two different exposed regions of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), a human C-type lectin, were conjugated to N418 using thiol-based chemistry. The N418 MAb served as the targeting molecule and synthetic peptides as the Ag (MAb-Ag). A rapid and peptide specific serum IgG response was produced by Day 7 when the synthetic peptides were linked to the N418 MAb, compared to peptide co-delivered with the N418 without linkage. Spleen cells from N418-peptide immunized mice were fused on Day 10, and three IgG1/k monoclonal antibodies (MAbs) were selected to one of the peptide epitopes (MID-peptide). One of the MAbs, Novik 2, bound to two forms of recombinant DC-SIGN protein in enzyme-linked immunosorbent assay (ELISA), and was specifically inhibited by the MID-peptide in solution. Two of these MAbs show specific binding to DC-SIGN expressed by cultured human primary DC. We conclude that in vivo DC targeting enhances the immunogenicity of synthetic peptides and is an effective method for the rapid generation of MAbs to predetermined epitopes.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12713687&dopt=Abstract [PubMed - in process]



Gen Comp Endocrinol. 2003 May;131(3):258-63.
Melatonin enhances cellular and humoral immune responses in the Japanese quail (Coturnix coturnix japonica) via an opiatergic mechanism.

Moore CB, Siopes TD.

Department of Poultry Science, North Carolina State University, Raleigh, NC 27695-7608, USA.

It is known that melatonin has important immunomodulatory properties in the Japanese quail. However, the mechanism of melatonin action on the immune system is not clearly understood in avian species. In mammals, the immunostimulatory properties of melatonin are mediated by the release of opioid peptides from activated T-lymphocytes. The present study was performed to determine if these same melatonin-induced opioids (MIO) are involved with the immunoenhancing effects of melatonin in quail. Three treatment groups were given melatonin (50 microg/ml) in the drinking water ad libitum along with naltrexone, a known opioid receptor-blocking agent. Melatonin was administered throughout the 3 week study and each bird received a daily intramuscular injection of naltrexone at a dose of 0.1, 1.0, or 10.0 mg/kg. In addition, three control groups were established that received only melatonin, naltrexone, or diluent. Evaluation of the cellular and humoral immune responses was initiated after 2 weeks of treatments. A cutaneous basophil hypersensitivity reaction to phytohemagglutinin (PHA-P) was measured to evaluate the cellular immune response. To evaluate the humoral immune response, primary antibody titers were determined 7 days post-intravenous injection with a Chukar red blood cell (CRBC) suspension. Both the cellular and humoral immune responses were significantly increased by 22 and 34%, respectively, upon melatonin exposure as compared to quail receiving diluent only. Concomitant administration of naltrexone and melatonin significantly reduced the immunoenhancing effect of melatonin across all naltrexone doses. We conclude that melatonin enhances a cellular and humoral immune response in Japanese quail via an opiatergic mechanism.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12714007&dopt=Abstract [PubMed - in process]



Mech Ageing Dev. 2003 Apr;124(4):371-8.
Interrelationships among brain, endocrine and immune response in ageing and successful ageing: role of metallothionein III isoform.

Giacconi R, Cipriano C, Muzzioli M, Gasparini N, Orlando F, Mocchegiani E.

Immunology Center, (Section Nutrition, Immunity and Ageing), Research Department Italian National Research Centres on Ageing (INRCA), Via Birarelli 8, 60121, Ancona, Italy

Metallothionein-III (MT-III) a brain-specific member of metallothionein family contributes to zinc neuronal homeostasis, and zinc is an important regulator of many brain functions, including the activity of hormone realising factors by hippocampus. Among them, somatostatin is pivotal because affecting thyroid hormones turnover and consequently thymic and peripheral immune efficiency (Natural Killer, NK) cell activity. Somatostatin is in turn affected by somatomedin-C, which is also zinc-dependent. Therefore, somatomedin-C may be a marker of somatostatin status in the hippocampus. MTs sequester and release zinc in transient stress, as it may occur in young age, to protect cells by reactive oxygen species. In order to accomplish this task, MTs are induced by IL-6 for a prompt immune and anti-inflammatory response. During ageing, MTs are high with a role of sequester of zinc, but with very limited role in zinc release because stress-like condition and inflammation is persistent. Therefore, high MTs may become to protective in young age to harmful during ageing leading to low zinc ion bioavailability for many body homeostatic mechanisms, including brain function. As a consequence, an altered physiological cascade from the brain (upstream) to endocrine and immune system (downstream) may occur. The aim of this work is to study the role of MT-III in the interrelationships among brain-endocrine-immune response in ageing and successful ageing. The main results are: (1) MT-III and IL-6 gene expressions increase in the hippocampus from old mice, in comparison with young and very old mice. (2) Somatomedin-C plasma levels decrease in old mice in comparison with young and very old mice. (3) Low zinc ion bioavailability (tested by the ratio total thymulin/active thymulin) is coupled with altered thyroid hormone turnover and depressed IL-2 in old mice in comparison with young and very old mice. (4) 'In vitro' experiments display more increments on NK cells activity by adding zinc-bound active thymulin than T3 alone. In conclusion, low MT-III in the hippocampus from young and very old mice leads to good zinc ion bioavailability that it is upstream coupled with normal hippocampal function affecting downstream normal thyroid hormones turnover and satisfactory NK cell activity, via complete saturation of zinc-bound active thymulin molecules. Therefore, a correct MTs homeostasis is pivotal for brain-endocrine-immune response in order to reach successful ageing.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12714242&dopt=Abstract [PubMed - in process]



Mech Ageing Dev. 2003 Apr;124(4):419-25.
Neutrophil immunity of the elderly.

Schroder AK, Rink L.

Institute for Immunology, RWTH Aachen, University Hospital, Pauwelsstr. 30, 52074, Aachen, Germany

Due to age-related changes of the immune system, elderly people are more susceptible to microbial infections than the young. Most research concerning immune senescence has been done on T and B cells, yet the first cells to migrate into microbe-infected tissue are neutrophils, which phagocytose and kill the pathogens. Long regarded as mere phagocytes, the neutrophils' importance for the immune response has been recognized in current publications, which acknowledge them an active participation in the cytokine network. Similarities in the symptoms of patients with genetical neutrophil deficiencies and those of the elderly indicate a leading role of neutrophils in the effects of immune senescence. While the number of circulating neutrophils remains unaltered in the elderly compared with young controls, phagocytosis and intracellular killing have been reported impaired. Oddly enough, the results for various stimuli differed: while some showed a decrease in neutrophil activation, the response to others remained unaltered. More research needs to be done on this, preferably using preparations of high purity to exclude monocytic interventions. Elucidation of immune deficiencies caused by neutrophil senescence can be an important contribution to a healthier elderly population.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12714248&dopt=Abstract [PubMed - in process]








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