PubMed Health⌕ Search

Biomedical subjects

Martin Raithel

Publications and source records attributed to Martin Raithel.

7 recordsLinked to original sources
PubMed2006

Response of respiratory flour allergics in an ingested flour challenge may involve plasmacytoid dendritic cells, CD25+ and CD152+ T cells.

BACKGROUND: A number of occupational respiratory allergens are food related, and little is known about the responses these allergens elicit in sensitized persons that ingest them. METHODS: Nine respiratory flour-allergic volunteers were exposed in a double-blind placebo-controlled food challenge with flour. Responses were monitored by spirometry, acoustic rhinometry, determination of urinary methyl histamine and tryptase and flow cytometric evaluation of basophil, dendritic and T cell numbers and markers. RESULTS: Significant increases in serum tryptase (compared with placebo post-exposure levels) and methyl histamine and a coordinated decrease in blood basophils and nasal volume after ingestion of allergen compared with placebo suggest an allergic response to ingested allergen. There was no change in forced expiratory volume in 1 s. The number of blood plasmacytoid dendritic cells (DC), but not of myeloid DC, decreased after exposure (p = 0.001). DC HLA DR was reduced after both exposures (p < 0.001). Expression of CXCR4 on DC was reduced after allergen (p = 0.033) but not after placebo exposure. CD4+ T cell expression of CD25 was elevated after placebo (p = 0.021) but reduced after allergen provocation. The reduction in CD25 expression after allergen compared with placebo was significant (p = 0.024). CD152 was downregulated on these cells after allergen (p = 0.039) but less so after placebo exposure. CONCLUSION: Persons with respiratory allergy respond after ingestion of the relevant allergen. Response to this allergen challenge may selectively recruit plasmacytoid DC through CXCR4 and T cells expressing CD25 and CD152, which may be a regulatory phenotype.

Adult↗
PubMed2004

Implication of peroxisome proliferator-activated receptor gamma and proinflammatory cytokines in gastric carcinogenesis: link to Helicobacter pylori-infection.

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-dependent transcription factor involved in various processes including the inflammation and carcinogenesis. The aim of the present study was 1) to examine the mRNA and protein expression of PPARgamma in gastric cancer (GC); 2) to evaluate the effect of PPARgamma ligand (ciglitazone) on the proliferation and apoptosis of GC cell line; and 3) to assess the levels of gastric tissue proinflammatory cytokines, IL-1beta and IL-8, and plasma gastrin in GC patients before and after Helicobacter pylori (H. pylori) eradication. The trial material included 30 H. pylori-negative controls and 30 sex- and age-matched GC patients without or with H. pylori before and after its eradication. Expression of tissue PPARgamma, tissue levels of IL-1beta and IL-8, and plasma concentration of gastrin were significantly higher in H. pylori-positive GC compared to controls, but H. pylori eradication significantly reduced these parameters. Kato III cells incubated with alive H. pylori upregulated PPARgamma expression and ciglitazone inhibited cell proliferation and induced apoptosis. PPARgamma, proinflammatory cytokines and plasma gastrin appear to be implicated in H. pylori-related gastric carcinogenesis and PPARgamma agonists may have potential in cancer therapy.

Adult↗
PubMed2004

Activation of NFkappaB represents the central event in the neoplastic progression associated with Barrett's esophagus: a possible link to the inflammation and overexpression of COX-2, PPARgamma and growth factors.

The molecular mechanisms responsible for the progression of malignant transformation in Barrett's esophagus (BE) are still poorly understood. This study was undertaken (1) to investigate the gene and protein expression of cyclooxygenase-2 (COX-2), peroxisome proliferator-activated receptor-gamma (PPARgamma), interleukin-8 (IL-8), hepatocyte growth factor (HGF), gastrin, and its receptor (CCK-2) in the Barrett's epithelium; (2) to analyze the activity of NFkappaB in Barrett's esophagus with low-grade dysplasia; and (3) to assess the effects of PPARgamma ligand (ciglitazone) and gastrin on cell proliferation in the cell line derived from esophageal adenocarcinoma (OE-33). COX-2, PPARgamma, IL-8, HGF, gastrin, and CCK-2 expression levels relative to the control gene encoding GAPDH were analyzed by RT-PCR and Western blot in specimens of BE with low-grade dysplasia (n = 20) and compared with that in the normal squamous esophageal mucosa from the middle portion of the esophagus (n = 20). In vitro experiments included the incubation of cell line OE-33 with ciglitazone (1-15 microM) and gastrin (100 nM). NFkappaB activity in biopsies specimens was measured by highly sensitive ELISA. COX-2, PPARgamma, IL-8, HGF, gastrin, and CCK-2 expressions were significantly increased in BE compared with normal squamous esophageal mucosa. NFkappaB activity was significantly upregulated in BE. Ciglitazone inhibited cell proliferation of OE-33 cells as assessed by BrdU and this effect was attenuated partly by gastrin. (1) COX-2, PPARgamma, HGF, gastrin, and its receptor are significantly upregulated in BE, suggesting a possible role for these factors in Barrett's carcinogenesis; (2) the increased NFkappaB activity is probably linked to increased IL-8 and COX-2 expression; and (3) PPARgamma ligands might be useful as a new therapeutic option in the prevention and treatment of Barrett's carcinoma.

Aged↗
PubMed2003

Immunoglobulin E production in chronic pancreatitis.

OBJECTIVES: Serum immunoglobulin E (IgE) was investigated in patients with chronic pancreatitis in order to elucidate possible disease mechanisms linking pancreatitis, adverse reaction to foods and allergy. DESIGN AND METHODS: Serum IgE was analysed in 86 non-atopic patients with advanced chronic pancreatitis and 54 non-atopic controls. IgE detection was performed by enzyme-linked immunofluorescence. RESULTS: Mean IgE levels (+/- standard error of mean) in chronic pancreatitis patients (286.1+/-49 kU/l) were found to be significantly elevated compared to controls (67.7+/-11 kU/l; P<0.0001). Normal IgE levels (<100 kU/l) were present in 40/54 control patients (74.1%), but only 39/86 pancreatitis patients (45.3%). Of the patients with chronic pancreatitis, 47/86 (54.6%) had clearly elevated IgE levels of >100 kU/l and their IgE values did not show a Gaussian distribution. However, nine-fold higher IgE levels were found in chronic pancreatitis patients with alcohol consumption of >25 g/day and exocrine insufficiency (915.5+/-240 kU/l) than in pancreatitis patients with normal exocrine function and no alcohol consumption (103.4+/-43 kU/l; P<0.001). Moreover, acute episodes of chronic pancreatitis were found to increase serum IgE levels. CONCLUSIONS: In patients with chronic pancreatitis, serum IgE production is markedly enhanced, especially during acute inflammatory episodes or when alcohol is consumed. Since abstinence from alcohol and pancreatic enzyme substitution are associated with clearly lower IgE levels, it may be concluded that pancreatic insufficiency with reduced nutrient digestion and alcohol consumption stimulate IgE production. This finding gives rise to the speculation that, apart from pancreatic inflammation, cross-linking of IgE with alimentary or other antigens might be involved in the pathophysiology of a sub-population of patients with chronic pancreatitis and manifest pancreatic insufficiency.

Adult↗
PubMed2003

Functional and morphologic characterization of eosinophils in the lower intestinal mucosa of patients with food allergy.

OBJECTIVE: The aim of this study was to characterize the functional and morphologic features of eosinophils in the intestinal mucosa of patients with food allergy. METHODS: Eighteen patients with food allergy and 11 controls took part in this study. In every patient, corresponding biopsy samples obtained during colonoscopy were quantitatively assessed by immunohistochemical methods (EPO-I) and subjected to mucosa oxygenation using eosinophilic cationic protein (ECP). Initial basal release, spontaneous and anti-IgE-dependent release, and the total ECP content of mucosal biopsies were studied. RESULTS: Morphologically, mucosal eosinophils in patients with food allergy have distinct features, occur in larger amounts, and show a distinct distribution pattern (i.e., intraepithelial, lamina propria, and submucosa). Their initial basal release is similar to that of controls, but stimulation of the IgE receptor with anti-IgE results in 40-fold activation (p < 0.001). In food allergy patients, the density of eosinophils, the presence of intraepithelial eosinophils, and the rate of degranulation showed a highly significant correlation to the initial basal release of ECP by mucosal tissue (Kendall tau = 0.619, 0.381, and 0.609, respectively; p < 0.05 for all) but not to their capability to be stimulated with anti-IgE. CONCLUSIONS: Eosinophils of the lower intestine of patients with food allergy show characteristic features with regard to morphology, distribution, and functional behavior to IgE receptor stimulation. Immunostaining of eosinophil peroxidase (EPO) detects important characteristic features that are missed with conventional hematoxylin-eosin staining.

Adult↗