Library

Notes: 1. Oleic acid was used to produce adult respiratory distress syndrome-like pulmonary micro-vascular injuries. The resulting injuries have previously indicated involvement of accumulating neutrophils (Hultkvist et al. 1988). Activated neutrophils release oxygen free radicals that may be possible to detect in the plasma.2. The dynamics of neutrophils and platelets were studied in the guinea-pig after oleic acid-induced injury (0.03 ml/kg per 10 min).3. As an indication of oxygen free radical activity, plasma levels of uric acid and red blood cell (RBC)-catalase, were analysed.4. Allopurinol (10 mg/kg, i.p.) was given prior to oleic acid infusion to block the production of uric acid.5. The neutropenia, in contrast to the thrombocytopenia seen at 15 min, was significantly inhibited in the allopurinol pretreated group compared with oleic acid and vehicle alone.6. The blood plasma concentration of uric acid was significantly elevated after 15 min from start of experiment. Allopurinol pretreatment significantly reduced the uric acid plasma level.7. The RBC catalase activity did not change with time within or between any groups.8. The results indicate that sequestration of activated neutrophils in the microvasculature are to some extent oxygen free radical dependent.

Notes: Background The mechanisms for adverse reactions to foods in the gastrointestinal tract are poorly understood. Presently, only hmited possibilities are available for identification of adverse immunological reactions to different foods.Objective The intestinal inflammatory reactions in adult patients with a history of milk-related gastrointestinal symptoms were studied after intestinal challenges by a jejunal perfusion technique and compared with the reactions in a control group. Methods Five skin-prick test and radioallergosorbent test negative and lactose tolerant patients with a history of milk-related gastrointestinal symptoms, verified by double-blind placebo-controlled challenge, and eight healthy controls were investigated. Perfusions were performed allowing analyses of a well-defined ‘closed’ jejunal segment. Milk perfusions were performed in patients and controls after an overnight fast. Ten millilitres of milk were administered to the segment at 3 mL/min, The jejunal fluid levels of hyaluronan (hyaluronic acid) and albumin were measured.Results In the five patients the milk challenges induced as a mean fivefold increased levels of hyaluronan compared with prcstitnulation values, whereas no such increases were seen in the control subjects. Albumin, as a marker of plasma leakage, was also increased in the patients but not in the control subjects.Conclusion The underlying mechanisms for locally increased levels of hyaluronan and also albutnin in the intestinal lumen may be secretion of lymph rich in hyaluronan and reflect the mucosal oedetna. This capacity of the intestinal mucosa to react with lymph leakage towards a locally infused allergen may be a possible way lo delineate gastrointestinal reactions in food-related disorders.

Notes: Background Immune-mediated food hypersensitivity affecting the gut is difficult to evaluate, and objective tools to diagnose local gastrointestinal (GI) inflammatory reactions are lacking.Objectives To determine whether allergic manifestations in adults with a history of food-related GI symptoms could be assessed in feces during symptomatic and non-symptomatic periods, using the surrogate markers, eosinophil cationic protein (ECP), eosinophil protein X (EPX) and myeloperoxidase (MPO).Methods Thirteen subjects with food hypersensitivity-related GI symptoms, confirmed by a positive double-blind placebo-controlled food challenge (DBPCFC), were subjected to an open kinetic food challenge design for 6 weeks. Symptoms were recorded and scored during the 3-week study period and stool samples were obtained every day. The surrogate markers ECP, EPX and MPO were measured in the supernatants from feces samples.Results A significant increase in abdominal pain, distension and flatulence was observed during challenge, with a gradual decrease during elimination diet. Both between days and subjects, EPX levels were more frequently increased compared to ECP and MPO. Individuals with a history of a short duration of symptoms had significantly higher mean levels of EPX and MPO than those with a longer duration of symptoms.Conclusions An overall increase in levels of eosinophil markers, in particular EPX, was observed in feces from patients with food-related GI symptoms. However, rather than being a tool to differentiate symptomatic from non-symptomatic periods, EPX might be used for detecting an ongoing clinical or subclinical chronic inflammation, that may have an impact on the patient's clinical course of GI symptoms.

Notes: Background Food intolerance in adults is mostly associated with vague symptoms and not clearly related to atopy and food allergy. A combination of different pathogenetic mechanisms may be responsible for the symptoms.Objective The aim of this study was to describe patients with a history of food-related gastrointestinal symptoms in relation to the presence of mucus in the stools, joint swelling and arthralgia and to determine whether or not there is an association between the presence of these parameters, atopic disease and the presence of immune complexes in serum.Methods Fifty-eight patients consecutively referred to our clinic with food-related gastrointestinal symptoms were investigated.Results Thirty-five patients (60%) had mucus in their stools, 24 patients (41%) complained about joint swelling and 41 patients (71%) had arthralgia. There were no correlations between these parameters and atopy according to Phadiatope test or skin prick test (SPT). No correlations were found between the occurrence of mucus in the stools, arthralgia and joint swelling. There were significantly higher levels of circulating immune complexes in patients with a history of arthralgia compared with patients with no such history (P 〈 0.03) and the number of individuals with the presence of such immune complexes was higher among the patients with arthralgia than among the patients without. In general the patients did not relate the exposure to certain foods to symptoms like joint swelling, arthralgia and presence of mucus in the stools. However, there were significant positive correlations between food-related gastrointestinal symptoms in the following instances: chocolate-induced gastrointestinal symptoms and mucus in the stools (P= 0.006), vegetable-induced gastrointestinal symptoms and mucus in the stools (P= 0.002) and meat-induced gastrointestinal symptoms and mucus in the stools (P= 0.003). In a group of individuals without foodrelated symptoms investigated separately, a very low frequency of mucus in the stools, joint swelling and arthralgia was seen (none, two and three individuals of the 20 subjects, respectively). Of 41 patients with immediate onset of gastrointestinal symptoms, 20 were atopic according to Phadiatope and SPT, Of 11 patients with late onset of symptoms 10 were negative in Phadiatope and SPT (P 〈 0.05). The most frequently involved foods were fruits, vegetables, milk, fish and meat.Conclusion The results suggest the involvement of different inflammatogenic mechan isms in food-related gastrointestinal symptoms.

Notes: The clinical outcome of peanut allergy and some factors associated with development of peanut allergy remain unsolved. It has not been clarified to what extent peanut intake affects immunoglobulin (IgE) antibody formation in peanut sensitized individuals. The aim of the study was to investigate the development of peanut hypersensitivity in children and adolescents with specific IgE antibodies to peanut, using questionnaires and current serum tests and comparing it to information obtained 5–6 yr earlier, to investigate how peanut intake during this period related to subject age, IgE antibody levels and symptoms and to investigate what information this patient group was given at the time of diagnosis regarding avoidance of peanut related food. All patients with detectable peanut-specific IgE antibodies investigated during 1994–1996 deriving from two allergy laboratories in the western region of Sweden were traced and reinvestigated (n=132). A total of 111 subjects (63 with peanut allergy and 48 peanut sensitized) participated in the questionnaire. Eighty-six of them consented to be enrolled in a further interview and renewed testing of specific IgE antibody to peanut 5 yr later. All tests were done using the Pharmacia CAP system®. Increased IgE antibody levels during follow-up was related to age; subjects 0–6 yr at initial test occasion were more likely to have higher IgE antibody class than the older individuals (p=0.018). Exposure to peanut during the study, i.e. 5–6 yr since diagnosis, did not seem to affect the result. During the follow-up period, 29 out of 86 (34%) increased their IgE antibody class. At the second test occasion the remaining subjects had similar (28%) or lowered (38%) levels of IgE antibodies. Exposure to peanut during follow-up was more common in subjects with IgE antibody class 1–3 compared to subjects with high value (〉3) at the initial test (p=0.003). Reported symptoms during follow-up were also more common in subjects with initially high IgE antibody value. Individuals with initially high IgE antibodies to peanut had been given more information about peanut allergy and cross-reacting allergens than other individuals. The subjects over 6 yr of age showed a decrease in peanut-specific IgE class over a 5-yr period. Together with the literature, our result suggest that follow-up and renewed testing is recommended, since there may be a change in IgE antibody classes and clinical sensitivity over time. Even in Sweden, with a low consumption of peanuts, the youngest individuals with peanut sensitization experienced a similar course of events that has been reported in other countries.

Notes: CD1 cell surface glycoproteins represent a family of non-major histocompatibility complex (MHC) encoded antigen-presenting molecules. All members of the CD1 family appear to mediate the recognition of microbial or endogenous lipid and glycolipid antigens. The recognition of CD1d by a unique subset of natural killer (NK) T cells that leads to rapid production of large amounts of both type 1 and type 2 cytokines can be augmented by some synthetic glycolipids. Because of the proposed role of such CD1d-restricted T cells in immunoregulation, we hypothesized that CD1d molecules participate in mucosal immune responses in patients with gastrointestinal symptoms owing to food hypersensitivity. Patients of that category represent a heterogeneous group in which poorly defined immunological mechanisms are believed to contribute to disease pathogenesis. The expression of CD1 in duodenal biopsy samples from six patients with verified intolerance to cow's milk and six healthy controls was studied by immunoperoxidase staining of cryostat sections using a panel of mouse monoclonal antibodies (MoAbs) specific for CD1a, b, c, and d. Large numbers of CD1d positive cells were found in the lamina propria of all the patients, both during the symptomatic and the asymptomatic periods, whereas healthy controls were virtually devoid of CD1d expression in the duodenum. The localization of CD1d positive cells corresponded to areas where B cells, plasma cells and dendritic cells (DC) were present. A positive correlation was found between the numbers of CD1d+ and CD19+ cells in the lamina propria. In contrast to previous reports, no CD1d expression was found on the epithelial cells. Although less numerous than CD1d+, the CD1c+ cells were also present in all the patients and in five out of six controls. No staining for CD1a or CD1b was detected in the duodenal biopsy samples from any of the subjects. The exclusive presence of CD1d in the duodenal lamina propria of the patients with cow's milk hypersensitivity might suggest the participation of these molecules in the pathogenesis of allergic reactions to food.