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Testing of visceral sensitivity

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Under normal circumstances most of the visceral input to the central nervous system is not perceived consciously. Visceral hypersensitivity associated with altered reflex activity seems to be a common pathophysiological mechanism in functional gastrointestinal disorders. Investigation of visceral sensitivity in humans is based on distension tests using barostat, or tensostat more recently. Tensostat may allow better standardization of distending stimuli, regardless of the capacity or compliance of the organ being tested. Other techniques include transmucosal electrical nerve stimulation, and chemical or thermal stimulation. Measurement of the responses to gut stimuli is based on the evaluation of conscious perception or objective responses, such as reflex activity or central processes. Recently, the assessment of the central responses has become available due to a variety of new brain imaging techniques. Several factors are thought to influence the results of visceral sensitivity studies: age, gender, physiological factors (postprandial testing) as well as psychological factors (stress, hypnosis, hypervigilance phenomenon). Technical conditions for performing tests like distension protocols may considerably affect the perception of sensory thresholds. Various mediators and pharmacological agents, in particular those acting on serotonin receptors, affect the sensory function of the gastrointestinal tract, and some of them have therapeutic potential in the treatment of visceral hypersensitivity.
One of the common side effects of acetylsalicylic acid (ASA) is the induction of pseudoallergic reactions that range from urticarial wheals to anaphylactic shock. At present there is no reliable detection method available for the diagnosis of ASA-hypersensitivity and its relation to clinical symptoms. The purpose of the present study was to evaluate the functional eicosanoid typing (FET) score taking into account several parameters of the equilibrium between prostaglandins (PG) and peptido-leukotriens (pLT). A total eicosanoid pattern score (TEP) ranging from 0.0 to 3.0, was defined that exhibited significant differences (p 0.001) between ASA-intolerant patients and healthy subjects. In addition to the differentiation of both groups at a TEP cut-off value of 1.0, the increasing TEP values correlated with an increasing severity of clinical symptoms in ASA-intolerant patients. We conclude that the FET has the potential for the safe and reliable detection of ASA-intolerance and, probably, other eicosanoid-related pseudoallergic reactions.
The aim of the study was to analyse the potential pea-peanut cross-reactivity using the mice BALB/c as a biological in vivo model in the research on immune response to peanut proteins (PnE). BALB/c mice were three-fold sensitised (on days 1, 7, and 21) by oral or intraperitoneal (IP) administration of PnE in 0.5 mg or 1 mg dose, with or without adjuvant – aluminum hydroxide gel (Alum). Serum immunoglobulins (IgE, IgG, IgG1 and IgG2a) and level of cytokines (IL-4, IL-10, IFN- γ), secreted by the isolated lymphocytes were examined. The highest increase in total IgE and peanut-specific IgG1 was noted in the group sensitised by IP administration of PnE in the presence of Alum. Lymphocytes from peanut-sensitised (with and without Alum) mice showed a significantly high level of IL-4 and this cytokine was secreted to a much higher extent as compared to IFN-γ. Stimulation of a culture of lymphocytes with pea proteins resulted in high IFN-γ secretion. A weak reaction of peanut-specific IgG1 present in mice serum with pea globulins (vicilin – PV and legumin – PL) can suggest that the cross-reactivity between peanut and pea proteins results from the presence of proteins other than 7S and 11S globulins. Due to the demonstrated low cross-reactivity between peanut proteins and pea globulins, the possibility of applying pea proteins in peanut-allergy immunotherapy may be suggested.
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