Comparison of endotoxin levels in cow’s milk samples derived from farms and shops

The observations on the protective effect of bacterial endotoxin in farm-derived cow’s milk on childhood asthma and allergy are contradictory. The aim of this study was to determine the endotoxin levels in ‘farm-derived whole raw’ and ‘processed shop’ sources of cow’s milk, and to test how the temperature and storing conditions might alter their endotoxin concentrations. Milk was collected from farms and shops. The level of endotoxin was measured by micro (gel-clot) Limulus amebocyte lysate test expressed as EU/ml. The concentration ranges of endotoxin were much higher and more widely scattered in the samples of whole raw farm milk than in the processed shop milk. Cold storage or heating increased the endotoxin concentrations in all samples of farm milk, but not in the processed shop milk. These results show that elevated levels of endotoxin in raw farm milk samples can occur from the cowshed or be formed during storage. In processed shop milk, storage does not cause any changes in the amount of endotoxin. Therefore, it is consistent that the handling and storage of raw milk alters the endotoxin concentrations, which may explain previous contradictory findings regarding the beneficial modulating effects on innate immunity toward allergy prevention in early childhood.L

Season dependent changes in the expression of Protein Kinase C isoenzymes in a female patient with Systemic Lupus Erythematosus

Europeanwhitewomen .Peripheral bloodmononuclear cells (PBMC) . Protein kinaseC(PKC) . Season dependence . Systemic lupus erythematosus (SLE

Index of Stimulation and TNFα Measurements Used for laboratory Diagnosis of Latent Tuberculosis as a New Principle

A new principle of a method for the laboratory diagnosis of latent Mycobacterium tuberculosis infection (LBTI) compared to the QuantiFERON (QFT) test is presented. The new elements, the calculation and introduction of an Index of Stimulation (IS) were based on the measurements of tumour necrosis-α (TNF-α) release in whole human blood stimulated by the peptides (TB-P) derived from Mycobacterium tuberculosis (Mtb) related proteins and Purified Protein Derivative (PPD). The amount of TNF-α was determined by ELISA. The calculation of IS values was carried by the formula: TNFα(pg/ml)TB-P/ TNF-α(pg/ml)PPD. The populations studied consisted of a) 15 healthcare workers dealing with Mtb- infected patients (HCWTB); b) 14 healthcare workers not being exposed to Mtb patients (HCW-C) as controls. The diagnosis of LTBI was established if IS was higher than 1.50. In the HCW-TB group the number of LTBI was 6/15 by the new method and 9/15 by QFT. Tested clinically, the number of false-positive results by QFT was 3/9. All members of HCW-C group were LTBI negative by both methods. This new assay did not result in any false positive reactions. Although these results are still preliminary data derived from few patients. However, the theoretical novelties in the principle of method: the calculation of IS from the TNF-α-TB-P/TNF-α –PPD values can mean a progress in the individual laboratory diagnosis of LTBI in further studies

Adenosine inhibits the release of arachidonic acid and its metabolites (AAM) in activated human peripheral mononuclear cells

Objective: The effects of adenosine (Ado) and subtype-specifi c activators of adenosine receptors (A1, A2A, A2B and A3) were studied on the release of arachidonic acid (AA) and its metabolites (AAM) from human peripheral mononuclear cells (monocytes). Materials and method: Adenosine and the selective agonists and antagonists of adenosine receptors were used. 3H-AA and its metabolites released into the medium were determined by measurement of the total 3H radioactivity released without separating the AAM. Results: In the cells activated by protein kinase C specifi c phorbol ester (phorbol 12-myristate 13?acetate) and Ca2+ ionophore (A23187), adenosine and two subtype-specifi c receptor agonists, CPA(A1) and CGS 21680 (A2A) induced concentration-dependent inhibition of the release of AAM, whereas stimulation of A2B or A3 receptors was ineffective. The rank order of potency for the inhibition of AAM release was as follows: CGS 21680 = CPA > adenosine > NECA (in the presence of ZM 24185 and DPCPX as A2A and A1 adenosine receptor antagonists, respectively) = IB-MECA. Adenosine inhibited the release of AAM only at and above the concentration of 100 ?M, whereas the inhibitory effect of A1 and A2A receptor specifi c agonists appeared at a concentration of 10-7 M. Conclusions: It can be concluded that adenosine physiologically may not have a signifi cant effect on the AAM release of circulating monocytes, but in pathological conditions, where the local Ado concentrations increases, this nucleoside, through activation of A2A and A1 receptors can exert, at least in part, an antiinfl ammatory action by decreasing proinfl ammatory AAM productio