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Relapsing polychondritis is a rare autoimmune disease, which is due to sporadic occurrence, unexplained etiology and wide range of symptoms resulting in the difficulties in diagnosis. Recurrent inflammation leads to destruction of cartilaginous tissues, such as ear, nasal septum, larynx, trachea and bronchi, peripheral joints and vertebral structures. Blood vessels, the central nervous system, eyes, and the urinary tract can be involved as well. Clinical course of relapsing polychondritis is often modified by co-existing systemic diseases and remains misdiagnosed. In case of inappropriate or delayed treatment, serious and life-thretening complications may develop. In this article we present the most characteristic clinical features of the disease, differential diagnosis, focusing on current approaches to treatment.

Complete arterial revascularisation using the radial artery (RA) is an attractive alternative to venous graft implantation for the coronary artery bypass grafting (CABG). In spite of the favourable long-term results of this approach, the sensitivity of RA to vasoconstriction and spasm is still limiting its use. It has been suggested that vasospastic properties of the artery may differ depending on the location (proximal or distal).To compare the vasoreactive properties of proximal and distal sections of RA grafts.Proximal and distal segments of RA were obtained from 27 patients undergoing CABG and isometric recordings of changes in smooth muscle force were performed mounted in the organ bath. Responses to cumulatively increasing concentrations of phenylephrine (PE), angiotensin II (AT-II), prostaglandin F2 (PGF2) and endothelin-3 (ET-3) were evaluated.Both proximal and distal segments of RA constricted in response to KCl, PE, AT-II, PGF2 and ET-3. Proximal segments demonstrate significantly greater spastic response to KCl, as well as to receptor-mediated agonists PE and more importantly vasoactive peptide AT-II. These differences remained statistically significant after correcting for vessel size and weight. In contrast, reactivity of both segments of RA to increasing cumulative doses of PGF2 and ET-3 was similar.Proximal segments of the radial artery are more susceptible to vasoconstriction induced by PE and AT-II, which should be taken into consideration in the clinical setting of CABG surgery. Increased muscle content in this segment does not fully explain this difference, which may result from varying receptor density and properties.

This study was designed to investigate changes in aggregability of red blood cells of patients with essential hypertension and concomitant hypercholesterolemia (total cholesterol level5.0 mmol/l) following the use of angiotensin converting enzyme inhibitors (ACE-I) along with or without inhibitor of reductase HMG-CoA (statin). Under standard pharmacotherapy (beta-receptor anatgonist, calcium chanel antagonist, and diuretic) aggregability of RBC in hypertensive patients was significantly increased in spite of the treatment. However, in patients receiving additionally ACE-I spontaneous aggregation of RBC was attenuated. We found that antihypertensive therapy consisting of ACE-I along with statin improved erythrocyte aggregation nearly to the level of normotensive and normocholesterolemic patients. Interestingly, this improvement of blood rheology was observed prior to statin-induced lowering of total cholesterol.

While immunopathogenesis of atherosclerosis is well defined, immunological mechanisms of hypertension (HTN) and its link to atherosclerosis remain unclear. We hypothesized, that primary HTN is associated with a pro-inflammatory and pro-atherogenic phenotype of circulating monocytes, characterized by co-expression of the Fc-gamma receptor (CD16+) and LPS receptor (CD14+high). Methods: 132 subjects (74M and 58F) with typical clinical risk factors of atherosclerosis were studied. HTN (85%) was diagnosed based on blood pressure monitoring and use of anti-HTN drugs. Monocyte characteristics in the peripheral blood were determined by flow cytometry and plasma cytokine levels by ELISA. Results: CD16+CD14+ cells were more prevalent in subjects with HTN and were highest in subjects whose blood pressure was poorly controlled (Figure ). A significant correlation between blood pressure levels at the time of study (JNC7) and prevalence of CD14+CD16+ monocytes was found (Figure ). These relationships remained significant in multi-variate analysis (p = 0.01; type 3 sum of squares ANOVA) taking into account other major risk factors for atherosclerosis or treatments. Further analysis of subpopulations showed that levels of CD16 +CD14+ (high) monocytes, rather than CD16 + CD14(dim) revealed a strong relationship to hypertension. These monocytes showed significantly higher expression of activation markers HLA-DR and CD45RA and TNF-α production(p

Superoxide anion is produced in human platelets predominantly by Nox2-dependent NADPH oxidases. In vitro experiments have shown that it might play a role in modulating platelet functions. The relationship between platelet superoxide production and aggregation remains poorly defined. Accordingly, we aimed to study superoxide production and aggregation in platelets from subjects with significant cardiovascular risk factors (hypertension, hypercholesterolemia, smoking and diabetes mellitus) and from control individuals. Moreover, we studied the effects of novel polyphenol-rich extracts of Aronia melanocarpa (chokeberry) berries on platelet function in vitro. Superoxide production was significantly increased in patients with cardiovascular risk profile when compared to controls, while platelet aggregation in response to either collagen or thrombin were borderline higher, and did not reach statistical significance. Interestingly, no relationship was observed between platelet aggregation ex vivo and platelet superoxide production in either of studied groups. No correlation was found between endothelial function (measured by FMD) and platelet aggregation ex vivo either. Polyphenol-rich extracts of A. melanocarpa berries caused a significant concentration dependent decrease in superoxide production only in patients with cardiovascular risk factors, while no effect was observed in the control group. A. melanocarpa extracts abolished the difference in superoxide production between risk factor patients and controls. A. melanocarpa extracts exerted significant concentration dependent anti-aggregatory effects in both studied groups, which indicated that these effects may be independent of it's ability to modulate superoxide production. The anti-aggregatory effects of chokeberry extracts were similar irrespective of aggregation inducing agent (collagen or thrombin). Moreover, they appear to be independent of platelet NO release as NOS inhibition by L-NAME did not lead to their abrogation.

The study was performed to find the relationship between rheological properties of erythrocytes and the effectiveness of antihypertensive therapy both in patients suffering from essential hypertension as well as in spontaneously hypertensive rats (SHR). Additionally, in patients receiving the same antihypertensive therapy we evaluated the effect of aspirin at a low and high dose on aggregation of erythrocytes. We found that in a consequence of uniformed antihypertensive therapy which in patients lasted minimum one year and consisted of one of ACE inhibitors (enalapril or perindopril or captopril), one of beta-antagonists (metoprolol or bisoprolol) and diuretic agent (indapamid), while SHR lasted 8 days and consisted of ACE inhibitor (chinapril), blood pressure lowered and red blood cell rheology was significantly improved. For the first time we observed that antihypertensive treatment which advantageously decreased the aggregability of erythrocytes was diminished by a high dose of aspirin (300 mg/day).

Sjögren's Syndrome (SS) is the second most common autoimmune disorder after rheumatoid arthritis (RA). It can be found as a lone condition (primary Sjögren's Syndrome) or may accompany other autoimmune rheumatic diseases (secondary Sjögren's Syndrome). Despite such frequent occurrence, accurate diagnosis of Sjögren Syndrome is difficult. These difficulties result from highly variable symptoms of SS as well as from common presence of other autoimmune disorders. In the following article authors present current knowledge concerning clinical symptoms, diagnostic methods and latest clinical guidelines on the diagnosis of SS. Differential diagnosis of SS and systemic lupus erythematosus (SLE) is also discussed.

The objective of the present study was to investigate the effect of beta2-adrenoreceptor polymorphisms Arg16Gly and Gln27Glu as well as their relationship to the pulmonary function parameters, and the clinical presentation in patients with asthma and allergic rhinitis. Investigated polymorphisms were in linkage disequilibrium, therefore their effects should be evaluated collectively. Although no significant association could be found with the presence of asthma or allergic rhinitis in studied population, polymorphisms of beta2-adrenoreceptor can influence pulmonary function in these patients. These effects significantly differ between men and women, possibly indicating the effect of sex hormones on genetic regulation of pulmonary function.

Summary Background Staphylococcus aureus has important implications for the pathogenesis of atopic dermatitis (AD). In some patients S. aureus can be eradicated from the skin during anti-inflammatory treatment, while in others bacterial colonization is persistent. Potential mechanisms and features of these two distinct groups of patients are not known. Objective Accordingly, we studied relationships between the ability to eliminate S. aureus during an anti-inflammatory treatment and selected clinical and immunological features. Methods Quantitative assessment of S. aureus on the skin, in nasal vestibule and throat, serum IgE levels, CD4/CD8 T-cell ratio, lymphocyte proliferation and phagocyte oxidative burst were determined during the exacerbation and after 4 and 12 weeks of the treatment using topical steroid and oral antihistamine in 34 patients with AD. Results S. aureus was found on the skin of all 34 patients during exacerbation. Disease severity scoring of atopic dermatitis (SCORAD) correlated with the density of bacteria. Treatment with oral antihistamine and topical steroid resulted in a significant alleviation of symptoms, which correlated with the elimination of S. aureus from the skin in 70% of patients. In the remaining 30% of patients, dense (more than 1010/cm2) S. aureus skin colonization, persisted despite the treatment. Patients with persistent S. aureus presented with higher serum IgE levels, lower lymphocyte proliferation in response to staphylococcal enterotoxin B, phytohaemagluttinin and anti-CD3. Persistence of S. aureus was more common in men. Conclusions Patients with AD differ in the ability to clear S. aureus from the skin during anti-inflammatory treatment, which appears to be related to the abnormalities in immunological parameters. Local antibiotic therapy should be considered only in patients with persistent S. aureus colonization.

Nitric oxide (NO) and reactive oxygen species exert multiple modulating effects on inflammation and play a key role in the regulation of immune responses. They affect virtually every step of the development of inflammation. Low concentrations of nitric oxide produced by constitutive and neuronal nitric oxide synthases inhibit adhesion molecule expression, cytokine and chemokine synthesis and leukocyte adhesion and transmigration. Large amounts of NO, generated primarily by iNOS can be toxic and pro-inflammatory. Actions of nitric oxide are however not dependent primarily on the enzymatic source, but rather on the cellular context, NO concentration (dependent on the distance from NO source) and initial priming of immune cells. These observations may explain difficulties in determining the exact role of NO in Th1 and Th2 lymphocyte balance in normal immune responses and in allergic disease. Similarly superoxide anion produced by NAD(P)H oxidases present in all cell types participating in inflammation (leukocytes, endothelial and other vascular cells etc) may lead to toxic effects, when produced at high levels during oxidative burst, but may also modulate inflammation in a far more discrete way, when continuously produced at low levels by NOXs (non-phagocytic oxidases). The effects of both nitric oxide and superoxide in immune regulation are exerted through multiple mechanisms, which include interaction with cell signalling systems like cGMP, cAMP, G-protein, JAK/STAT or MAPK dependent signal transduction pathways. They may also lead to modification of transcription factors activity and in this way modulate the expression of multiple other mediators of inflammation. Moreover genetic polymorphisms exist within genes encoding enzymes producing both NO and superoxide. The potential role of these polymorphisms in inflammation and susceptibility to infection is discussed. Along with studies showing increasing role of NO and free radicals in mediating inflammatory responses drugs which interfere with these systems are being introduced in the treatment of inflammation. These include statins, angiotensin receptor blockers, NAD(P)H oxidase inhibitors, NO-aspirin and others. In conclusion in this mini-review we discuss the mechanisms of nitric oxide and superoxide dependent modulation of inflammatory reactions in experimental animals and humans. We also discuss potential roles of nitric oxide as a mediator of allergic inflammation.

Using automatic erythrocyte aggregometer type MA-1 (Myrenne gmbh, Germany), we investigated the hypothesis that therapeutic effectiveness of quinapril--angiotensin converting enzyme inhibitor (ACEI)--in the treatment of hypertension would correlate with improvement of red blood cell (RBC) aggregability. Experiments were performed on commercially available inbred strain of spontaneously hypertensive male rats (SHR) aged 19-21 weeks. Age-matched normotensive Wistar-Kyoto (WKY) rats genetically related to SHR were used as a control. Aggregability of RBC in hypertensive rats was significantly higher than in control WKY animals. Quinapril (100 microg/kg) administered i.p. for 8 days improved RBC aggregability in normotensive rats but surprisingly not in SHR animals. Beneficial effect of quinapril on RBC aggregation observed in normotensive animals did not occur when this drug was injected in combination with aspirin (1 or 50 mg/kg) or with indomethacin (20 mg/kg) or with L-NAME (10 mg/kg). However, much the same damaging effects on RBC aggregability were observed when aspirin, indomethacin or L-NAME were each administered into normotensive animals without quinapril. In contrast with normotensive rats, aggregability of RBC in SHR was not affected either by quinapril or by indomethacin and by L-NAME, given separately or in combination. The only compound significantly worsening RBC aggregability in SHR was aspirin but this effect was not dose-dependent. Quinapril-induced improvement of RBC aggregability in normotensive rats (but not in SHR) was completely abolished by simultaneous administration of B2 receptor antagonist icatibant and successfully mimicked by 8 days of treatment with bradykinin. In vitro aggregability of RBC isolated from WKY was not affected by previous incubation (30 min at 37 degrees C) with quinapril, indomethacin or L-NAME. Only aspirin (3 mM) significantly increased RBC aggregability as compared to placebo. It is concluded that under physiological conditions quinapril efficiently inhibits RBC aggregability and this effect is modulated by secretion of endothelial mediators, mainly prostacyclin and nitric oxide. In hypertension quinapril, in spite of lowering of arterial blood pressure, is unable to display its beneficial effects on RBC aggregability possibly due to the hypertension-induced/accompanied dysfunction of vascular endothelium. Aspirin revealed unique erythrocyte damaging properties, presumably independent of inhibition of cyclooxygenase but related to a direct membrane protein acetylation.

Pathogenesis of atopic dermatitis (AD) is multifactorial, therefore despite many different treatment protocols none of the available methods is effective enough. In the present study we analysed the effects of oral antihistamines and topical steroids on selected parameters of humoral (immunoglobulin levels) and cellular (lymphocyte proliferation index, granulocyte oxidative burst, lymphocyte phenotype CD4:CD8) immunity. These parameters were analysed in 34 AD subjects during the exacerbation of the disease and after 4 and 12 weeks of the treatment.Along with the clinical status improvement (change form 3.17 +/- 0.1 to 1.3 +/- 0.2; 0-4 scale; p0.001), total serum IgE levels decreased significantly from 1563 +/- 459 to 1266 +/- +/- 364 IU/ml (p0.05). Other immunoglobulin levels did not change. Total blood chemiluminescence in response to latex stimulation was relatively higher during exacerbation than during remission, but this difference was not significant (p = 0.1). Mean spontaneous or PMA stimulated chemiluminescence did not differ either. CD4:CD8 index decreased significantly during the treatment (from 2.7 +/- 0.3 to 1.8 +/- 0.2; p = 0.03). Lymphocyte proliferation in response to PHA was significantly lower during exacerbation than during remission (10.4 +/- 2.8 vs. 27.1 +/- +/- 5.2; p0.03) and the improvement was observed after first 4 weeks of the treatment reaching the levels found in healthy controls. Proliferation index in response to anti-CD3 mAb (OKT-3) was in turn significantly higher during exacerbation (19.1 +/- 3.4 vs. 11.2 +/- 2.0; p = 0.04).Oral antihistamine in combination with topical steroids leads to several significant changes in the immune parameters (IgE levels, CD4:CD8 and proliferation indexes) which may explain its high effectiveness in majority of patients with AD.

Tobacco dust contains various immunologically active as well as toxic substances. However the relationship between allergic reactivity or lung function with chronic exposure to tobacco dust remains unclear. Accordingly the aim of the present study was to investigate the relationship between occupational chronic exposition to tobacco dust, respiratory function and some allergic reaction parameters.40 tobacco factory workers (47.5% women and 52.5% men) aged 25-59 years (mean 36.5) chronically (5-31 years, mean 12.6) exposed to tobacco dust were included into the study. Control group consisted of 30 subjects (46.7% women, 53.3% men) aged 25-60 years (mean 36.6) not exposed to tobacco leaves' dust. Detailed epidemiological data was collected. Additionally total IgE, specific (tobacco) IgE, eosinophil blood counts, skin tests (mixed grass and weed pollens, house dust, feather, tobacco extracts), basophil degranulation and neutrophil destruction tests with tobacco extracts as well as spirometry were studied in these groups. We found that FEV1/VC was significantly lower in tobacco industry workers chronically exposed to tobacco dust than in the control group (91.5 +/- 11.6% vs. 101.7 +/- 10.7% n; p = 0.0004). These subjects were also characterized by higher occurrence of mild bronchial obturation (FEV1/VC88% and FEV170%) which was present in 30% tobacco factory workers and in 6.7% of control group (p = 0.035). Levels of total IgE and tobacco-specific IgE, eosinophil counts, skin test reactivity, basophil degranulation and neutrophil destruction tests were not different between groups.Occupational chronic exposition to the dust of tobacco leaves is associated with significant increase in the occurrence of mild obturative ventilatory disturbances. Simultaneously no increased frequency of allergization to tobacco or other allergens was observed in tobacco industry workers.

Many diseases of the heart and circulatory system have been linked with both dysfunction of vascular endothelium and insufficient deformability of erythrocytes. Using shear stress laser diffractometry we investigated whether deformability of erythrocytes would be regulated endogenously by generation of two endothelial secretogogues: prostacyclin and nitric oxide. Experiments were performed in rats ex vivo and with whole blood or isolated erythrocytes in vitro. Iloprost--a stable analogue of prostacyclin (10 microg/kg i.v.) and SIN-1 (NO-donor) at a dose of 2 mg/kg/min i.v induced a significant improvement of deformability of erythrocytes ex vivo. Improvements of deformability by these two compounds were also evident in vitro when they were applied at a range of concentrations of 1 microM and 3 microM, respectively. Cyclooxygenase (indomethacin 20 mg.kg i.v.) and nitric oxide synthase (L-NAME 10 mg/kg i.v.) inhibitors while worsening deformability ex vivo, they did not affect (3 mM and 10 microM, respectively) rheological functions of erythrocytes in vitro. Aggravating effects of these inhibitors on erythrocyte deformability ex vivo were reversed by prostacyclin and nitric oxide supplemented exogenously. Aspirin at a low (1 mg/kg i.v.) and high dose (50 mg/kg i.v.), contrary to indomethacin and L-NAME, aggravated erythrocyte deformability either ex vivo or in vitro. It is concluded that autocrine function of vascular endothelium plays an important role in regulation of rheology of red blood cells in flowing blood. The mechanism of this phenomenon is unclear but some possible explanations are discussed. In addition, in our experiments aspirin revealed unique erythrocyte damaging properties, possibly independent of inhibition of cyclooxygenase, but related to a direct protein acetylation.

Essential hypertension is one of the most important risk factors for cardiovascular diseases. Its pathophysiological mechanism is unknown. Recent data suggests that deformability and aggregation of red blood cells may play an important role in the regulation of blood rheology in hypertension. Simultaneously there are reports suggesting that antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) could be counteracted by high doses of aspirin. We postulate that these effects could be related to the changes in blood rheology. Accordingly we designed a study to evaluate the effect of low or high dose of aspirin on deformability and aggregability of red blood cells from patients with essential hypertension. Deformability and aggregability of red blood cells were measured by laser diffractometer (Rheodyn SSD, Myrenne GmbH) and computerized automatic aggregometer (MA1 Myrenne GmbH, Germany), respectively. The effects of aspirin on deformability and aggregation of red blood cells were studied ex vivo in whole blood from three groups of patients with essential hypertension (group I: 10 patients receiving placebo, group II: 23 patients receiving 75 mg/day p.o. aspirin for 3 days, and group III: 23 patients receiving 300 mg/day p.o. aspirin for 3 days). Subjects in all groups received the same combination of antihypertensive agents consisting of: one of ACEI (enalapril or perindopril), one of beta-antagonists (metoprolol or bisoprolol), and diuretic agent (indapamid). In patients receiving high dose of aspirin (300 mg/day) we observed that erythrocyte aggregability was 25% higher than in the placebo group (MEA = 25.8 +/- 6 SD, vs MEA = 20.6 +/- 3 SD, p0.05). Aspirin had no effects on deformability of erythrocytes or on arterial blood pressure. High doses of aspirin or possibly also other nonsteroidal anti-inflammatory drugs (NSAID) in patients receiving antihypertensive therapy can directly affect rheological properties of the blood due to the activation of red blood cell aggregation. Increased aggregation of red blood cells during antihypertensive therapy may be an important indicator of the worsening of organ perfusion.

Background: Leukotrienes are potent mediators of allergic inflammation and their role in the pathogenesis of allergic disorders, particularly asthma, is well established. Their importance in the pathogenesis of atopic eczema/dermatitis syndrome (AEDS) is still unclear. We aimed to compare urinary cysteinyl leukotriene (Cys-LT) levels during exacerbation and remission of AEDS in relation to clinical status, IgE levels, and eosinophil counts. Methods: Urinary Cys-LTs were measured by direct enzyme immunoassay in 17 adult patients with AEDS and in 17 healthy controls in whom atopy had been excluded. Cys-LTs were compared during exacerbation and remission of AEDS in relation to the clinical status measured by SCORAD. Total IgE levels were measured by enzyme-linked immunoassay (ELISA). Results: Mean clinical score during the exacerbation was 64.3 ± 3.1 and during remission 22.4 ± 4 ( P

Despite the great progress, our understanding of the pathogenesis of atopic dermatitis (AD) is still incomplete. In particular, the clinical importance of various changes of the immune system parameters is unclear. Accordingly we have undertaken the study to compare selected parameters of cellular and humoral immunity between AD subjects (n = 26) and healthy controls (n = 10). These parameters included immunoglobulin levels (IgE in particular), neutrophil respiratory, oxygen burst, peripheral blood lymphocyte phenotype and response to mitogens. We also analysed the relationship between these parameters and clinical severity of skin lesions.Mean total immunoglobulin E levels were very significantly increased in the AD group (1563 +/- 459 vs 35.5 +/- 12.1 IU/ml; p = 0.001). Simultaneously total serum IgE levels varied extensively between individual subjects with AD and were significantly correlated to clinical severity of the disease (Rs = 0.44; p = 0.02). Atopic dermatitis was also associated with the increase in the number of CD4+ and simultaneous decrease in the CD8+ lymphocytes causing statistically significant difference in CD4:CD8 ratio compared to the control group. We also observed changes of proliferation indices to phytohaemagglutinin (decrease) and increase of responses to anti CD3 mAb (OKT-3) and staphylococcal enterotoxin B. None of these immune parameters however, appeared to be statistically correlated to clinical status.We find that atopic dermatitis is associated with significant changes of several important indices of cellular and humoral immunity including increased IgE levels and altered peripheral lymphocyte proliferation capacity and phenotype. Change of total IgE levels appears to be the most important from clinical point of view.

Inflammation is a major process in the pathogenesis of bronchial asthma. Pivotal role in the induction of the inflammation in atopic subjects is played by mast cells and eosinophils and their mediators. Lymphocytes T and macrophages modulate this process. Although the pathogenesis of asthma in non-atopic subjects is not totally clear the inflammation has similar course as in asthma with IgE overproduction. Current research emphasise e.g. the role of adhesion molecules, bronchial epithelial cells and nitric oxide in the pathogenesis of asthma. Selectin E, ICAM-1, VCAM-1 take part in the migration of inflammatory cells in the asthmatic lung. Expression of these molecules is included by IL-1, TNF-alpha, and IL-4. Inflammation leads to the bronchial epithelial damage and release of proinflammatory cytokines, which augment the above process. The epithelial damage causes exposure of nerve endings, which can lead to the activation of axon reflexes. The concentration of NO in the exhaled air of asthmatics is much higher than in healthy subjects. It may be produced by inflammatory cells and may augment the inflammation as well as cause bronchial hyperresponsiveness. The better understanding of inflammatory patterns of bronchial asthma has major influence on the therapeutic approach. Inhaled anti-inflammatory drugs are of the first choice in pharmacotherapy of even mild forms of asthma.

Clinical study was conducted on 77 adult patients with hypersensitivity to honey bee venom (HBV) to determine clinical characteristics and pathogenesis of hypersensitivity to HBV as well as the effect of specific immunotherapy(ITS) with HBV on several clinical and immunological parameters. The patients studied (43 women and 34 men of age ranging between 18-61 years with a mean age at 30 years) were divided into two groups: Group 1-44 patients with a history of anaphylactic shock following honey bee sting, who received specific immunotherapy with HBV. Group 2-33 patients hypersensitive to HBV(9 people reacted with severe anaphylactic systemic reaction, while others had skin reactions) who were not treated by ITS method. In all patients skin tests with HBV allergen were conducted before and at various stages of immunotherapy. Specific IgE (I1), s-IgG4 (I1), total IgE, IgG, IgA, IgM, C3c, C4 were estimated in sera samples obtained at the beginning, during the course and at the end of ITS. Dynamics of changes of these parameters were studied during a 3-year period of ITS. The challenge tests were conducted at the end of the treatment. 86.9% of treated patients reacted with IgE-mediated reactions. They showed elevated levels of s-IgE before immunotherapy, and significant decrease in s-IgE and increase in s-IgG4 titers after ITS. 10.4% of patients showed clinical symptoms of anaphylaxis, but non-IgE mediated. IgE titer in these patients wasor = 0.2 IU/ml and has not significantly changed during immunotherapy. s-IgG, levels were in these patients below 2 micrograms/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell mediated immunity (CMI) was assessed in 43 patients with chronic bronchitis and asthma and in 41 healthy subjects. The relative and absolute number of T lymphocytes, delayed hypersensitivity skin tests to tuberculin (PPD), streptokinase-streptodornase (SKSD) andCandida antigens, the in vitro stimulation of protein synthesis in peripheral blood lymphocytes (PBL) cultured with phytohaemagglutinin (PHA) and specific antigens were determined. Serum immunoglobulin levels were also assessed. It has been found that the relative number of T lymphocytes was not changed in the patient group and the absolute number was increased. Eight patients did not respond to any of the skin-test antigens and their serum IgA was increased. PBL of nonresponding patients showed poor stimulation in vitro with PHA and no response to antigens. The clinical course of the illness in patients with depressed CMI was on average more severe when compared to the remaining patients. The results indicate that patients with chronic bronchitis and asthma may have depressed CMI but intact humoral immunity.