D. Maslinska

Distribution of tryptase-containing mast cells and metallothionein reactive astrocytes in human brains with amyloid deposits.

Alzheimer’s disease (AD) is the most common neurodegenerative disorder of the elderly, causing severe and permanent impairment of multiple cognitive faculties. The two most striking pathological features of AD are extracellular deposits of beta-amyloid plaques in the cerebral cortex and intracellular neurofi brillary tangles of hyperphosphorylated tau proteins [1]. A variety of different mechanisms has been suggested to contribute to neuronal death in AD, including genetic and environmental factors [2, 3]. Increasing data support the hypothesis that infl ammation is involved in the pathogenesis of the disease [4]. Mast-cell tryptase is a protease with proinfl ammatory activity and an important indicator of mast cell activation and degranulation [5]. Metallothionein (MT) has several putative roles in metal detoxifi cation, in scavenging free radicals, and in acute phase responses [6]. Therefore, we have studied the distribution of these two proteins in the brains of individuals with AD and in brains of patients who died within a few minutes after cardiac arrest.

Increased production of β-defensin 3 (hBD-3) by human amniotic epithelial cells (HAEC) after activation of toll-like receptor 4 in chorioamnionitis

Placenta and fetal membranes may become exposed to pathogenic microorganisms which may infl uence the embryo/fetus health. Recent investigations suggest that the placental unit may function as an active barrier, recognizing and responding to pathogens via toll-like receptors (TLRs) [1]. The TLR4 recognize lipopolysaccharide (LPS) microbial endotoxins associated with gram-negative bacteria. Various antimicrobial molecules are expressed on the surfaces of monocytes and epithelial cells [2]. Human amniotic epithelial cells (HAEC) produce antimicrobial β-defensins, especially human β-defensin 3 (hBD-3) [3]. Here we comparatively examined in vitro, infl uence of LPS on hBD-3 synthesis in normal HAEC and obtained after chorioamnionitis.

Mast cell-derived VEGF and VEGF receptor type 1, 2, and 3 expression in human term trophoblast culture—influence of hypoxia

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Mast cell number, histamine concentration and placental vascular response to histamine in preeclampsia

The pathogenesis of preeclampsia is not clear but it is believed that the placenta is the primary cause of the problem [1]. Among many theories, allergic reactions to placental products (toxins) and pathological processes that limit the uteroplacental circulation (ischaemia) must be considered [2]. The role of vasoactive agents in placental vessels is more significant than in other sites, because of the lack of sympathetic innervation in placental vessels. Histamine exerts a vasoconstrictor effect upon the placental vasculature [3]. Available literature and our own data indicate that mast cell numbers and histamine concentrations are altered in human placentas obtained after complicated pregnancies [4, 5]. The aim of the study was to examine mast cell number, histamine concentration and placental vascular response to histamine in preeclampsia.

6. Human and clinical aspects of histamine

Rheumatoid arthritis (RA) is a chronic infl ammatory disease, characterized mainly by immunological disturbances and synovial infl ammation. The importance of various endogenous mediators was confi rmed in the development of RA, however the pathogenesis of RA remains still unclear [1, 2]. Arthritic synovium manifests many pathological changes. During synovium infl ammation critical events such as neoangiogenesis, cellular hyperplasia and a massive infl ux of infl ammatory cells occurs. Normal synovial tissue consists of a scraggly intimal lining and the synovial sublining, however RA synovial tissue manifests oedema. Finally, in RA, this results in the formation of a mass of tissue (“pannus”) which serves as the origin of joint erosion [2]. Histamine is an important chemical mediator which acts at the site of infl ammation. Mast cells present in synovium are major sources of histamine [1, 3]. There are four subtypes of histamine receptors; H1, H2, H3 and H4 [4]. The H4R is proposed to be exclusively expressed on the cells with hematopoietic lineage (eosinophils, T cells, dendritic cells, basophils and mast cells) [5, 6]. Excess of expression of H4R in organs of the immune system (e. g. spleen, thymus and leukocytes) has implicated H4R in the immune system [3, 7]. The H4R mediates eosinophil histamine-induced chemotaxis and has a role in secretion of IL-16 from CD8+ T cells. Activation of H4R can cause calcium mobilization and chemotaxis in mast cells [7, 8]. While the presence of H4R in cultured synovial cells of RA patients has been documented by RTPCR technique [3], the distribution pattern of this receptor in the synovial tissue has not yet been determined. Materials and methods

Placental mast cells (MC) and histamine (HA) in pregnancy complicated by diabetes class C - relation to the development of villous microvessels

Summary The role of histamine (HA) and other mast cells (MC) mediators in local placental angiogenesis is still under consideration. In human placentae obtained after normal and complicated pregnancies MC distribution, MC numbers and HA concentrations are different. Altered vascularization in diabetes is strictly related to the severity of metabolic disorders. The White class C of diabetes in pregnancy is the last stage without recognized vascular changes. The aim of the study was to find the correlation between MC number, HA concentration and density of the network of placental vessels in diabetes White class C. Nine diabetic placentas and 9 controls were examined. HA concentration in placental samples was estimated fluorimetrically. MC in sections were marked both by tryptase/chymase antibodies and stained with toluidine blue or alcian blue. In light microscopy, using computed morphometry for quantitative analysis, the development of villous microvessels was measured in calibrated areas of the placental sections. Vascular/extravascular tissular index (V/EVTI) was calculated. The results showed that in diabetes White class C increased density of the villous network of vessels (V/EVTI: 0.33±0.027 vs 0.26±0.031 in control) correlates with higher HA concentration (365.1±36.2 ng/g of wet weight vs 251.7±22.1 ng/g of wet weight in control) and increased number of MC (5134 vs 3726 in control).

Histamine H4 receptors on mammary epithelial cells of the human breast with different types of carcinoma

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Expression of histamine H4 receptor in human osteoarthritic synovial tissue

Osteoarthritis (OA) is a progressive non-infl ammatory disorder of the joints caused by gradual loss of cartilage and resulting in the development of bony spurt and cysts with the most common location being the knee [1]. Histamine (H) affects a variety of functions in the human body including joints. Mast cells present in the synovium are the major source of histamine [2]. They often increase in number at site of active cartilage erosion. Recently histamine has been implicated in the pathophysiological processes of OA and H receptors H1 and H2 as well as histamine decarboxylase expression were demonstrated immunohistochemically in OA chondrocytes [3]. This suggests that immuno/infl ammatory reactions are involved in the pathogenesis of OA. Histamine receptors are classifi ed into four subtypes, H1, H2, H3 and H4. The histamine H4 (HH4) receptor is a member of G-protein coupled receptors (GPCRs) and preferentially expressed on the cells of hematopoietic lineage (eosinophils, T cells, dendritic cells, basophils and mast cells) [4]. We have previously shown that the novel HH4 receptor is localized in synoviocytes found in infl amed tissue of patients with rheumatoid arthritis (RA) [5]. Here we report the studies of expression of HH4 receptor in various types of synovial cells of patients with OA.

Taurine chloramine modifies adjuvant arthritis in rats.

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Taurine – chloramine is a potent antiinflammatory substance

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