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Here we evaluated the ability of l-theanine in preventing experimental hepatic cirrhosis and investigated the roles of nuclear factor-κB (NF-κB) activation as well as transforming growth factor β (TGF-β) and connective tissue growth factor (CTGF) regulation. Experimental hepatic cirrhosis was established by the administration of carbon tetrachloride (CCl4) to rats (0.4 g/kg, intraperitoneally, three times per week, for 8 weeks), and at the same time, adding l-theanine (8.0 mg/kg) to the drinking water. Rats had ad libitum access to water and food throughout the treatment period. CCl4 treatment promoted NF-κB activation and increased the expression of both TGF-β and CTGF. CCl4 increased the serum activities of alanine aminotransferase and γ-glutamyl transpeptidase and the degree of lipid peroxidation, and it also induced a decrease in the glutathione and glutathione disulfide ratio. l-Theanine prevented increased expression of NF-κB and down-regulated the pro-inflammatory (interleukin (IL)-1β and IL-6) and profibrotic (TGF-β and CTGF) cytokines. Furthermore, the levels of messenger RNA encoding these proteins decreased in agreement with the expression levels. l-Theanine promoted the expression of the anti-inflammatory cytokine IL-10 and the fibrolytic enzyme metalloproteinase-13. Liver hydroxyproline contents and histopathological analysis demonstrated the anti-fibrotic effect of l-theanine. In conclusion, l-theanine prevents CCl4-induced experimental hepatic cirrhosis in rats by blocking the main pro-inflammatory and pro-fibrogenic signals. [ABSTRACT FROM AUTHOR]

The kinetics of gene expression and the cellular source of murine beta -defensin-3 (mBD3) and murine beta -defensin-4 (mBD4) were determined in mouse models of progressive pulmonary tuberculosis and latent infection induced by high or low infecting doses, respectively. During progressive disease, there was an initial rapid expression of both defensins by respiratory epithelial cells that correlated with temporary control of bacillary proliferation, but expression decreased during the later progressive phase of the disease. In latent infection, both defensins were expressed continuously, but they were suppressed after reactivation of the disease. Thus, mycobacterial infection induces the expression of mBD3 and mBD4, and both might participate in the control of mycobacterial growth. [ABSTRACT FROM AUTHOR]

Existing descriptions of morphological correlates of light- and dark-adaptation in crayfish photoreceptors are primarily concerned with changes of the rhabdom or components derived from it, and little is known about mechanisms involved in screening pigment migration and other transformations that take place in the cytoplasm of the retinula cells. In the present study, electron microscopy was used to examine the effects of light and darkness on the cytoplasmic structure of the retinula cells. In the light-adapted state a multitude of pigment granules and many small vacuoles are dispersed throughout the cells (Figs. 1 a and 2a). On dark-adaptation the granules are withdrawn towards the axon and many of the small vacuoles in the cell body are replaced by large cisternae (Figs. 1b and 2b). The cisternae attain maximal development in the distal cytoplasm, close to the nucleus, and they do not show a preferential association with the rhabdom. Vacuoles of intermediate size and some pigment granules are seen in partly-adapted retinula cells (Fig. 3). A decrease in the density of the ground substance is observed in the cell body of dark-adapted specimens. At least part of the ground substance is constituted by a fuzzy filamentous material that in thin-sections appears surrounding and often interconnecting the pigment granules and other structures (Fig. 4). In thick-sections observed with stereo high-voltage electron microscopy, this material is revealed as a threedimensional fibrous matrix in which the pigment particles are suspended (Fig. 5). This matrix appears more compact where the granules aggregate, suggesting that it moves with the pigment. The transformation of small vacuoles into large cisternae, interpreted as equivalent to the growth of a subrhabdomal palisade in other compound eyes, is proposed to represent a structural adjustment related to the withdrawal of a cytoskeletal complex of pigment granules and their associated matrix during dark-adaptation (Fig. 6). [ABSTRACT FROM AUTHOR]

Los péptidos antimicrobianos son moléculas efectoras clave en la inmunidad innata. Generalmente contienen de 15 a 45 residuos de aminoácidos y en su gran mayoría poseen carga positiva, además de que tienen la propiedad de ser anfipáticos. Estos péptidos son secretados por células epiteliales y leucocitos, como es el caso de los macrófagos y neutrófilos. En la actualidad, con base en la traducción de secuencias en programas computacionales se han descrito más de 800 tipos de péptidos antimicrobianos distribuidos en los reinos animal y vegetal. Estos péptidos pueden ser clasificados de acuerdo con su conformación estructural y la ubicación de sus puentes disulfuro. Las defensinas constituyen uno de los tipos de péptidos antimicrobianos más estudiados, y se dividen en dos familias de acuerdo con la ubicación de sus puentes disulfuro: alfa-defensinas y beta-defensinas. Algunas de estas defensinas pueden ser inducidas por citocinas proinflamatorias, así como por moléculas propias de patógenos, y se ha observado que están relacionadas con la inmunopatogenia de varias enfermedades. El papel principal de los péptidos antimicrobianos es la lisis directa de microorganismos; sin embargo, a la fecha también se han descrito propiedades quimiotácticas, que le permiten modular el sistema inmune y de esta forma constituir un puente entre la inmunidad innata y la inmunidad adaptativa. Actualmente se han iniciado estudios con la posibilidad de utilizar esta clase de moléculas como nuevos fármacos en diferentes tipos de enfermedades infecciosas.