An evaluation of potential correlations between pathophysiologic mechanisms, clinical manifestations, and management of rosacea.

This article discusses rosacea, a common facial dermatosis of uncertain etiology and recent investigations that have begun to shed considerable light on the sequence of events leading to clinical manifestations of rosacea. The article content is based on a dedicated meeting about rosacea sanctioned by the American Acne & Rosacea Society (AARS) and represents the consensus of the authors and AARS Board of Directors.

[Study of anti-inflammatory activity of some organic and inorganic magnesium salts in rats fed with magnesium-deficient diet].

The purpose of the present research was comparative study of anti-inflammatory action of some Mg salts in rats fed with Mg-deficient diet. It was shown in our study that administration of Mg L-aspartate with pyridoxine leads to higher compensation of Mg deficiency in rats with diet-induced Mg depletion as compared with other Mg supplementations. According to the Mg deficiency correction rate Mg salts may be ranged in the following order: Mg L-aspartate with pyridoxine > or = Mg chloride with pyridoxine > or = Mg lactate with pyridoxine > or = Mg L-aspartate > Mg chloride > Mg orotate. In our study administration of Mg salts resulted in decreased number of blood leukocytes, reduced peripheral vasodilation visible in the external ear, decreased spleen weight, and as consequences in reduced inflammatory and immunological response. According to correction rate of the inflammatory response Mg salts may be ranged in the following order: Mg orotate > or = Mg chloride > or = Mg chloride with pyridoxine > or = Mg L-aspartate > or = MgL-aspartate with pyridoxine > or = Mg lactate with pyridoxine.

Uric acid, a nucleic acid degradation product, down-regulates dsRNA-triggered arthritis.

Uric acid, the naturally occurring degradation product of purine metabolism, is a danger signal, driving maturation of dendritic cells. It is well known that uric acid crystals display potent proinflammatory properties--the cause of gout--whereas the biological properties of soluble uric acid are less well documented. We have demonstrated previously that nucleic acids of endogenous and exogenous origin display proinflammatory properties. The aim of the present study was to assess the impact of soluble uric acid on in vivo inflammatory responses. Mice were administered with uric acid suspension in saline or saline alone prior to induction of neutrophil-mediated inflammation, delayed-type hypersensitivity, histamin-induced edema (measure of vasodilation capacity), as well as double-stranded (ds)RNA-triggered arthritis. Frequency and severity of arthritis were decreased significantly in mice exposed to dsRNA and simultaneously treated with uric acid as compared with saline-treated controls. Also, granulocyte-mediated inflammatory response and vasodilation capacity were reduced significantly in mice treated with uric acid as compared with their control group. The data suggest that down-regulation of inflammation was mediated by skewing the inflammatory response from the peripheral sites to the peritoneal cavity and down-regulating vasodilatatory capacity and thereby affecting leukocyte migration. In contrast, the T cell-mediated delayed-type hypersensitivity reaction was not affected significantly in mice exposed to uric acid. These findings demonstrate that uric acid displays a potent, distant anti-inflammatory effect in vivo. This property seems to be mediated by down-regulation of neutrophil influx to the site of inflammatory insult.

Markedly increased nasal blockage by intranasal leukotriene D4 in an experimental allergic rhinitis model: contribution of dilated mucosal blood vessels.

We examined whether nasal hyperresponsiveness to leukotriene (LT) D4 is seen in our allergic rhinitis model, which showed sneezing and biphasic nasal blockage by repeated antigen inhalation challenge, and whether a dilatation of mucosal blood vessels contributes to this hyperresponsiveness. Nasal blockage [increase of specific airway resistance (sRaw)] was indexed as nasal (hyper)responsiveness. The sensitized-challenged guinea pig showed a remarkable dose-dependent increase in sRaw by intranasal instillation of LTD4 (10 microl/nostril) at 10(-10) to 10(-6) M 10 h and 2 days but not 7 days after the challenge. The increase in sRaw induced by LTD4 was largely blocked by pranlukast or naphazoline, and this was dose-dependently suppressed by N(omega)-nitro-L-arginine methyl ester. Sodium nitroprusside induced an elevation of sRaw in the sensitized-challenged animal in the hyperresponsiveness state, but the degree did not differ from that in the non-sensitized-non-challenged group. The amount of NO2- and NO3- in nasal cavity lavage fluid after LTD4 instillation in the sensitized-challenged animal in the hyperresponsiveness state was significantly greater than that before the instillation. These results demonstrate that the hyperresponsiveness to LTD4 acquired by repeated antigen challenge is mainly due to dilatation of nasal blood vessels, which can be related to hyperproduction of nitric oxide through cysteinyl LT1-receptor activation.