Culture of mouse peritoneal macrophages with mouse serum induces lipid bodies that associate with the parasitophorous vacuole and decrease their microbicidal capacity against Toxoplasma gondii

Lipid bodies [lipid droplets (LBs)] are lipid-rich organelles involved in lipid metabolism, signalling and inflammation. Recent findings suggest a role for LBs in host response to infection; however, the potential functions of this organelle in Toxoplasma gondii infection and how it alters macrophage microbicidal capacity during infection are not well understood. Here, we investigated the role of host LBs in T. gondii infection in mouse peritoneal macrophages in vitro. Macrophages cultured with mouse serum (MS) had higher numbers of LBs than those cultured in foetal bovine serum and can function as a model to study the role of LBs during intracellular pathogen infection. LBs were found in association with the parasitophorous vacuole, suggesting that T. gondii may benefit from this lipid source. Moreover, increased numbers of macrophage LBs correlated with high prostaglandin E2 (PGE2) production and decreased nitric oxide (NO) synthesis. Accordingly, LB-enriched macrophages cultured with MS were less efficient at controlling T. gondii growth. Treatment of macrophages cultured with MS with indomethacin, an inhibitor of PGE2 production, increased the microbicidal capacity against T. gondii. Collectively, these results suggest that culture with MS caused a decrease in microbicidal activity of macrophages against T. gondii by increasing PGE2 while lowering NO production.

Interleukin 1 and receptor expression, kinetics of cyclooxygenase and synthesis of prostaglandin E2 in keratoconus cells

As inetrleukin increases secretions of prostaglandin E2 and collagenase, we have investigated the number of membrane receptors for this cytokine on keratoconus fibroblasts and determined the corresponding dissociation constant [Kd]. We have also studied kinetics of cyclooxygenase, synthesis of prostaglandins E2, interleukin 1 and collagen. The data were compared with those from human normal cornea fibroblasts. Eight normal corneas and eight keratoconus were studied. Cells were seeded in 24-well plated, at a concentration of 50,000 cells per well and cultured for 24 hours before the experiments. Increasing concentrations of 125 I labelled IL1 were added to the wells. The number of receptors for IL1 was found to be 4 fold higher for keratoconus. Consequently, synthesis of PGE2 is ten times more in keratoconus than in normal cornea cells, and collagen synthesis decreased in keratoconus. Relation between inflammatory disease and keratoconus are discussed

Prostaglandin E, cortisol and thyroid hormones in cases of rhinoscleroma

Prostaglandin E, cortisol and T[3] and T[4] were assayed in sera of rhinoscleromatous patients [40 subjects], contacts [20 subjects] and controls [20 subjects]. Prostaglandin E was found significantly elevated [P < 0.001] in patients with rhinoscleroma as compared to controls. This finding can be explained on the ground of increased production at the site of inflammatory process and its transport to blood. No changes were reported in contacts [P > 0.05]. Statistically significant changes were not found when cortisol levels were considered [P > 0.05]. Cortisol is known to be correlated with prostaglandin only when given in therapeutic doses, but in this work all patients and contacts were not under steroid therapy. Thyroid hormones were also not changed in group II and III subjects [P > 0.05]. It appears that there is no role of prostaglandin-which are increased in rhinoscleroma-in thyroid hormones production in euthyroid subjects as it can only induce thyroid hormones production in hyperthyroid subjects

Prostaglandin E in chronic liver disease: relation to specific pathology

Recent works have substantiated the possible role of prostaglandins [PGs] in the pathogenesis of various manifestations and complications of liver cirrhosis. The relation to specific pathology and hepatic functional class in Egyptians with chronic liver disease is not known. Plasma PGE was measured by radioimmunoassay in 40 males with chronic liver disease compared with 10 healthy controls. Specific liver disease was determined according to histopathologic criteria, Functional class was graded as A, B and C according to Pugh Scale. Plasma PGE [Mean +/- SD ng/ml] was higher in patients with chronic liver disease than in healthy controls [5.12 +/- 1.02 VS 1.61 +/- 0.28, P < 0.01]. Patients with pure cirrhosis and those with mixed cirrhosis had higher levels than those with pure schistosomal [Sch] fibrosis [5.45 +/- 1.15, 5.54 +/- 0.94 VS 4.19 +/- 0.31, P < 0.01] with no significant difference between the two cirrhotic groups. PGE was higher in grade B and C than in grade A [6.13 +/- 0.37, 6.03 +/- 0.32 VS 4.15 +/- 0.30, P < 0.05] with no significant difference between grade B and C. Ascetics had higher PGE than non-ascetics [6.09 +/- 0.28 VS 4.15 +/- 0.30, P < 0.01]. Patients with skin vascular changes had higher levels than those without [6.4 +/- 0.28 VS 4.93 +/- 0.96, P < 0.01]. We conclude that plasma PGE is high in chronic liver disease. Cirrhotics with or without Sch. fibrosis have higher levels than those with pure Sch. fibrosis. Ascites and the functional class of liver disease are determining factors

El sistema monocito-macrófago en la enfermedad de Hodgkin / The monocyte-macrophage system in Hodgkin's disease

La enfermedad de Hodgkin (EH) se caracteriza por la aparición de un tumor en los ganglios linfáticos constituido por una gran variedad de células que se asemejan a una reacción inflamatoria inespecífica. Las células de Reed-Sternberg (R-S) presentes en la granuloma tienen características citogenéticas, de cultivo y de heterotransplantabilidad que parecen neoplásicas. Su origen más probable es en las células interdigitantes ganglionares derivadas de los macrófagos. Al ser el ganglio linfático un órgäo inmunológico, sus alteraciones se manifestan en defectos de la respuesta inmune, los cuales pueden deberse tanto a la expresión de la calidad de las mismas. En la EH la alteración de la respuesta inmune se observa en estadíos precoces, aún con una mínima extensión de compromiso ganglionar, lo que sugiere más una lesión cualitativa que cuantitativa. Teniendo en cuenta que el origen más probable de esta extraña neoplasia es la célula de R-S y que ésta deriva de los macrófagos, investigamos la capacidad funcional de los monocitos sanguíneos transformados in vitro en macrófagos. Se estudió su capacidad fagocítica y lítica a través de la generación de productos tóxicos del oxígeneo, medidos por quimioluminiscencia y citomorfologia. Se encontró un defecto en la generación de productos tóxicos del oxígeno, que se debía a un exceso en la producción de PGE2 y era corregido por inhibidores de la síntesis de prostaglandinas (ciclooxigenasas); este defecto aparece precozmente en la EH y continúa...