ABSTRACT
Brachiaria spp. is the predominate pasture grass for cattle grazing in the Orinoco watershed in Colombia. However, it has been recognized that this grass can cause liver damage, leading to photosensitization in ruminants; such injury is caused by the steroidal saponins found in this plant. Liver samples taken from five clinically-healthy bulls' left and right liver lobes and portal vein entrance were processed by routine histological techniques to evaluate liver lesions caused by Brachiaria decumbens in cattle grazing on Colombia's Eastern plains. The main lesions observed in these tissues were mononuclear cell cholangiohepatitis, foamy macrophages, moderate bile pigment accumulation, hepatocyte death, binucleated hepatocytes, moderate bile duct hyperplasia and multiple foci of mild fibrosis in portal areas; these were corroborated by Masson's trichrome staining. Such lesions were predominantly distributed at the portal vein entrance, frequently being located in the periportal region. This type of lesion has usually been attributed to Brachiaria decumbens consumption, and was present in clinically healthy animals exclusively feeding on this type of grass. Thus we conclude that the tissue alterations found herein were caused by Brachiaria decumbens. This research should be expanded to involve a larger selection of cattle populations, throughout a broader geographical region.
En la Orinoquía colombiana hay una considerable cantidad de ganado bovino que se alimenta predominantemente de Brachiaria spp. Sin embargo, se ha reconocido que esta pastura puede ocasionar daño hepático y posterior fotosensibilización en rumiantes, por las saponinas esteroidales que contiene. Con el propósito de evaluar las lesiones hepáticas en ganado bovino procedente de los Llanos Orientales colombianos, se tomaron y procesaron, mediante técnicas histológicas de rutina, muestras de hígado de los lóbulos derecho e izquierdo, así como de la entrada de la vena porta de cinco toros clínicamente sanos. Las principales lesiones observadas en estos tejidos fueron colangiohepatitis mononuclear, macrófagos espumosos, acumulación moderada de pigmentos biliares, muerte de hepatocitos, hepatocitos binucleados, moderada hiperplasia de ductos biliares y múltiples focos de fibrosis leve en áreas periportales, que fueron corroborados por tinción tricrómica de Masson. Estas lesiones se distribuyeron predominantemente en la entrada de la vena porta y se localizaron con frecuencia en la entrada de la región periportal. Dado que estas lesiones se atribuyen comúnmente al consumo de Brachiaria decumbens, y estaban presentes en animales clínicamente sanos exclusivamente alimentados con esta pastura, se concluye que las lesiones aquí encontradas fueron causadas por la Brachiaria decumbens. Se sugiere ampliar este estudio involucrando más bovinos, granjas y municipios.
ABSTRACT
Macrophages harvested from the peritoneal cavities of rats release a neutrophil chemotactic factor (MNCF) in response to stimulation with Gram-negative bacterial lipopolysaccharide (LPS). MNCF has been shown to be active in rats treated with dexamethasone, a glucocorticoid that usually inhibits the neutrophil migration induced in this species by interleukin (IL)-1, tumour necrosis factor alpha (TNFalpha), IL-8, C5a and leukotriene B(4) (LTB(4)). Here we report that macrophages harvested from peritoneal cavities of mice, and stimulated in vitro with LPS, also release a factor that induces neutrophil migration in dexamethasone-treated animals. This chemotactic activity was neutralized by the incubation of the LPS-stimulated macrophage supernatants with a purified polyclonal IgG anti-mouse TNFalpha. In addition, significant amounts of TNF were detected in the supernatants. The neutrophil migration induced by intraperitoneal administration of recombinant murine TNFalpha was also unaffected by pretreatment of the mice with dexamethasone. Moreover, neutrophil migration induced by intraperitoneal injection of LPS was completely blocked by pretreatment of the mice with a monoclonal antibody against murine TNFalpha. In conclusion, our results support the hypothesis that, in contrast to the role of TNF in rats (where it indirectly induces neutrophil migration), in mice, it may be an important mediator in the recruitment of neutrophils to inflammatory sites.