Semen collection and evaluation of captive coatis (Nasua nasua) / Coleta e avaliação de sêmen de coatis (Nasua nasua) mantidos em cativeiro

Semen samples (n=105) were collected through eletroejaculation from six adult male coatis (Nasua nasua) between January 2007 and December 2008 at Universidade Federal de Mato Grosso Zoo, Cuiabá, Brazil. Mean values were: volume (mL); concentration (sperm/mL); total motility (%); progressive sperm motility (scale, 0-5); live spermatozoa (%); acrossome integrity (%); primary defects (%); and secondary defects (%). There was high correlation between total motility and live sperm; total motility and progressive sperm motility; total motility and acrossome integrity; live sperm and progressive motility; live sperm and acrossome integrity and volume and concentration. The method for semen collection was considered safe and efficient. It can be used for the evaluation of breeding potential of coati in captivity and for the establishment of new assisted reproductive technology (ART) for threatened neotropical carnivores species.

Amostras de sêmen (n=105) foram coletadas por eletroejaculação em seis coatis (Nasua nasua) machos adultos entre Janeiro de 2007 a Dezembro de 2008 no Zoológico da Universidade Federal de Mato Grosso, Cuiabá, Brasil. Os valores mensurados foram: volume (mL); concentração (espermatozoides/mL); motilidade (%); vigor (escala: 0-5); espermatozoides vivos (%); acrossomas íntegros (%); defeitos primários (%) e defeitos secundários (%). Houve alta correlação entre motilidade e espermatozoides vivos, motilidade e vigor; motilidade e integridade de acrossoma; espermatozoides vivos e vigor; espermatozoides vivos e integridade de acrossoma; e volume e concentração. O método de colheita de sêmen foi seguro e eficiente podendo ser indicado para avaliação do potencial reprodutivo de coatis mantidos em cativeiro e para o estabelecimento de tecnologias de reprodução assistida (TRA) para espécies de carnívoros neotropicais ameaçadas de extinção.

Eicosanoid-mediated proinflammatory activity of Pseudomonas aeruginosa ExoU.

As Pseudomonas aeruginosa ExoU possesses two functional blocks of homology to calcium-independent (iPLA(2)) and cytosolic phospholipase A(2) (cPLA(2)), we addressed the question whether it would exhibit a proinflammatory activity by enhancing the synthesis of eicosanoids by host organisms. Endothelial cells from the HMEC-1 line infected with the ExoU-producing PA103 strain exhibited a potent release of arachidonic acid (AA) that could be significantly inhibited by methyl arachidonyl fluorophosphonate (MAFP), a specific PLA(2) inhibitor, as well as significant amounts of the cyclooxygenase (COX)-derived prostaglandins PGE(2) and PGI(2). Cells infected with an isogenic mutant defective in ExoU synthesis did not differ from non-infected cells in the AA release and produced prostanoids in significantly lower concentrations. Infection by PA103 induced a marked inflammatory response in two different in vivo experimental models. Inoculation of the parental bacteria into mice footpads led to an early increase in the infected limb volume that could be significantly reduced by inhibitors of both COX and lipoxygenase (ibuprofen and NDGA respectively). In an experimental respiratory infection model, bronchoalveolar lavage (BAL) from mice instilled with 10(4) cfu of PA103 exhibited a marked influx of inflammatory cells and PGE(2) release that could be significantly reduced by indomethacin, a non-selective COX inhibitor. Our results suggest that ExoU may contribute to P. aeruginosa pathogenesis by inducing an eicosanoid-mediated inflammatory response of host organisms.

Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages.

After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease, a debilitating cardiac illness caused by the protozoan Trypanosoma cruzi. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with T. cruzi fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-beta (TGF-beta) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-beta release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it in vivo. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.