Salivary, serum, and abomasal mucus IgA as an immune correlate of protection against Haemonchus contortus infection in naturally infected lambs.

This study aimed to evaluate salivary, serum, and abomasal mucus IgA levels in lambs naturally infected with Haemonchus contortus. Thirty-seven crossbred lambs (½ Texel or ½ Ile de France) with an average age of 193 days were evaluated for 56 days after grazing on a contaminated pasture. Fecal samples were collected every 7 days to evaluate the EPG. Blood and saliva samples were collected for IgA measurement every 14 days. On D56, 29 animals were killed for parasite counting and IgA quantification in the abomasal mucus. Salivary, serum, and abomasal mucus IgA were measured by ELISA using third-stage larvae antigens. Salivary and mucus IgA were not correlated, but D14 salivary IgA correlated with EPG on D28 (r = -0.37) and D56 (r = -0.36); D28 salivary IgA correlated with D49 (r = -0.40) and D56 EPG (r = -0.44). Abomasal mucus IgA negatively correlated with EPG from D28 to D56 (r varied from _0.51 to -0.62) and with the counts of all parasitic stages (-0.60 to -0.67). The lambs were classified as susceptible (S) or resistant (R) according to EPG (D56 EPG and cumulative EPG) or IgA (salivary, serum, and mucus IgA). Based on D56 EPG and cumulative EPG, resistant lambs had higher D14 salivary IgA, mucus IgA, and total worm counts. For evaluations based on IgA levels, the EPG of S and R animals differed, indicating that IgA was an immune correlate of protection against natural infection with Haemonchus sp., mainly in the saliva sample of D14.

Relevance of antibodies against the Chicken Anaemia Virus.

Chicken Infectious Anaemia (CIA) Virus (CAV) inhibits the function of multiple immune compartments. Mortality due to clinical infection is controlled in broilers by passive immunization derived from vaccinated breeders. Therefore, serological tests are often used in chicks to determine maternally-derived antibodies (MDA). We used a vaccine overdose-induced model of CIA. The model replicated the most common features of the disease. This model was used to determine the role of MDA in the protection of chicks. Hatchlings were tested for anti-CAV titers by ELISA and were sorted into groups based on antibody levels. SPF chicks were used as a no-antibody control. Lower specific antibody levels seemed to facilitate viral entry into the thymus, but viral levels, CD4+ and CD8+ counts, thymus architecture, and haematocrit were preserved by MDA, regardless of its levels. Levels of MDA are not correlated with protection from CIA, but are important for the progression CAV infection.

De novo galectin-3 expression influences the response of melanoma cells to isatin-Schiff base copper (II) complex-induced oxidative stimulus.

Galectin-3, a ubiquitous member of the galectin family, has been shown to control cellular proliferation, adhesion, migration and apoptosis; thus, it has a role in tumor development and progression. Galectin-3 expression is both up- and down-regulated during melanoma progression. However, conflicting data regarding its roles in tumor biology prompted us to investigate if the presence of galectin-3 influences the response of melanoma cells to a novel metallodrug because metastatic melanoma acquires chemo resistance and is reported to be redox-sensitive. Previously, it was demonstrated that the complex [bis-(2-oxindol-3-yl-imino)-2-(2-aminoethyl) pyridine-N,N'] copper (II) perchlorate, herein referred to as [Cu(isaepy)], induces ROS formation and apoptosis in neuroblastoma cells through mitochondrial uncoupling and the activation of AMPK/p38/p53 signaling. Here, we used a model of vertical growth melanoma (TM1), in which GAL3 expression is lost during tumor progression. When de novo expressed, galectin-3 was found to be ubiquitously present in all subcellular compartments. Our results demonstrate that de novo galectin-3 expression impairs the cellular antioxidant system and renders TM1G3 cells more susceptible than GAL3-null TM1MNG3 cells to [Cu(isaepy)] treatment. This compound, in contrast with the redox inactive [dichloro (2-oxindol-3-yl-imino)-2-(2-aminoethyl) pyridine-N,N'] zinc (II), herein referred to as [Zn(isaepy)], leads to increased intracellular ROS accumulation, increased carbonyl stress, increased mitochondrial depolarization, decreased cell adhesion, increased p38 activation and apoptosis in TM1G3, compared with TM1MNG3. Cell death was shown to be dependent on a hydrogen peroxide-derived species and on the activation of p38. Because mitochondria are a target of both [Cu(isaepy)] and galectin-3, we propose that the presence of galectin-3 in this organelle favors increased ROS production, thereby inducing oxidative cellular damage and apoptotic death. Therefore, [Cu(isaepy)] may be envisaged as a possible anti-melanoma strategy, particularly for melanomas that express galectin-3.