Perinuclear antineutrophil cytoplasmic autoantibodies in dogs infected with various vector-borne pathogens and in dogs with immune-mediated hemolytic anemia

Abstract Objective—To determine the prevalence of perinuclear antineutrophil cytoplasmic autoantibodies (pANCA) in dogs with confirmed or suspected immune-mediated hemolytic anemia (IMHA) or dogs infected with various vector-borne pathogens, including Rickettsia rickettsii, Bartonella henselae, Bartonella vinsonii subsp berkhoffii, Ehrlichia canis, Borrelia burgdorferi, and Leishmania infantum. Animals—55 dogs with confirmed or suspected IMHA, 140 dogs seroreactive for vector-borne pathogens, and 62 healthy dogs and dogs seronegative for vector-borne pathogens. Procedures—Samples were allocated to subgroups on the basis of the health status of the dogs and the degree of seroreactivity against various vector-borne pathogens. Serum samples were tested retrospectively via indirect immunofluorescence assay to determine pANCA status. Results—26 of 55 (47%) dogs with confirmed or suspected IMHA and 67 of 140 (48%) dogs seroreactive for vector-borne pathogens had positive results when tested for pANCA. Serum samples with the highest antibody concentrations against L infantum antigen had the highest proportion (28/43 [65%]) that were positive for pANCA. One of 20 (5%) dogs seronegative for tick-borne pathogens and 8 of 22 (36%) dogs seronegative for L infantum had positive results for pANCA. One of 20 (5%) healthy dogs had serum antibodies against pANCA. Conclusions and Clinical Relevance—pANCA were detected in a high percentage of dogs with IMHA and vector-borne infectious diseases. Therefore, pANCA may be a relatively nonspecific marker for dogs with inflammatory bowel disease, although they could represent a biomarker for immune-mediated diseases and infections.</jats:p

The effect of race training on the basal gene expression of alveolar macrophages derived from Standardbred racehorses

Mild-to-moderate equine asthma is prevalent in young racehorses, particularly early in their training period. Although the precise etiopathogenesis remains undetermined, it is possible that the susceptibility of this population might partly reflect an exercise-associated immune derangement at the level of the airway. We performed a genome-wide basal gene expression scan on alveolar macrophages (AMs) isolated from Standardbred racehorses before and after commencement of competition race training with a view to identifying any exercise-associated gene expression modulation consistent with functional alterations, which might reflect training-associated immunological derangement. Microarray technology was used to analyze the basal gene expression profiles of bronchoalveolar fluid–derived AMs, harvested from six systemically healthy Standardbred racehorses before (T0) and after (T1) entry into training. In addition, AM lipopolysaccharide (LPS)-induced TNF-α and IL-10 release at T0 and T1 was assessed. Although the data revealed significant interhorse heterogeneity in relation to the magnitude of individual gene expression at each timepoint, within each horse, several inflammatory-related genes [e.g., chemokine ligands, interferons, and nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB)] declined in expression from T0 to T1. Entry into training did not significantly alter AM LPS-induced TNF-α or IL-10 release. The data support a direct effect of training on AM basal gene expression, particularly with respect to immune-related genes. The pattern of training-associated differential gene expression may indicate relative downregulation of inflammatory-related genes, consistent with an immunosuppressive effect of training and an increased susceptibility to opportunistic pathogens