Background: Phagocytic activity of neonatal foals has been reported to be similar to that of adult horses, but serum opsonization capacity develops with age and may be further altered when opsonins are consumed during infection.
Hypothesis: Phagocytosis, oxidative burst activity, and serum opsonization capacity in neonatal foals admitted to an intensive care unit are reduced in comparison with control foals.
Animals: Blood samples were collected from hospitalized neonatal foals and from control foals. Hospitalized foals were characterized as sick or septic on the basis of a sepsis score and received intravenous plasma transfusion.
Methods: Phagocytosis, oxidative burst activity, and serum opsonization capacity were tested with flow cytometric analysis. Serum immunoglobulin and complement component 3 concentrations were determined with radial immunodiffusion. Serum amyloid A concentration was assayed with a commercially available solid-phase Sandwich ELISA Kit. Data were analyzed with nonparametric and regression methods. Alpha was set at P = .05.
Results: Phagocytic functions of septic and sick foals were lower than control foals in the initial phase of the study (P = .01). Opsonization capacity was significantly higher when bacteria were opsonized with serum from septic (P = .029) and sick (P = .006) foals than from control foals on day 1. Opsonization capacity in septic foals was comparable with control foals on days 2 and 5. This effect was not accompanied by an increase in serum complement C3 or immunoglobulin G concentrations independently.
Conclusions And Clinical Importance: Our results suggest that phagocytic function could be decreased in hospitalized foals. The synergistic effect of opsonic elements provided by plasma transfusion may sustain opsonization capacity during sepsis.
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http://dx.doi.org/10.1892/0891-6640(2007)21[797:socpao]2.0.co;2 | DOI Listing |
FEMS Microbes
October 2024
Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL 32610, United States.
is ranked among the top five bacterial pathogens responsible for catheter-associated urinary tract infections, wound infections, secondary root canal infections, and infective endocarditis. Previously, we showed that inactivation of either the manganese- and iron-binding (EfaA) or zinc-binding (AdcA and AdcAII) lipoproteins significantly reduced virulence. Here, we explored whether immunization using a multi-valent approach induces protective immunity against systemic enterococcal infections.
View Article and Find Full Text PDFVaccine
December 2024
Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7DQ, UK; Department of Biology, University of Oxford, Oxford OX1 3RB, UK. Electronic address:
A new and more effective tuberculosis (TB) vaccine is urgently needed, but development is hampered by the lack of validated immune correlates of protection. Bacillus Calmette Guérin (BCG) vaccination by the aerosol (AE) and intravenous (IV) routes has been shown to confer superior levels of protection from challenge with Mycobacterium tuberculosis (M.tb) in non-human primates (NHP) compared with standard intradermal (ID) administration.
View Article and Find Full Text PDFFront Vet Sci
August 2024
Department of Specialty Medicine, College of Veterinary Medicine, Midwestern University, Glendale, AZ, United States.
Naturally occurring diabetes mellitus (NODM) is one of the most common endocrine disorders in dogs and its etiology closely resembles type 1 diabetes mellitus (T1DM) in people. Human patients with T1DM commonly have cellular derangements consistent with inflammation, impaired immune function, and hypovitaminosis D. There is little information available regarding inflammatory biomarkers, immune function, and vitamin D status in diabetic dogs.
View Article and Find Full Text PDFPLoS One
August 2024
Department of Life Sciences, Syed Babar Ali School of Science and Engineering, Lahore University of Management Sciences, Lahore, Pakistan.
Vaccine
October 2024
School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD 4072, Australia. Electronic address:
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