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Veterinary immunology and immunopathology2006; 112(3-4); 199-209; doi: 10.1016/j.vetimm.2006.02.010

Foals are interferon gamma-deficient at birth.

Abstract: The increased vulnerability of foals to specific pathogens such as Rhodococcus equi is believed to reflect an innate immunodeficiency, the nature of which remains poorly understood. Previous studies have demonstrated that neonates of many species fail to mount potent Th1 responses. The current research investigates the ability of circulating and pulmonary lymphocytes of developing foals to produce interferon gamma (IFNgamma). Peripheral blood mononuclear cells (PBMC) were prepared from up to 10 horse foals at regular intervals throughout the first 6 months of life. Bronchoalveolar lavage (BAL) samples were collected at 1, 3 or 6 months of age from three groups of five foals. The PBMC and BAL cells were stimulated in vitro and IFNgamma production was measured by intracellular staining. In addition, RNA was extracted from freshly isolated and in vitro stimulated PBMC and BAL cells for quantitation of IFNgamma gene expression by real time PCR. Newborn foals exhibited a marked inability to express the IFNgamma gene and produce IFNgamma protein. This deficiency was observed in both circulating and pulmonary lymphocytes. However, IFNgamma gene expression and protein production increased steadily throughout the first 6 months of life, reaching adult levels within the first year of life. These findings suggest that foals are born with an inherent inability to mount a Th1-based cell mediated immune response which may contribute to their susceptibility to intracellular pathogens.
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Publication Date: 2006-04-18 PubMed ID: 16621024DOI: 10.1016/j.vetimm.2006.02.010Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research suggests that baby horses (foals) are born with a significant deficiency in creating interferon gamma, a protein that’s vital for immune response. This deficiency, present in both their circulating and pulmonary lymphocytes, could contribute to their susceptibility to intracellular pathogens.

Objectives and Methodology of the Study

  • The study aimed to understand the nature of the seemingly innate immunodeficiency in foals, contributing to their increased vulnerability to specific pathogens such as Rhodococcus equi. A particular focus was on the foals’ ability to produce interferon gamma, an essential part of Th1 responses, which are critical for immunity against intracellular pathogens.
  • The foals’ ability to produce interferon gamma was assessed by preparing peripheral blood mononuclear cells (PBMC) from up to 10 foals at regular intervals throughout their first six months of life.
  • Bronchoalveolar lavage (BAL) samples were also collected from three groups of five foals at 1, 3 or 6 months of age.
  • The team then stimulated the PBMC and BAL cells in vitro (in a controlled, experimental environment outside of the organism), and measured IFNgamma production by staining the intracellular components. Simultaneously, RNA was extracted from both freshly isolated and in vitro stimulated PBMC and BAL cells, in order to quantify IFNgamma gene expression using real-time polymerase chain reaction (PCR).

Findings and Implications

  • The team observed that newborn foals demonstrated a severe inability to express the IFNgamma gene and to produce IFNgamma protein. This deficiency was found both in the circulating and pulmonary lymphocytes – cells which play a significant role in the immune system.
  • This capacity to express the IFNgamma gene and to produce the associated protein, however, increased gradually over the first six months of life, reaching the levels found in adult horses within the first year.
  • These findings provide evidence suggesting foals are born with an inherent incapacity to mount an effective Th1-based cell-mediated immune response, which possibly makes them more susceptible to intracellular pathogens.
  • The observations of this study contribute significant insights to understanding the immunodeficiency in foals, and could pave the way for potential preventive strategies or treatments to boost immune responses during the early stages of their life.

Cite This Article

APA
Breathnach CC, Sturgill-Wright T, Stiltner JL, Adams AA, Lunn DP, Horohov DW. (2006). Foals are interferon gamma-deficient at birth. Vet Immunol Immunopathol, 112(3-4), 199-209. https://doi.org/10.1016/j.vetimm.2006.02.010

Publication

Veterinary immunology and immunopathology
ISSN: 0165-2427
NlmUniqueID: 8002006
Country: Netherlands
Language: English
Volume: 112
Issue: 3-4
Pages: 199-209

Researcher Affiliations

Breathnach, C C
  • Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA.
Sturgill-Wright, T
    Stiltner, J L
      Adams, A A
        Lunn, D P
          Horohov, D W

            MeSH Terms

            • Age Factors
            • Animals
            • Animals, Newborn
            • Bronchoalveolar Lavage Fluid / cytology
            • Bronchoalveolar Lavage Fluid / immunology
            • Colostrum / immunology
            • Flow Cytometry / veterinary
            • Gene Expression Regulation
            • Horses / genetics
            • Horses / immunology
            • Immunity, Innate / immunology
            • Interferon-gamma / deficiency
            • Interferon-gamma / genetics
            • Interferon-gamma / immunology
            • Ionomycin / pharmacology
            • Leukocytes, Mononuclear / drug effects
            • Leukocytes, Mononuclear / immunology
            • Lymphocyte Activation
            • Lymphocytes / immunology
            • RNA, Messenger / biosynthesis
            • RNA, Messenger / genetics
            • Random Allocation
            • Reverse Transcriptase Polymerase Chain Reaction / veterinary
            • Tetradecanoylphorbol Acetate / pharmacology

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