Foals are interferon gamma-deficient at birth

Area of Science:

• Equine immunology
• Neonatal immunology
• Cell-mediated immunity

Background:

• Foals exhibit increased susceptibility to pathogens like Rhodococcus equi, possibly due to innate immunodeficiency.
• Neonatal immune responses, particularly Th1 responses, are often underdeveloped in many species.
• The specific nature of foal immunodeficiency, especially regarding cell-mediated immunity, is not well understood.

Purpose of the Study:

• To investigate the capacity of circulating and pulmonary lymphocytes in developing foals to produce interferon gamma (IFNγ).
• To assess the developmental trajectory of IFNγ gene expression and protein production in foals from birth to six months of age.

Main Methods:

• Peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage (BAL) cells were collected from foals aged 0-6 months.
• Cells were stimulated in vitro, and IFNγ production was measured using intracellular staining.
• IFNγ gene expression was quantified via real-time PCR on freshly isolated and stimulated cells.

Main Results:

• Newborn foals demonstrated a significant inability to express the IFNγ gene and produce IFNγ protein in both PBMC and BAL cells.
• IFNγ gene expression and protein production progressively increased in foals throughout the first six months of life.
• These levels approached adult levels within the first year of life.

Conclusions:

• Foals are born with an inherent deficiency in mounting a Th1-based cell-mediated immune response.
• This neonatal immunodeficiency may contribute to the heightened susceptibility of foals to intracellular pathogens.
• Understanding this immune gap is crucial for managing foal health and disease prevention.