The HPA Axis

HPA Axis

The HPA axis has been receiving a lot of attention in recent studies. The studies are looking at potential pre-natal and post-natal roles it plays in schizophrenia. When the body becomes under stress, the hypothalamic-pituitary-adrenal axis (HPA) is used by the hypothalamus to mediate cortisol output (Walker, 2002). For pre- and post-natal development, the HPA axis is an important stress defense (Zhang et al., 2014). The HPA axis releases corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH) and glucocorticoids (GC) (Misiak et al., 2014). Glucocorticoids, like cortisol, are stress hormones and function multiple ways which include the inhibition of inflammatory response and also has an influence on cognitive functioning

Fetal exposure to prenatal stress is capable of reprograming the HPA axis to have an increased responsiveness to glucocorticoids later in life as well as inhibit the secretion of glucocorticoids due to stress (Koenig, Kirkpatrick and Lee, 2002).

The Immune system and Inflammatory Response

The immune system is composed of two parts, the innate and acquired, which respond to antigens present in the body. The innate side is the first line of defense against antigens and matures in the thymus. An antigen that produces an immune response are called immunogens (Delves and Roitt, 2000). A mechanism used in defense by the innate side is inflammation, cytokines in this process that are pro-inflammatory include IL-1ß, IL-6 and tumor necrosis factor (TNF)-alpha (Meyer, 2013). The acquired side is slower in response and matures in the bone marrow. Both cells start in the bone marrow, but T-cells migrate to the thymus, as thymocytes, at an early stage to finish maturation; if the thymocytes do no complete their journey to the thymus they die by performing apoptosis (Parkin and Cohen,

The research that is out there does implicate immune system dysfunction in prenatal immune activation as a role in the development of schizophrenia. More research needs to be conducted on looking at the effects of cytokines on the neurodevelopmental processes in humans. There are multiple animal studies that have found neurodevelopmental effects of cytokines on the offspring due to prenatal immune activation (Meyer et al., 2005; Meyer 2013; Patterson 2009; Deverman and Patterson, 2009). The found effects have implications on cytokines on the neurodevelopmental processes in humans. Stress research has shown the decreased effectiveness of the prenatal enzyme 11ß-HSD2 which protects the developing fetus from maternal factors (O'Donnell, O'Connor and Glover, 2009). Future studies are needed to look at what other possible placenta enzymes are down regulated and if that allows other cytokines to cross. More studies like the one conducted by Ellman et al. (2010) needs to be done looking at individual cytokine effects during maternal presentation. The data discussed in the paper supports that prenatal immune activation is linked with structural and functional abnormalities of the neurodevelopment of the fetus's brain. The key factors suggested are the timing, dosage and type of cytokine.