We also today (in another thread) have mentioned the HPA axis hyperactivity in MS.
To recap, some of the main points regarding influencing specific cytokines and the immune system in MS, what has been found is that you want to control NK cells (inhibition), reduce IL1b, reduce TNFa, reduce IL6, increase IL10 as much as possible (this strengthens the BBB), and even perhaps more importantly, we have recently found that in progressive MS, we want to decrease the hyperactivity of the HPA.
Look at this regarding interferon 1b (i.e. Betaseron). I have run across this before regarding the interferons, but this is the first time (don't ask me why) I have run across all of this information in one publication. Is this why for the most part, the interferons are NOT prescribed for progressive MS?
Psychoneuroendocrinology. 2002 Nov;27( 8 ):881-92. Related Articles, Links
Acute interferon beta-1b administration alters hypothalamic-pituitary-adrenal axis activity, plasma cytokines and leukocyte distribution in healthy subjects.
Goebel MU, Baase J, Pithan V, Exton M, Saller B, Schedlowski M, Limmroth V.
Department of Medical Psychology, Medical Faculty, University of Essen, Hufelandstr 55, 45122, Essen, Germany. firstname.lastname@example.org
It has been suggested that the immune-endocrine communication plays an important role in development and progression of multiple sclerosis (MS). Interferon beta (IFN beta-1b) treatment is the therapy of choice in patients suffering from relapsing remitting or secondary chronic progressive multiple sclerosis. While typical adverse events of IFN beta-1b treatment such as flu-like symptoms or fatigue are well studied, little is known about the acute changes in the immune and neuroendocrine system. Therefore, we analyzed the short-term effects of IFN beta-1b on cortisol, epinephrine, norepinephrine, prolactin and growth hormone (GH) plasma levels before and 4, 8 and 24 h after IFN beta-1b administration in healthy subjects. Moreover, we determined heart rate, blood pressure, body temperature, leukocyte and lymphocyte subsets and plasma levels of interleukin (IL)-1 beta, IL-6, IL-10 and tumor necrosis factor (TNF)-alpha. IFN beta-1b led to an increase in body temperature and heart rate, and in parallel, elevated cortisol, prolactin and GH plasma levels at 4 and 8 h after IFN beta-1b injection. There were no significant alterations in blood pressure, norepinephrine or epinephrine plasma levels. Simultaneously, IFN beta-1b injection led to an immediate granulocytosis while concomitantly decreasing peripheral lymphocytes, especially natural killer (NK) cells. At the same time, IL-6, IL-10 and TNF-alpha plasma levels showed an overall increase. Overall, cytokine administration exerts strong stimulatory effects on the hypothalamic-pituitary-adrenal (HPA)-axis that may contribute to the side effects of IFN beta-1b therapy and affect the efficacy of IFN beta-1b treatment.
PMID: 12383450 [PubMed - indexed for MEDLINE]