Stress-induced suppression of experimental allergic encephalomyelitis in the rat

Abstract

Numerous experiments have demonstrated that physical stress can alter immunological parameters. However, little attention has been paid to the interrelationship between stress and autoimmune processes. The present study was designed to determine the influence of electric shock and sound stress on the development of experimental allergic encephalomyelitis (EAE). Ten-week-old male DA rats highly susceptible to EAE were used. Rats were subjected to the stress procedure during 19 days either before or after immunization with intradermal injection of 0.1 ml of an emulsion containing guinea pig spinal cord (20 mg/rat) in an equal volume of complete Freund's adjuvant (CFA). In addition, rats received subcutaneous injection of Bordetella pertussis in the dorsum of the same foot. Electric stress procedure consisted of 80 inescapable, unpredictable tail shocks (5 s, 1 mA) delivered at the same time each day. Sound stress procedure consisted of exposure of rats to a 90 dB fire alarm bell which rings 60 times for 5 s during one hour, at the same time of the day. Rats were observed daily for clinical signs of EAE and survived animals were sacrificed on day 20 after immunization. The brain and spinal cord sections were examined histologically for mononuclear cell infiltrates characteristics for EAE. The results clearly indicate that inescapable tail shocks suppressed the appearance and development of EAE when rats were subjected to stress procedure during 19 days after immunization, but not when rats were stressed during 19 day before the induction of EAE. On the other hand, in rats exposed to sound stress there was only delay in the onset of the disease.

Neonatal Maternal Separation Alters Immune, Endocrine, and Behavioral Responses to Acute Theiler’s Virus Infection in Adult Mice

“…Although the etiology of multiple sclerosis remains uncertain, epidemiological studies suggest that viral infection during adolescence may be an initiating factor in genetically susceptible individuals (Acheson 1977; Alter et al 1986; Hernan et al 2001; Kurtzke et al 1995; Sospedra and Martin 2005). Psychological stress has also been shown to have a profound impact on animal models of multiple sclerosis, such as Theiler's virus infection (Campbell et al 2001; Johnson et al 2004, 2006; Meagher et al 2007a, b; Mi et al 2004, 2006a, b; Sieve et al 2004, 2006; Steelman et al 2009; Welsh et al 2004; Young et al, in press) and Experimental Autoimmune Encephalomyelitis (EAE; Bukilica et al 1991; Dowdell et al 1999; Griffin and Whitacre 1990; Griffin et al 1993; Levine and Saltzman 1987; Levine et al 1962; Stephan et al 2002; Teunis et al 2002; Whitacre et al 1998). Although several studies have shown that early life stress can alter the course of EAE (Laban et al 1995a, b; Stephan et al 2002; Teunis et al 2002), the impact on Theiler's virus infection remains unexplored.…”

Effects of Anxiolytic Drugs in Animal Models of Multiple Sclerosis

“…e. Experimental model of MS (Table 1): Several authors have observed that stress exacerbates the early viral infection (Campbell et al, 2001;Sieve et al, 2004) and the later demyelinating disease in Theiler's virus infection. However, this does not coincide with studies using EAE, which show no effect of stress prior to disease induction, and a suppression during disease induction (Bukilica et al, 1991;Dowdell et al, 1999;Griffin et al, 1993;Levine & Saltzman, 1987;Levine et al, 1962). The differences in how stress affects EAE and Theiler's virus infection may lie in their immunological mechanisms of demyelination and neuronal destruction.…”

“…In contrast, if restraint stress is applied concurrent with infection, the disease is again exacerbated (Campbell et al, 2001;Sieve et al, 2004). Likewise, Bukilica et al (1991) indicated that whereas 19 daily sessions of inescapable tail-shock (80, 5 s, 1 mA) have no effect when administered prior to EAE induction, stressor exposure following EAE induction has a protective effect. Specifically, tail-shock reduces the incidence and duration of EAE, delays disease onset, and decreases the severity of clinical and histological symptoms.…”

Injection of bleomycin in newborn mice induces autoimmune sialitis that is transferred by CD4 T cells

“…However, autoantigen immunization with adjuvant has been shown to induce tissue‐specific autoimmune disease in a disease‐specific background. For example, experimental autoimmune encephalomyelitis in mice can be induced by exposure to peptides, suggesting that both genetic and environmental stresses can induce autoimmune disease 6 , 7 , 8 . The environmental factors, which induce cell apoptosis, are considered one of the main causes of autoimmune disease.…”