[A Cross-sectional Study of Hepatitis B Virus Infection in Mianyang, Sichuan Province].

OBJECTIVES: To determine the prevalence and distribution of hepatitis B virus (HBV) infection in Mianyang. METHODS: Data were extracted from the 12th five-year National Science and Technology Major Projects-Integrated Prevention and Control of Major Infectious Diseases in Mianyang. A two-level logistic regression model was established to determine factors associated with HBV infection. RESULTS: About 4.91% of people in Mianyang were HBsAg positive, which increased with age. HBV infection showed aggregation at townships. Governmental spending ≥¥1 000 000 on public health was a protective factor in the regression model; whereas, age, male gender, medical workers, absent from HBV vaccination, more than 80 g/d alcohol consumption were risk factors of HBV infection. CONCLUSIONS: Mianyang had medium level of HBV infections. But high HBV prevalence can be found in some townships. The known behavior risk factors all exist in Mianyang, which can serve as a screening tool for identifying high risk populations.

Neonatal endotoxin exposure suppresses experimental autoimmune encephalomyelitis through regulating the immune cells responsivity in the central nervous system of adult rats.

Early-life exposure to bacterial endotoxin (lipopolysaccharide, LPS) affects the susceptibility to a variety of systemic organic inflammation in adulthood. To determine the long-term effects of neonatal LPS exposure on inflammatory responses in the central nervous system (CNS) in adulthood, we examined the effects on the development of experimental autoimmune encephalomyelitis (EAE) in adult rats as well as the potential regulatory immune mechanisms involved. The results showed that neonatal LPS exposure significantly reduced the morbidity (p<0.01) and severity (p<0.05) of EAE in adult rats, and decreased inflammatory cell infiltration and demyelination in the CNS compared with neonatal saline controls (p<0.05). Neonatal LPS-treated animals showed reduced activation of microglia and astrocytes, as detected by immunocytochemistry, accompanied by down-regulation of the pro-inflammatory cytokines interleukin-17 and interferon-gamma but up-regulation of anti-inflammatory cytokine interleukin-10 in the CNS (p<0.05). At the same time, cerebrum mRNA levels of the transcription factors T-bet and RORgammat were lower in neonatal LPS-compared with saline- treated animals (p<0.05) accompanied with increased STAT-6 and Foxp3 levels in the neonatal LPS-treated group (p<0.05). These findings suggest that early-life exposure to LPS could provide an important neuroprotective effect on the development of EAE in adult rats due to modulation of inflammatory responses in the CNS.

Chronic caffeine treatment protects against experimental autoimmune encephalomyelitis in mice: therapeutic window and receptor subtype mechanism.

Chronic treatment with caffeine, the most widely consumed psychoactive drug and a non-selective antagonist of adenosine receptors, can protection against myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In this study, we investigated the mechanism underlying caffeine-mediated neuroprotection against EAE by determining the effective therapeutic time-window of caffeine and the involvement of adenosine A2A and A1 receptor. We found that administration of caffeine during the effector phase (10 â†’ 20 days post-immunization, d.p.i., corresponding to appearance of neurological deficits) but not the induction phase (0 â†’ 10 d.p.i., before the appearance of ascending flaccid paralysis) significantly ameliorated EAE-induced neurobehavioral deficits, reduced the infiltration of inflammatory cells into the spinal cord and reduced the demyelination of spinal cord. Furthermore, genetic deletion of the A2AR exacerbated MOG-induced brain damage and caffeine administering to A2AR knockout mice reversed this EAE pathology by acting at non-A2AR target. The protective effect of chronic caffeine treatment was associated with up-regulation of brain A1R (but not A2AR). The identification of the effective therapeutic window of caffeine at the effector phase and clarification of non-A2AR target (likely A1R) in caffeine action in EAE models advance the therapeutic prospective that chronic caffeine consumption may attenuate brain damage in MS.

[The change of periphery and centra CD4(+);CD25(+);Treg, CD8(+);CD28(-);Treg in the MOG induced model of experimental autoimmune encephalomyelitis].

AIM: To observe the change of periphery and centra CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg of MOG35₋55; induced EAE disease in mouse, and to explore the potential mechanism of cellular immunity in the process of EAE. METHODS: MOG35₋55; were used to establish EAE model on femina C57BL/6 mice.The behavioral changes and the histological scores were recorded. The changes of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg on periphery and centra lymphocyte in spleen , brain were analyzed by flow cytometry. RESULTS: MOG35₋55;-induced EAE group Showed the typical clinical behavior and pathological manifestations, CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes were detected in the brain and spinal cord of EAE group mice, but they were not detected in the brain of control group. CD8(+); CD28(-); Treg in the spleen of EAE group were lower than those in control group (P < 0.01). CD4(+); CD25(+); Treg lymphocytes were slight higher than the control group. CONCLUSION: CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes all play important roles in the pathogenesy of EAE. The distribution of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg in the CNS and peripheral of EAE is different, suggesting that their entry into the CNS and regulate of local inflammation.