Epstein-Barr virus-induced infection-associated hemophagocytic lymphohistiocytosis with acute liver injury: A case report.

BACKGROUND: Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory reaction, which is rare and life-threatening. According to the pathogen, HLH is divided into genetic and acquired. The most common form of acquired HLH is infection-associated HLH, of which Herpes viruses, particularly Epstein-Barr virus (EBV), are the leading infectious triggers. However, it is difficult to distinguish between simple infection with EBV and EBV-induced infection-associated HLH since both can destroy the whole-body system, particularly the liver, thereby increasing the difficulty of diagnosis and treatment. CASE SUMMARY: This paper elaborates a case about EBV-induced infection-associated HLH and acute liver injury, aiming to propose clinical guides for the early detection and treatment of patients with EBV-induced infection-associated HLH. The patient was categorized as acquired hemophagocytic syndrome in adults. After the ganciclovir antiviral treatment combined with meropenem antibacterial therapy and methylprednisolone inhibition to inflammatory response, gamma globulin enhanced immunotherapy, the patient recovered. CONCLUSION: From the diagnosis and treatment of this patient, attention should be paid to routine EBV detection and a further comprehensive understanding of the disease as well as early recognition and early initiation are keys to patients' survival.

Electroacupuncture prevents cognitive impairment induced by lipopolysaccharide via inhibition of oxidative stress and neuroinflammation.

Oxidative stress and neuroinflammation play an important role in the pathophysiology of lipopolysaccharide (LPS)-induced cognitive impairment. This study aims to observe the effect of electroacupuncture (EA) on the cognitive function in LPS-induced mice, and its regulation on hippocampal α7 nicotinic acetylcholine receptors (α7nAChR), oxidative and proinflammatory factors. Adult male C57BL/6 nice were used to establish animal model of LPS-induced cognitive impairment, and were randomly divided into three groups (n = 16): control group, model group (LPS: 5 mg/kg), and EA group. The cognitive function was measured by Morris water-maze test, and protein expression of α7nAChR in hippocampus was detected by immunohistochemistry. Enzyme-linked immunosorbent assay (ELISA) was used to measure hippocampal proinflammatory cytokines. The results showed that LPS significantly impaired working and spatial memory of mice, which could be attenuated by EA treatment. EA prevented LPS-induced decrease of α7nAChR protein, acetylcholine (ACh) content and choline acetyltransferase (ChAT) activity, and prevented LPS-induced increase of acetylcholinesterase (AChE) activity (P < 0.05). EA significantly decreased malondialdehyde (MDA) and hydrogen peroxide (H2O2), and increased the contents of catalase (CAT) and glutathione (GSH) in hippocampus of LPS-treated Mice (P < 0.05). EA also prevented LPS-induced increase of proinflammatory cytokines interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) in hippocampus (P < 0.05). In conclusion, electroacupuncture can improve the learning and memory in LPS-treated mice, and its mechanism may be related to enhanced expression of α7-nAChR and cholinergic factors, and suppression of oxidative stress and neuroinflammation in hippocampus.

Effect of dexmedetomidine on rats with convulsive status epilepticus and association with activation of cholinergic anti-inflammatory pathway.

Convulsive status epilepticus (CSE) is a neurological disease with contraction and extension of limbs, leading to damage of hippocampus and cognition. This study aimed to explore the effects of dexmedetomidine (DEX) on the cognitive function and neuroinflammation in CSE rats. All rats were divided into control group, CSE group and DEX group. Morris water maze test was used to measure cognitive function. Acute hippocampal slices were made to detect long-term potentiation (LTP). Immunohistochemistry was used to determine the expression of α7-nicotinic acetylcholine receptor (α7-nAChR) and interleukin-1ß (IL-1ß). Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of IL-1ß, tumor necrosis factor-α (TNF-α), S-100ß and brain-derived neurotrophic factor (BDNF). Our results showed that DEX improved the memory damage caused by CSE. DEX reduced seizure severity and increased the amplitudes and sustainable time of LTP, and also inhibited the hippocampal expression of α7-nAChR and IL-1ß in CSE rats. DEX treatment decreased serum IL-1ß, TNF-α and S-100ß levels and increased BDNF levels. The effects of DEX on seizure severity and LTP could be simulated by nicotine or attenuated by concurrent α-bungarotoxin (α-BGT) treatment. In conclusions, DEX significantly improved spatial cognitive dysfunction, reduced seizure severity and increased LTP in CSE rats. Improvements by DEX were closely related to enhancement of cholinergic anti-inflammatory pathway.