IL-27 Alleviates Airway Inflammation and Airway Hyperresponsiveness in Asthmatic Mice by Targeting the CD39/ATP Axis of Dendritic Cells.

Interleukin-27 receptor (IL-27R) is expressed in a variety of immune cells and structural cells, including dendritic cells. The mechanism of IL-27 in asthma has not been fully elucidated. This study aimed to examine whether IL-27 regulated the CD39/ATP axis of dendritic cells in asthma. Our results showed that in ovalbumin (OVA)-induced asthma mouse model, IL-27Rα-/- asthmatic mice showed increased airway resistance, increased infiltration of inflammatory cells in lung tissue, proliferation of goblet cells, enhanced expression of Muc5 AC around airway epithelium, increased total number of cells and eosinophils, increased levels of total IgE, OVA-IgE, IL-4, IL-5, IL-13 and IL-17 A, and increased expression of transcription factors GATA-3 and RORγt in lung tissue. The expression of CD39 mRNA and protein in the lung tissue of IL-27Rα-/- asthmatic mice decreased, and the expression of NLRP3, ASC and Caspase-1 in NLRP3 inflammasome components increased. The concentration of ATP was significantly increased compared with WT asthmatic mice. In vitro experiments showed that the expression of CD39 in lung dendritic cells of IL-27Rα-/- asthmatic mice decreased, while the expression of NLRP3 inflammasome components NLRP3, ASC and Caspase-1 increased. These findings indicate that IL-27 directly and indirectly regulates immunoinflammatory responses in asthma by acting on dendritic cells CD39/ATP Axis.

Epstein-Barr virus (EBV) induced pneumonitis in a patient with breast cancer receiving neoadjuvant chemotherapy: A case report.

Background: Epstein-Barr virus (EBV) usually leads to latent infection and is reported mostly in infectious mononucleosis, lymphoma, and cancer in adolescents and adults, but pneumonitis due to EBV infection in adults is rare. Case presentation: We hereby reported a case of a 52-year-old woman with breast cancer who developed acute pneumonia during neoadjuvant chemotherapy. Her serologic workup revealed a low CD4+ count and positive anti-EBV antibodies. Chest computed tomography (CT) shows multiple patchy ground-glass shadows in the bilateral lung. Microscopic examination of stained sputum and bronchoalveolar lavage fluid (BALF) smear specimens did not find any pathogens. Metagenomic next-generation sequencing (mNGS) of BALF indicated a large number of EBV reads, allowing to confirm the diagnosis of EBV induced pneumonitis. The patient was then treated with ganciclovir with subsequent dramatic clinical and radiological improvement. Conclusions: This case highlights the combined application of mNGS and traditional tests in the clinical diagnosis of invasive pulmonary infection. In the meanwhile, clinicians should be aware neoadjuvant chemotherapy for breast cancer carries a risk of EBV induced pneumonitis, so that EBV induced pneumonitis could be considered in differential diagnosis while similar patients present, to orchestrate improvements in diagnosis, treatment, and prognosis.

Pleural effusion caused by Trichinella spiralis infection: two case reports.

BACKGROUND: Trichinosis is a worldwide food-borne zoonotic parasitic disease, which is mainly obtained by ingesting undercooked meat containing infected larvae. The purpose of our article is to introduce and discuss two rare cases of pleural effusion caused by Trichinella spiralis. CASE PRESENTATION: Here we described two male patients who presented to the respiratory department of our hospital with a massive unilateral pleural effusion, their serum eosinophils were in the normal range, laboratory serological tests revealed that Trichinella spiralis IgG antibody was positive. After the oral administration of antiparasitic drugs, the pleural effusion of two patients was completely absorbed. CONCLUSION: Both patients were diagnosed with Trichinosis complicated with pleural effusion, which is very rare in the clinic and easy to be misdiagnosed because of normal eosinophils.

Efficacy and safety of treatment with benralizumab for eosinophilic asthma.

Eosinophilic asthma accounts for 40% to 50% of asthmatic patients. However, 5% to 10% of patients with asthma need high-dose drug control, which is clinically referred to as severe asthma patients. Interleukin (IL)-5 plays an important role in the proliferation, maturation, and migration of eosinophils. Benralizumab, as an antagonist of the IL-5 receptor, can treat eosinophilic asthma by promoting the apoptosis of eosinophils. The implications for efficacy and/or adverse events are unclear. This article reviews the findings about benralizumab in the treatment of severe eosinophilic asthma in recent years. Results indicated the effectiveness of benralizumab for the treatment of severe asthma.

Modified Burr-Hole Craniostomy for the Treatment of Chronic Subdural Hematoma in Adults.

BACKGROUND: Burr-hole craniostomy (BHC) is considered to be the most effective method for the treatment of chronic subdural hematoma (CSDH), and middle meningeal artery embolization is a new therapy used in clinical practice in recent years to treat CSDH. However, the optimal therapeutic effect of these 2 procedures is still controversial. This study prospectively designed a modified burr-hole craniostomy (mBHC) with drainage to treat CSDH. METHODS: A total of 101 patients diagnosed with CSDH from January 2019 to April 2020 were prospectively included in this study. They were divided into BHC and mBHC groups. Among them, 40 selected CSDH patients received mBHC treatment. For comparison, 61 CSDH patients who received BHC treatment were used as the control group. Primary outcomes were hematoma recurrence and postoperative complications. Secondary outcomes included midline recovery, hematoma clearance, operation time, and hospital stay. The Chi-square test was used to compare the 6-month follow-up results between the 2 groups. RESULTS: Among patients treated with mBHC, 39 patients had a good prognosis, and one 87-year-old patient with bilateral hematoma died of postoperative heart failure. Of the patients treated with BHC, 52 patients had good prognoses, and one 53-year-old patient with unilateral hematoma died of postoperative acute intracranial bleeding. During the 6-month follow-up period, no relapse occurred in the patients treated with mBHC, whereas 8 (13%) of the patients treated with BHC relapsed. There was a significant difference in the recurrence rate between the 2 groups (P < 0.05). In addition, midline recovery, hematoma clearance rate, operation time, and complications were found to be significantly different statistically (P < 0.05), and other characteristics of operation and outcome were not significantly different (P > 0.05) between the 2 groups. CONCLUSIONS: Modified burr-hole craniostomy has a positive therapeutic effect on patients with CSDH and is more effective than conventional BHC therapy.

Pharmacological Targeting of CSF1R Inhibits Microglial Proliferation and Aggravates the Progression of Cerebral Ischemic Pathology.

Ischemic stroke can induce rapid activation of the microglia. It has been reported that the microglia's survival is dependent on colony-stimulating factor 1 receptor (CSF1R) signaling and that pharmacological inhibition of CSF1R leads to morphological changes in the microglia in the healthy brain. However, the impact of CSF1R inhibition on neuronal structures and motor ability after ischemia-reperfusion remains unclear. In this study, we investigated microglial de-ramification, proliferation, and activation after inhibition of CSF1R by a tyrosine kinase inhibitor (ki20227) in a mouse model of global cerebral ischemia induced by bilateral common carotid artery ligation (BCAL). In addition to microglial morphology, we evaluated the mRNA expression of cytokines, chemokines, and inflammatory receptors. Our results show that pharmacological inhibition of CSF1R in ischemic mice resulted in the blockade of microglial proliferation and a shift in microglial morphology reflected by excessive de-ramification and a more activated phenotype accompanied by an enhanced innate immune response. Furthermore, we show that pharmacological inhibition of CSF1R in ischemic mice resulted in the aggravation of neuronal degeneration and behavioral impairment. Intravital two-photon imaging revealed that although pharmacological inhibition of CSF1R did not affect the recovery of dendritic structures, it caused a significant increase in spine elimination during reperfusion in ischemic mice. These findings suggest that pharmacological inhibition of CSF1R induces a blockade of microglial proliferation and causes acute activation of the microglia accompanied by a severe inflammatory response. It aggravates neuronal degeneration, loss of dendritic spines, and behavioral deficits after transient global cerebral ischemia.