Background: Allergic asthma is characterized by type 2 inflammation. We have shown the presence of increased type 2 inflammation in patients with severe asthma and those with frequent exacerbations. However, it is not known whether increased type 2 inflammation drives asthma exacerbations. This study aims to determine Th2 immune parameters in patients presenting to the emergency department (ED) with an acute asthma exacerbation and correlate these parameters with clinical and physiological measures of asthma. Methods: Sixteen adults presenting to the ED with acute asthma exacerbations were recruited after giving informed consent. Ten patients returned 2 weeks later for follow-up. Physiological parameters, asthma control (ACQ6), asthma quality of life (AQLQ) questionnaires, and venous blood were collected during both visits. An immune cell profiling was performed by whole blood flow cytometry: CD4 + T cells, Th2 cells (CD4 + CRTh2 + T cells and % of CD4 + T cells expressing CRTh2), eosinophils and innate lymphoid cells (ILC2). Results: During exacerbation, peripheral blood Th2 cell numbers correlated with ACQ6 and AQLQ scores, while ILC2 and eosinophil numbers did not. Subjects had higher % of CD4 + T cells expressing CRTh2 and worse FEV 1 during exacerbation compared with the follow-up. The decrease in the % of CD4 + T cells expressing CRTh2 seen during the follow-up visit correlated with the improvement in lung function. Conclusions: These data suggest that Th2 cells in peripheral blood may be a sensitive measure of increasing symptoms in patients with asthma exacerbations and may serve as a biomarker of an asthma exacerbation.

No abstract

No abstract

Cerebrospinal fluid (CSF) shunts are commonly used for the long-term management of hydrocephalus in children. Shunt infection remains a common complication, occurring in about 5%–15% of CSF shunts. This narrative review summarises key evidence from recent literature on the epidemiology, pathogenesis, clinical presentation, diagnosis, management, outcomes and prevention of CSF shunt infections in children. The majority of shunt infections occur due to contamination at the time of surgery, with coagulase-negative staphylococci andStaphylococcus aureusbeing the most common infecting organisms. Clinical presentations of shunt infection can be varied and difficult to recognise. CSF cultures are the primary test used for diagnosis. Other CSF and blood parameters may aid in diagnosis but lack sensitivity and specificity. Core aspects of management of shunt infections include systemic antimicrobial therapy and surgical removal of the shunt. However, many specific treatment recommendations are limited by a lack of robust evidence from large studies or controlled trials. Shunt infections may result in long hospital stays, worsening hydrocephalus, neurological sequelae and other complications, as well as death. Therefore, reducing the incidence of infection and optimising management are high priorities. Antibiotic prophylaxis at the time of shunt placement, improved surgical protocols and antibiotic-impregnated shunts are key strategies to prevent shunt infections. Nevertheless, further work is needed to identify additional strategies to prevent complications and improve outcomes.