Microbiota and neurologic diseases : potential effects of probiotics

Background: The microbiota colonizing the gastrointestinal tract have been associated with both gastrointestinal and extra-gastrointestinal diseases. In recent years, considerable interest has been devoted to their role in the development of neurologic diseases, as many studies have described bidirectional communication between the central nervous system and the gut, the so-called "microbiota-gut-brain axis". Considering the ability of probiotics (i.e., live non-pathogenic microorganisms) to restore the normal microbial population and produce benefits for the host, their potential effects have been investigated in the context of neurologic diseases. The main aims of this review are to analyse the relationship between the gut microbiota and brain disorders and to evaluate the current evidence for the use of probiotics in the treatment and prevention of neurologic conditions. Discussion: Overall, trials involving animal models and adults have reported encouraging results, suggesting that the administration of probiotic strains may exert some prophylactic and therapeutic effects in a wide range of neurologic conditions. Studies involving children have mainly focused on autism spectrum disorder and have shown that probiotics seem to improve neuro behavioural symptoms. However, the available data are incomplete and far from conclusive. Conclusions: The potential usefulness of probiotics in preventing or treating neurologic diseases is becoming a topic of great interest. However, deeper studies are needed to understand which formulation, dosage and timing might represent the optimal regimen for each specific neurologic disease and what populations can benefit. Moreover, future trials should also consider the tolerability and safety of probiotics in patients with neurologic diseases

Point‐of‐care testing for influenza in a university emergency department: A prospective study

Background: Seasonal influenza is a burden for emergency departments (ED). The aim of this study was to investigate whether point-of-care (POC) PCR testing can be used to reduce staff sick days and improve diagnostic and therapeutic procedures. Objectives The aim of this study was to investigate whether point-of-care (POC) PCR testing can be used to reduce staff sick days and improve diagnostic and therapeutic procedures. Methods: Using a cross-over design, the cobas (R) Liat (R) Influenza A/B POC PCR test (Liat) was compared with standard clinical practice during the 2019/2020 influenza season. All adult patients (aged >= 18 years) with fever (>= 38 degrees C) and respiratory symptoms were included. Primary end points were the prevalence of influenza infections in the ED and staff sick days. Secondary end points were frequency of antiviral and antibacterial therapy, time between admission and test result or treatment initiation, patient disposition, ED length of stay (LOS), and for inpatients mortality and LOS. Nurses were interviewed about handling and integration of POC testing. The occurrence of SARS-CoV-2 infections coincided with the second half of the study. Results A total of 828 patients were enrolled in the study. All 375 patients of the intervention group were tested with Liat, and 103 patients of them (27.6%) tested positive. During the intervention period, staff sick days were reduced by 34.4% (P = .023). Significantly, more patients in the intervention group received antiviral therapy with neuraminidase inhibitors (7.2% vs 3.8%, P = .028) and tested patients received antibiotics more frequently (40.0% vs 31.6%, P = .033). Patients with POC test were transferred to external hospitals significantly more often (5.6% vs 1.3%, P = .01). Conclusion: We conclude that POC testing for influenza is useful in the ED, especially if it is heavily frequented by patients with respiratory symptoms

Therapeutic administration of a monoclonal anti-Il-1β antibody protects against experimental melioidosis

BACKGROUND:: Melioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, is a common cause of community-acquired sepsis in Southeast Asia and Northern Australia. The NLRP3-inflammasome and its downstream product interleukin-1 beta (IL-1β) have been proposed to play crucial roles in melioidosis. In this study we characterized the role of IL-1β more closely and we assessed its therapeutic potential. METHODS:: mRNA expression of inflammasome components was determined in isolated leukocytes of 32 healthy controls and 34 patients with sepsis caused by B. pseudomallei.Wild-type (WT), NLRP3-deficient (Nlrp3) and Asc mice were infected with B. pseudomallei. In additional experiments, infected WT mice were treated with an anti-IL-1β antibody. After 24, 48 and 72?hours (h) mice were sacrificed and organs were harvested. Furthermore, survival studies were performed. RESULTS:: Patients with melioidosis exhibited lower mRNA levels of caspase-1, NLRP3 and ASC. Bacterial dissemination and organ damage were increased in B. pseudomallei-infected Nlrp3 and Asc mice, together with a reduced pulmonary cell influx. Anti-IL-1β treatment of B. pseudomallei challenged mice resulted in strongly reduced bacterial counts, organ damage and pulmonary granulocyte influx together with reduced mortality. Postponement of anti-IL-1β treatment for 24?h post-infection still protected mice during melioidosis. CONCLUSION:: Expression of caspase-1, NLRP3 and ASC is altered in melioidosis patients. In mice, both NLRP3 and ASC contribute to the host defense against melioidosis. Anti-IL-1β treatment protects mice against B. pseudomallei infection and might be a novel treatment strategy in melioidosis

Therapeutic administration of a monoclonal anti-Il-1β antibody protects against experimental melioidosis

BACKGROUND:: Melioidosis, caused by the Gram-negative bacterium Burkholderia pseudomallei, is a common cause of community-acquired sepsis in Southeast Asia and Northern Australia. The NLRP3-inflammasome and its downstream product interleukin-1 beta (IL-1β) have been proposed to play crucial roles in melioidosis. In this study we characterized the role of IL-1β more closely and we assessed its therapeutic potential. METHODS:: mRNA expression of inflammasome components was determined in isolated leukocytes of 32 healthy controls and 34 patients with sepsis caused by B. pseudomallei.Wild-type (WT), NLRP3-deficient (Nlrp3) and Asc mice were infected with B. pseudomallei. In additional experiments, infected WT mice were treated with an anti-IL-1β antibody. After 24, 48 and 72?hours (h) mice were sacrificed and organs were harvested. Furthermore, survival studies were performed. RESULTS:: Patients with melioidosis exhibited lower mRNA levels of caspase-1, NLRP3 and ASC. Bacterial dissemination and organ damage were increased in B. pseudomallei-infected Nlrp3 and Asc mice, together with a reduced pulmonary cell influx. Anti-IL-1β treatment of B. pseudomallei challenged mice resulted in strongly reduced bacterial counts, organ damage and pulmonary granulocyte influx together with reduced mortality. Postponement of anti-IL-1β treatment for 24?h post-infection still protected mice during melioidosis. CONCLUSION:: Expression of caspase-1, NLRP3 and ASC is altered in melioidosis patients. In mice, both NLRP3 and ASC contribute to the host defense against melioidosis. Anti-IL-1β treatment protects mice against B. pseudomallei infection and might be a novel treatment strategy in melioidosis