http://nova.newcastle.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 Oral administration of the probiotic lactobacillus fermentum VRI-003 and mucosal immunity in endurance athletes http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:9301 Objective: To evaluate the ability of a probiotic Lactobacillus fermentum VRI-003 (PCC) to enhance the mucosal immune system of elite athletes. Design and setting: A double-blind, placebo-controlled, crossover trial was conducted over a 4-month period of winter training. Participants: 20 healthy elite male distance runners. Interventions: PCC was given at a daily dose of 1.2x10(10) as a freeze-dried powder in gelatin capsules. Placebo capsules contained an inert excipient. Main outcome measures: Treadmill performance (monthly), mucosal and systemic immunity (monthly), training (daily) and illness (daily) were assessed. Serum cytokine levels, salivary IgA levels and incidence, duration and severity of respiratory tract infections were measured. Results: Subjects reported less than half the number of days of respiratory symptoms during PCC treatment (30 days) compared with placebo (72 days, p<0.001). Illness severity was also lower for episodes occurring during the PCC treatment (p = 0.06). There were no significant differences in the mean change in salivary IgA and IgA1 levels, or in interleukin (IL) 4 and IL12 levels, between treatments. However, PCC treatment elicited a twofold (p = 0.07) greater change in whole-blood culture interferon gamma (IFN gamma) compared with placebo. No substantial changes in running performance measures were seen over the study period. Conclusions: Prophylactic administration of PCC was associated with a substantial reduction in the number of days and severity of respiratory illness in a cohort of highly trained distance runners. Maintenance of IFN gamma levels may be one mechanism underpinning the positive clinical outcomes. 2011-11-09T23:00:03.865Z ]]> Interleukin-10 gene expression in acute virus-induced asthma http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:217 Rationale: Virus-induced asthma is characterized by marked neutrophil influx and eosinophil degranulation, suggesting a mode of immunopathogenesis different from that of allergen-induced asthma. Objectives: This study compared induced sputum cytokine responses in subjects with severe asthma exacerbation and respiratory virus infection with those of patients with stable asthma, healthy control subjects, and virus-infected nonasthmatic subjects. Methods: Subject infection status and pulmonary history were established on the basis of common cold and asthma questionnaires, and lung function and atopy tests were performed. Respiratory virus infection was diagnosed by cell culture and direct polymerase chain reaction, using induced sputum. The induced sputum cellular profile was examined and cytokine gene expression was assessed by quantitative real-time polymerase chain reaction. Results:A respiratory virus was detected in 78% of subjects with acute asthma. Specific viruses detected were rhinovirus (83%), influenza (15%), enterovirus (4%), and respiratory syncytial virus (2%). Virus-infected subjects with acute asthma or no asthma had increased RANTES (regulated on activation, normal T cell expressed and secreted) and macrophage inflammatory protein-la messenger RNAs compared with other groups. Interleukin (IL)-10 mRNA was significantly increased in virus-infected acute asthma and reduced on recovery from acute asthma. IL-5, eotaxin, and IL-8 mRNA transcripts were similar across groups. Conclusions: Asthma exacerbation triggered by respiratory virus infection is characterized by increased IL-10 gene expression that may explain the suppressed eosinophil influx in acute asthma. Airway neutrophilia due to respiratory virus infection is associated with chemokine gene expression involving RANTES and macrophage inflammatory protein-la. 2010-04-27T06:00:43.360Z ]]> Apoptosis is a major cause of so-called 'caseous necrosis'' in mycobacterial granulomas in HIV-infected patients http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:4489 Aim: To demonstrate that so-called "caseous necrosis" is the result of apoptosis and investigate the association of B and T cells, and macrophages with the granulomas and their relationship to some apoptosis-related proteins. Methods: Cervical lymph node biopsy specimens from 55 HIV-infected Thai patients with caseating granulomas, confluent caseating granulomas, sarcoid-like granulomas, foamy macrophage response, pseudo-inflammatory tumour response or non-specific lymphoid hyperplasia were examined histologically and for apoptosis by immunostaining for caspase 3 and TUNEL. Classic tuberculoid caseating granulomas in cervical lymph node and lungs from non-HIV-infected patients were also stained with caspase 3. Results: All areas of caseous necrosis frequently displayed extensive apoptosis that readily accounted for the so-called "necrosis". Small foci of apoptosis were present in the other reaction patterns and fibrotic granulomas often showed residual apoptosis. The extent of apoptosis was inversely related to the numbers of identifiable acid-fast bacilli; all epithelioid macrophages revealed strong immunoexpression of the pro-apoptotic proteins Bax and Fas, whereas the anti-apoptotic protein Bcl-2 was not present. Apoptosis occurred in CD68+ macrophages and CD3+ CD8+ T cells; all nodes were deficient of CD4+ cells. CD8+ T cells were intimately related to the apoptotic foci, suggesting a role in the process, particularly in the absence of CD4+ cells. In non-HIV-infected cases, similar extensive apoptosis was confirmed with caspase 3. Conclusions: So-called "caseous necrosis" is shown for the first time to be the result of apoptosis. In the absence of CD4+ cells the findings negate many of the postulated mechanisms of apoptosis in the murine model and have implications for the treatment of mycobacterial infections. 2010-04-27T04:58:04.255Z ]]>