https://nova.newcastle.edu.au/vital/access/ /manager/Index en-au 5 Apoptosis is a major cause of so-called 'caseous necrosis'' in mycobacterial granulomas in HIV-infected patients https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:4489 Wed 11 Apr 2018 11:29:51 AEST ]]> The duodenal mucosa associated microbiome, visceral sensory function, immune activation and psychological comorbidities in functional gastrointestinal disorders with and without self-reported non-celiac wheat sensitivity https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51213 Thu 24 Aug 2023 14:59:28 AEST ]]> Neonatal chlamydial infection induces mixed T-cell responses that drive allergic airway disease https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22114 Chlamydia-induced lung disease was observed 10–15 days after infection, as evidenced by increased bacterial numbers and histopathology in the lung and a reduction in weight gain. After 6 weeks, infection and histopathology had resolved and the rate of weight gain had recovered. Neonatal but not adult infection resulted in significant decreases in interleukin-5 production from helper T cells and by the numbers of eosinophils recruited to the lung in response to ovalbumin exposure. Remarkably, the effects of early-life infection were associated with the generation of both type 1 and 2 ovalbumin-specific helper T-cell cytokine and antibody responses. Furthermore, although neonatal infection significantly attenuated eosinophilia, the generation of the mixed T-cell response exacerbated other hallmark features of asthma: mucus hypersecretion and airway hyperresponsiveness. Moreover, infection prolonged the expression of AAD and these effects were restricted to early-life infection. Conclusions: Early-life chlamydial infection induces a mixed type 1 and 2 T-cell response to antigen, which differentially affects the development of key features of AAD in the adult.]]> Sat 24 Mar 2018 07:13:18 AEDT ]]>