BackgroundAs a way to determine markers of infection or disease informing disease management, and to reveal disease-associated immune mechanisms, this study sought to measure antibody and T cell responses against key lung pathogens and to relate these to patients’ microbial colonization status, exacerbation history and lung function, in Bronchiectasis (BR) and Chronic Obstructive Pulmonary Disease (COPD).MethodsOne hundred nineteen patients with stable BR, 58 with COPD and 28 healthy volunteers were recruited and spirometry was performed. Bacterial lysates were used to measure specific antibody responses by ELISA and T cells by ELIspot. Cytokine secretion by lysate-stimulated T cells was measured by multiplex cytokine assay whilst activation phenotype was measured by flow cytometry.ResultsTypical colonization profiles were observed in BR and COPD, dominated by P.aeruginosa, H.influenzae, S.pneumoniae and M.catarrhalis. Colonization frequency was greater in BR, showing association with increased antibody responses against P.aeruginosa compared to COPD and HV, and with sensitivity of 73% and specificity of 95%. Interferon-gamma T cell responses against P.aeruginosa and S.pneumoniae were reduced in BR and COPD, whilst reactive T cells in BR had similar markers of homing and senescence compared to healthy volunteers. Exacerbation frequency in BR was associated with increased antibodies against P. aeruginosa, M.catarrhalis and S.maltophilia. T cell responses against H.influenzae showed positive correlation with FEV1% (r = 0.201, p = 0.033) and negative correlation with Bronchiectasis Severity Index (r = − 0.287, p = 0.0035).ConclusionOur findings suggest a difference in antibody and T cell immunity in BR, with antibody being a marker of exposure and disease in BR for P.aeruginosa, M.catarrhalis and H.influenzae, and T cells a marker of reduced disease for H.influenzae.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0811-2) contains supplementary material, which is available to authorized users.

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Potassium bromate is an oxidizing agent and one of the cheapest dough improvers in the baking and food industry. This agent is classified as carcinogenic in rats and nephrotoxic in both man and experimental animals when given orally. The red onion, Allium cepa, is used in the daily diet for taste. Compounds in onions also have various medicinal properties, such as being anticancer, antifungal, antioxidant, anti-ulcer, and anti-inflammatory. We therefore sought to investigate whether aqueous extract of red onion would be protective against injury to the intestine Materials and Methods: 36 Wistar male rats were divided into 6 batches. Over a 4-weeks experimental period, group I rats served as a control and group II received 100 mg/kg b.w of KBrO3 on the 24th and 27th days. Group III received red onion juice at 1ml/100 g bw every day and 100 mg/kg bw of KBrO3 on the 24th and 27th days. Group IV received 50 mg/kg bw of KBrO3 twice per week, group V received red onion juice daily at 1ml/100 g bw and 50 mg/kg bw of KBrO3 twice per week, and group VI received 30 mg/kg KBrO3 every day. The body and four organs weights, including the kidney, testis, lung and liver of all experimental rats were measured. The histopathological investigation was performed for the intestine tissues of all groups. Results: KBrO3-treated small intestines exhibited destruction in the villi, decreased number of goblet cells, crypt loss and cell infiltration in the epithelial lining. Treatment with extract of red onion appeared to significantly ameliorate the toxic effects of KBrO3. Conclusion: Our findings suggest that red onion ameliorates the extent of intestinal injury and appears to act as an antioxidant. This study supports that red onion has beneficial properties, although no direct clinical conclusions can be drawn from these data.

BackgroundPeople with chronic lung diseases, such as Bronchiectasis (BE) and smoking-induced Chronic Obstructive Pulmonary Disease (COPD), are susceptible to lung infections which can exacerbate their disease and can be life threatening. A relatively limited range of pathogens cause infections in these conditions and patients suffer repeated infections. It is unclear why such infections do not elicit protective adaptive immune responses. We wish to better understand immune responses against lung-infecting microbes in people with underlying lung disease since immune responses may be connected to disease pathology and also to protection from infection, and may provide a useful marker of colonisation.MethodsWe took peripheral blood samples from 114 BE and 47 COPD patients attending secondary care clinics, and 25 healthy controls, and extracted PBMC and serum. The patients were well-characterised clinically, including their history, aetiology, lung function and longitudinal microbial colonisation. T cell and antibody responses were measured against a panel of common lung-infecting microbial antigens (bacteria, fungi and viruses) using our in-house well-characterised assays (ELISA and ELIspot, respectively). These provided quantitative outputs of specific antibody titre and reactive gamma-interferon-secreting T cells per million PBMC, validated using positive controls. The sputum of patients was cultured, and microbial colonisation defined using prior definitions. Correlations between culture status and bacterial immune responses were analysed.ResultsThe predominant pathogens varied between BE and COPD as expected (percentages in Table 1). These included Pseudomonas, Haemophilus influenzae, Streptococcus pneumoniae and Moraxella spp. We found that specific IgG antibody responses correlated with bacterial sputum culture data for Pseudomonas (R = 0.61, p = 0.0001), but not with lung function nor number of exacerbations. In contrast, specific T cell responses did not correlate with microbiology.Abstract S71 Table 1 ConclusionsOur findings suggest that immune responses measured in the blood against potential lung pathogens contribute minimally to protection from infection or pathology. These tests may however help define colonisation status and could be used as surrogate markers of pathogens in the lung. The poor correlation between T cell responses may be a facet of the disease.