To assess the effect of Lactobacillus supplementation on Helicobacter pylori eradication rates and side effects of the triple therapy. PubMed, Embase, Web of Science and Cochrane Library were searched for articles published up to July, 2019. Review Manager 5.3 and Stata 12.0 were used for statistical analyses. The initial database search resulted in 852 articles. Through exclusion and screening, 11 randomized controlled trials involving a total of 724 patients were finally included in this meta-analysis. The H. pylori elimination rate in the Lactobacillus supplement group was significantly higher than that in the control group (RR 1.16, 95% CI 1.08–1.25, P<0.0001). Subgroup analysis showed that the eradication rates were significantly enhanced in both adults and children group, and no significant difference was detected between Asia and Europe group. In addition, sub-analysis based on duration of Lactobacillus supplementation showed the pooled RRs in the long-term and short-term groups were 1.17 (95%CI 1.06–1.30) and 1.16 (95% CI 1.04–1.30), respectively. Regarding the Lactobacillus strains, the pooled RR was 1.33 (95% CI 1.10–1.62) in the L. casei group, 1.18 (95% CI 1.03–1.34) in the L. reuteri group while 1.02 (95% CI 0.87–1.21) in the Lactobacillus GG group. As for the total side effects, Lactobacillus supplementation significantly reduced the incidence of taste disturbance (RR = 0.36, 95% CI 0.17–0.74, P = 0.005). Lactobacillus supplementation during the treatment of Helicobacter pylori infection can effectively improve the eradication rates, and reduce the incidence of therapy-related taste disturbance.

Background: Helicobacter pylori (H pylori) infection may be a risk factor for cardiovascular disease (CVD), but the reported researches have given conflicting results.Aims: To investigate the association between H pylori infection and risk of atherosclerotic CVD.Materials and Methods: The studies were retrieved in Embase, PubMed, Web of Science (published from Jan 1, 1990, to Jan 31, 2020, language restrictions: English). All studies included used data from case‐control studies and cohort studies of cardiovascular adverse events. Random effect models were used to measure pooled estimates. All data were analyzed with Stata 11.2 SE (StataCorp, College Station, TX).Results: Helicobacter pylori infection increased the risk of adverse cardiovascular events by 51% (40 studies, n = 19 691, odd ratio [OR] = 1.51, 95% confidence interval [CI]: 1.34‐1.70). The effect was greater for studies that the type of CVDs was myocardial infarction (MI) and cerebrovascular disease (MI OR = 1.80, 95% CI: 1.42‐2.26, cerebrovascular disease OR = 1.54, 95% CI: 1.27‐1.89). Meanwhile, CagA seropositive H pylori strains were associated with a significantly increased risk of cardiovascular adverse events based on published research data (OR = 1.73, 95% CI: 1.40‐2.14).Conclusion: In conclusion, H pylori infection enhanced the risk of atherosclerotic cardiovascular adverse events, especially in some patients with MI and cerebrovascular disease. This study will provide guidance for the targeted prevention and treatment of CVDs. But this association need to be confirmed by more prospective studies.

Helicobacter pylori neutrophil-activating protein A subunit (NapA) has been identified as a virulence factor, a protective antigen and a potent immunomodulator. NapA shows unique application potentials for anti-H. pylori vaccines and treatment strategies of certain allergic diseases and carcinomas. However, appropriate production and utilization modes of NapA still remain uncertain to date. This work has established a novel efficient production and utilization mode of NapA by using L. lactis as an expression host and delivery vector, and demonstrated immune protective efficacy and immune modulatory activity of the engineered L. lactis by oral vaccination of mice. It was observed for the first time that H. pylori NapA promotes both polarized Th17 and Th1 responses, which may greatly affect the clinical application of NapA. This report offers a promising anti-H. pylori oral vaccine candidate and a potent mucosal immune modulatory agent. Meanwhile, it uncovers a way to produce and deliver the oral vaccine and immunomodulator by fermentation of food like milk, which might have striking effects on control of H. pylori infection, gastrointestinal cancers, and Th2 bias allergic diseases, including many food allergies.

Enterovirus 71 (EV71) infection has become a major threat to global public health, especially in infants and young children. Epidemiological studies have indicated that EV71 infection is responsible for severe and even fatal cases of hand, foot, and mouth disease (HFMD). Accumulated evidence indicates that EV71 infection triggers a plethora of interactive signaling pathways, resulting in host immune evasion and inflammatory response. This review mainly covers the effects of EV71 infection on major antiviral and inflammatory cellular signal pathways. EV71 can activate cellular signaling networks including multiple cell surface and intracellular receptors, intracellular kinases, calcium flux, and transcription factors that regulate antiviral innate immunity and inflammatory response. Cellular signaling plays a critical role in the regulation of host innate immune and inflammatory pathogenesis. Elucidation of antiviral and inflammatory cellular signaling pathways initiated by EV71 will not only help uncover the potential mechanisms of EV71 infection-induced pathogenesis, but will also provide clues for the design of therapeutic strategies against EV71 infection.