The Protective Effects of Helicobacter pylori Infection on Allergic Asthma.

As an ancient Gram-negative bacterium, Helicobacter pylori has settled in human stomach. Eradicating H. pylori increases the morbidities of asthma and other allergic diseases. Therefore, H. pylori might play a protective role against asthma. The "disappearing microbiota" hypothesis suggests that the absence of certain types of the ancestral microbiota could change the development of immunology, metabolism, and cognitive ability in our early life, contributing to the development of some diseases. And the Hygiene Hypothesis links early environmental and microbial exposure to the prevalence of atopic allergies and asthma. Exposure to the environment and microbes can influence the growing immune system and protect subsequent immune-mediated diseases. H. pylori can inhibit allergic asthma by regulating the ratio of helper T cells 1/2 (Th1/Th2), Th17/regulatory T cells (Tregs), etc. H. pylori can also target dendritic cells to promote immune tolerance and enhance the protective effect on allergic asthma, and this effect relies on highly suppressed Tregs. The remote regulation of lung immune function by H. pylori is consistent with the gut-lung axis theory. Perhaps, H. pylori also protects against asthma by altering levels of stomach hormones, affecting the autonomic nervous system and lowering the expression of heat shock protein 70. Therapeutic products from H. pylori may be used to prevent and treat asthma. This paper reviews the possible protective influence of H. pylori on allergic asthma and the possible application of H. pylori in treating asthma.

Role of TLR4/NF-κB Signalling Pathway in Pulmonary Arterial Hypertension in Patients with Chronic Obstructive Pulmonary Disease.

OBJECTIVE: To determine the role of toll-like receptor 4 (TLR4)/ nuclear factor kappa B (NF-κB) signalling pathway in pulmonary arterial hypertension (PAH) in patients with chronic obstructive pulmonary disease (COPD). STUDY DESIGN: An experimental study. PLACE AND DURATION OF STUDY: Department of Respiratory Disease, The Hospital Affiliated to Jiangnan University, Wuxi, Jiangsu, China, from June 2018 to December 2019. METHODOLOGY: Subjects included 98 COPD patients and 22 healthy individuals (control group). COPD patients were divided into two groups as PAH group (PAH group, n=57) and normal pulmonary arterial pressure group (nPAP group, n=41). TLR4 and NF-κB in peripheral blood mononuclear cells (PBMC) were measured by real-time polymerase chain reaction (RT-PCR); and inflammatory cytokine of IL-6 and TNF-α were estimated by enzyme-linked immunosorbent assay (ELISA) of three groups. RESULTS: The levels of TLR4, NF-κB and inflammatory cytokine of IL-6 and TNF-α of PAH group were higher than those in nPAP group and controls (all p<0.05); and controls had a lower levels of TLR4, NF-κB and TNF-α than those n PAP group patients (all p<0.05) except for PAP and IL-6 (p=0.121 and p=0.304, respectively). The expression levels of TLR4 and NF-κB in PBMC were positively related to that PAP and inflammatory cytokine of IL-6 and TNF-α in PAH patients with COPD (all p<0.05), but the positive correlation betweenIL-6 and TNF-α expression level was not established (p=0.170). All parameters in the nPAP group had no significant correlation to each other, it is the same in control (all p>0.05). CONCLUSIONS: Inflammatory mechanisms play an important role in the development of PAH in patients with COPD. TLR4/NF-κB signal transduction pathway is involved in the pathogenesis of PAH, and the expression levels of TLR4/NF-κB may reflect the severity of PAH in patients with COPD. Key Words: Toll-like receptor 4, Nuclear factor kappa B, Pulmonary arterial hypertension, Chronic obstructive pulmonary disease, Inflammatory cytokine.

Prognostic value of FGFR1 gene copy number in patients with non-small cell lung cancer: a meta-analysis.

BACKGROUND: A number of studies have investigated the relationship between fibroblast growth factor receptor1 (FGFR1) gene copy number and survival in non-small cell lung cancer (NSCLC) patients. However, conclusions reported by different parties seem to be inconsistent, especially regarding the differences among different histopathologic subtypes. To derive a more precise estimate of the prognostic significance of FGFR1 gene copy number, we have reviewed published studies and carried out a meta-analysis. METHODS: The meta-analysis was conducted in accordance with PRISMA guidelines. The required data for estimation of individual hazard ratios (HRs) for survival were extracted from the publications and an overall HR was calculated. RESULTS: We identified 6 eligible studies, all dealing with NSCLC. The global quality score ranged 32.5-80%, with a median of 53.33%. For FGFR1 amplification in three studies including differed according to histological type, the overall RR was 0.86 which 95% confidence interval (CI) was 0.75 to 0.99 and P value was 0.048. Combined HR for the six evaluable studies was 1.17 (95% CI: 0.95 to 1.43). In the subgroup of squamous cell lung cancer (SQCC), the combined HR was 1.24 (95% CI: 0.89 to 1.73). For the Asian populations' studies, the combined HR was 1.67 (95% CI: 1.1 to 2.52). CONCLUSIONS: FGFR1 amplification significantly was more frequent in SQCC. FGFR1 was not associated with poorer survival in patients with NSCLC. Furthermore studies will be needed in terms of survival implications.

Diagnostic and prognostic significance of lysophosphatidic acid in malignant pleural effusions.

BACKGROUND: Lysophosphatidic acid (LPA) is an important extracellular signal transmitter and intracellular second messenger in body fluids. It can be detected in the ascitic fluid of patients with ovarian cancer. Increasing evidence shows that LPA can stimulate cancer cell proliferation and promote tumor invasion and metastasis. Our study aimed to evaluate the diagnostic value of LPA in differentiating between malignant pleural effusions (MPEs) and benign pleural effusions (BPEs) and to evaluate the association between the level of LPA in MPE and the prognosis of lung cancer patients. PATIENTS AND METHODS: The level of LPA in the pleural effusions (PEs) of 123 patients (94 MPE, 29 BPE) with lung cancer was evaluated using an enzyme-linked immunosorbent assay. The performance of LPA was analyzed by standard Receiver operator characteristic curve (ROC) analysis methods, using the area under the curve (AUC) as a measure of accuracy. Overall survival (OS) curves and progression-free survival (PFS) curves were based on the Kaplan-Meier method, and the survival differences between subgroups were analyzed using the log-rank or Breslow test (SPSS software). A multivariate Cox proportional hazards model was used to assess whether LPA independently predicted lung cancer survival. RESULTS: The levels of LPA differed significantly between MPE (22.08±8.72 µg/L) and BPE (14.61±5.12 µg/L) (P<0.05). Using a cutoff point of 18.93 µg/L, LPA had a sensitivity of 60% and a specificity of 83% to distinguish MPEs from BPEs with an AUC of 0.769±0.045 (SE) (P=0.000) (95% CI, 0.68-0.857). In the three pathological types of lung cancer patients with MPE, there were no significant associations between LPA levels and the length of PFS and OS (P=0.58 and 0.186, respectively). Interestingly, in the patients with MPE caused by lung adenocarcinoma there were significant associations between the LPA levels and the PFS and OS (P=0.018 and 0.026, respectively). Multivariate analysis showed that the LPA level was an independent prognostic factor for PFS in lung adenocarcinoma. CONCLUSIONS: Our results indicate that LPA can be used as a new biomarker for the diagnosis of MPE caused by lung cancer and that higher levels of LPA are related to shorter PFS in adenocarcinoma of the lung.