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COPD is a prevalent lung disease with significant impacts on public health. Affected airways exhibit pulmonary neutrophilia and consequent secretion of pro-inflammatory cytokines and proteases, which result in lung emphysema. Probiotics act as nonspecific modulators of the innate immune system that improve several inflammatory responses. To investigate the effect of Lactobacillus rhamnosus (Lr) on cigarette smoke (CS)-induced COPD C57Bl/6 mice were treated with Lr during the week before COPD induction and three times/week until euthanasia. For in vitro assays, murine bronchial epithelial cells as well as human bronchial epithelial cells exposed to cigarette smoke extract during 24 hours were treated with Lr 1 hour before CSE addition. Lr treatment attenuated the inflammatory response both in the airways and lung parenchyma, reducing inflammatory cells infiltration and the production of proinflammatory cytokines and chemokines. Also, Lr-treated mice presented with lower metalloproteases in lung tissue and lung remodeling. In parallel to the reduction in the expression of TLR2, TLR4, TLR9, STAT3, and NF-κB in lung tissue, Lr increased the levels of IL-10 as well as SOCS3 and TIMP1/2, indicating the induction of an anti-inflammatory environment. Similarly, murine bronchial epithelial cells as well as human bronchial epithelial cells (BEAS) exposed to CSE produced pro-inflammatory cytokines and chemokines, which were inhibited by Lr treatment in association with the production of anti-inflammatory molecules. Moreover, the presence of Lr also modulated the expression of COPD-associated transcription found into BALF of COPD mice group, i.e., Lr downregulated expression of NF-κB and STAT3, and inversely upregulated increased expression of SOCS3. Thus, our findings indicate that Lr modulates the balance between pro-and anti-inflammatory cytokines in human bronchial epithelial cells upon CS exposure and it can be a useful tool to improve the lung inflammatory response associated with COPD.

BACKGROUND: Cardiovascular disease is the main cause of death in patients with type 1 diabetes. Since oxidized low density lipoprotein (LDL) is considered to be a critical factor in the atherosclerotic process, the aim of our study was to assess the influence of different parameters of glycemic control on susceptibility to oxidative stress from low density lipoprotein (LDL) in patients with type 1 diabetes without microvascular or macrovascular complications. METHODS: Forty patients and 33 non-diabetic individuals matched for gender, age and body mass index (BMI) were evaluated. The two groups underwent determination of lipid profile, fasting and postprandial glucose control and measurement of glycated hemoglobin (HbA1c). Spectrophotometric analysis of the LDL oxidation index was performed before and 1, 3, 6 and 24 h after the addition of copper sulfate to purified LDL fractions. RESULTS: The oxidation coefficient for LDL presented similar basal values in the two groups; however, at 3 h, LDL showed a higher degree of oxidation in patients with type 1 diabetes. Correlations with the metabolic control variables were significant only for postprandial glycemia. Stepwise multiple regression showed that postprandial glycemia and sex were the significant independent variables. CONCLUSION: LDL from patients with type 1 diabetes showed high susceptibility to oxidative stress and this susceptibility was markedly related to the postprandial glucose levels. The influence of our findings on the development of chronic complications in patients with type 1 diabetes must be addressed in prospective studies.

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The potential participation of PAF-acether (PAF) on the paw oedema triggered by enterolobin was investigated. Intraplantar injections of enterolobin )5-20 µg/paw) yielded a dose response curve for edema which appeared after 30 min, peaked in the interval between 2-4 h and faded after 24h. The pre-treatment with BN 52021, but not with other PAF antagonists such as PCA 4248 or WEB 2086, significantly blocked enterolobin-induced oedema. To clarify better the discrepant results obtained with the PAF antagonists, desensitization to PAF was performed. The oedema triggered by enterolobin was not modified in paf desensitized animals. It was concluded that the paw inflammation induced by enterolobin does not require PAF mechanism