This study aims to analyze the relationship between social isolation and loneliness with smoking in older adults. This is a cross-sectional, population-based study performed with 986 individuals aged 60 years or older. Data were collected from the Health Survey of the Municipality of Campinas (ISACamp 2014/2015), state of São Paulo, Brazil. We estimated the prevalence of smoking and smoking cessation according to independent variables and tested the associations using the chi-square test, considering a 5% significance level. Adjusted prevalence ratios were calculated using simple and multiple Poisson regression. Smoking and smoking cessation were not associated with most variables that indicate objective social isolation. “Often or always” loneliness was related to a higher prevalence of smoking (PR = 2.25; 95%CI: 1.38-3.66) whereas loneliness accompanied of self-reported emotional problems or common mental disorders was strongly associated with smoking and with lower smoking cessation (PR = 6.24; 95%CI: 1.37-28.47 and PR = 0.46; 95%CI: 0.28-0.77, respectively). These findings indicate that loneliness is a psychosocial aspect related to tobacco use which hinders smoking cessation in older adults, emphasizing the importance of emotional problems in this association.

A polarização de células TCD4+ é um dos mecanismos mais importantes da resposta imunológica. Cada um dos subtipos ou padrões de células são originados a partir da polarização decorrente da interação de células TCD4+ naives com antígenos apresentados por células apresentadoras de antígenos. A expressão de determinados fatores de transcrição e a produção de interleucinas específicas constituem a identidade de cada um deles. Além de Th1 e Th2 já comumente descritos, o papel das polarizações Th17 e Th9 se mostram cada vez mais presentes na fisiopatologia de  diversas doenças e constituem um caminho promissor para traçar possíveis estratégias terapêuticas.

Background Celiac disease (CeD) is an autoimmune T-cell mediated enteropathy, triggered by gluten, a group of proteins found in wheat, barley, and rye. The defined role of gluten as a dietary trigger, necessary genes (HLA-DQ2 and/or DQ8), and tissue transglutaminase (TG2) as the autoantigen together, are unique features of CeD. Although CeD onset can occur at any age, first dietary introduction of gluten during infancy is a critical window of exposure, especially in infants homozygous for the HLA DQ2.5 allele. While adult sensitization studies have been recently performed in DR3-DQ2 mice, the consequences of early life gluten sensitization timing remain unexplored. Aims Our aim was to characterize gluten-immunopathology and CeD-specific serology in specific pathogen free (SPF) DR3-DQ2 transgenic mice sensitized to gluten, 1 week before weaning. Methods Seven-week-old SPF DR3-DQ2 transgenic mice, kept on a gluten-free diet (GFD), were paired for breeding. At post-natal day 3, pups were standardized to 4 per litter (n=2 male, n=2 female) to ensure equal nutrition across litters. At 14 days of age, pups were sensitized with pepsin-trypsin digested gliadin and cholera toxin (CT) three times in one week (n=15). At 21 days of age, pups were weaned and placed either on a gluten-containing diet (n=7), (equivalent of 20g/d of gluten in a human diet -high dose-) or an isocaloric GFD (n=8) until 10 weeks of age. Non-sensitized controls (n=7) received only CT and were kept on the GFD. At sacrifice, serum was collected for anti-TG2 and anti-gliadin antibodies (AGA). Jejunal tissue was collected for histological analysis using villus-to-crypt (V/C) ratios and CD3+ intraepithelial lymphocytes (IEL) counts. Results Gluten-sensitized mice placed on a gluten-containing diet post-weaning had lower V/C ratios and higher CD3+ IEL counts compared with controls (p<0.01). Pre-weaning sensitized mice that were kept on a GFD post-weaning had sustained decreases in V/C ratios and higher CD3+ IEL counts (p<0.01). Out of 15 sensitized mice, 7 developed positive anti-gliadin IgA (p=0.02) and 4 had positive anti-TG2 IgA antibodies (p=0.01) in intestinal contents, irrespective of gluten in the diet. None of the controls had detectable AGA or anti-TG2 antibodies. Conclusions Pre-weaning gluten sensitization of DR3-DQ2 mice induced prolonged gluten immunopathology that did not reverse after 5 weeks on a GFD. Our results indicate that young DR3-DQ2 mice are susceptible to gluten sensitization, with sustained immunopathology, suggesting a critical window of vulnerability in familial carriers of DQ2.5. This novel model will be useful to investigate environmental cofactors at the first time of gluten introduction to the diet. Funding Agencies CIHR