The expression of HSP70 in embryonic cells of mammals and its role for their normal development and protection is an important aspect to be investigated in pregnancy and/or mild diabetes. In this sense, the present study evaluated the effects of mild diabetes on maternal reproductive parameters and HSP70 levels in Wistar rats at different stages of life and in their offspring. Mild diabetes was induced by a betacytotoxic drug (streptozotocin) at birth. Four experimental groups were evaluated: at 90 days of age: nonpregnant nondiabetic (ND90) and nonpregnant mild diabetic (D90) female rats, and at term pregnancy: pregnant female rats of both glycemic status were examined (NDP and DP, respectively). The rats were submitted to oral glucose tolerance test, and blood samples were collected for determination of HSP70 levels. In addition, the reproductive performance of pregnant rats was assessed and HSP70 levels determined in their offspring blood samples. The HSP70 levels and maternal reproductive performance presented no difference between ND and D rats, regardless of the life stage. The HSP70 levels were increased in D90 rats and lower in offspring from D rats. Maternal HSP70 levels were positively correlated to the number of dead embryos. In conclusion, mild diabetes did not affect maternal reproductive performance, but high maternal HSP70 levels compromised embryo development. In addition, offspring from D rats exhibited lower HSP70 levels, showing that this protein can be used as an indicator of metabolic consequences of diabetes and predictor of related disorders in adulthood.

Citation: Moreira Santos TM, Vesentini G (2017) Incentive for the research that highlights the relationship between smoking and the development of chronic obstructive pulmonary disease (COPD). Chron Obstruct Pulmon Dis 2: 21. Letter to EditorSmoking, one of the most important public health problems, is responsible for a large number of preventive deaths in the world. It is also the main risk factor for the development of numerous diseases. For the last few decades, it has become a relevant topic for studies, especially because of the damage to the population health with negative consequences to the social, economic and sanitary sector.Cigarette users are exposed to a variety of chemical agents that can cause a series of detrimental health effects. Previous studies have shown that smoking can cause irreparable damage to the genetic material, cell damage and, consequently, the development of pulmonary diseases such as COPD.Likewise, research showing the relationship between smoking and the development of lung diseases should be further explored in order to understand the damage caused by smoking and to encourage people to quit smoking.Although there are several studies about this specific topic, there are few studies that investigate the chronic asymptomatic smokers and its relation with mild and moderate COPD. Such research theme would be essential to demonstrate the changes caused by the use of cigarrete and how these changes are close to patients who already have the disease.Our research team investigates the changes caused by cigarette and studies the relationship between chronic asymptomatic smoker and non-smokers, and patients with mild and moderate COPD. Results are being found (data not yet published), which could enlighten the pathophysiological process involved between cigarette and the risk of disease, including the risk of autoimmune diseases. Among our study variables, we seek to clarify the action of non-physiological stress caused by cigarettes, the genotoxicity, the inflammatory process and the immunological changes.We believe that research in this area tends to improve the understanding, both in basic science and in clinical issues of the pathological processes related to the use of cigarette, which may lead to the development of new therapies. Molecular and immunological techniques may be essential tools for detecting specific molecules and solving existing issues involving these diseases.These studies may open pathways for new research and contribute to the advancement of knowledge about the risk factor involved in smoking and COPD. We hope that this letter will encourage fellow scientists in the areas to invest in this field of research whose main objective is to clarify the changes caused by cigarette and to show that these changes are close and connected to the pathophysiology of COPD. Also, this research can be used as an incentive to smoking cessation and as strategies to effect reduction, consequently decreasing COPD in the population.

Chronic obstructive pulmonary disease (COPD) is an inflammatory airway disease whose incidence and mortality increases every year. COPD is characterized by irreversible airflow limitation based on obstructive bronchiolitis and emphysema. It is associated with an abnormal inflammatory response of the lung to toxic particles or gases, such as cigarette smoke. Recently, an increasing body of evidence has been accumulated for a link between inflammation and autoimmunity in the development of COPD. The idea that autoimmunity could contribute to the development of COPD provides a new angle to understand the pathogenesis of the disease. However, the non-physiological stress caused by environmental factors such as cigarette smoking is linked to the inflammatory process and autoimmunity, and all these factors may contribute to the occurrence of exacerbation in COPD. It will be demonstrated some evidences that support this paradigm and the need to invest in research in this area.

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