We analyzed the main karyologic changes that have occurred during the dispersion of Triatoma infestans, the main vector of Chagas disease. We identified two allopatric groups, named Andean and non-Andean. The Andean specimens present C-heterochromatic blocks in most of their 22 chromosomes, whereas non-Andean specimens have only 4–7 autosomes with C-banding. These heterochromatin differences are the likely cause of a striking DNA content variation (approximately 30%) between Andean and non-Andean insects. Our study, together with previous historical and genetic data, suggests that T. infestans was originally a sylvatic species, with large quantities of DNA and heterochromatin, inhabiting the Andean region of Bolivia. However, the spread of domestic T. infestans throughout the non-Andean regions only involved insects with an important reduction of heterochromatin and DNA amounts. We propose that heterochromatin and DNA variation mainly reflected adaptive genomic changes that contribute to the ability of T. infestans to survive, reproduce, and disperse in different environments.

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Cystic fibrosis is a genetic disease caused by mutations in the CFTR gene, whereas chronic obstructive pulmonary disease (COPD) is mainly caused by environmental factors (mostly cigarette smoking) on a genetically susceptible background. Although the etiology and pathogenesis of these diseases are different, both are associated with progressive airflow obstruction, airway neutrophilic inflammation, and recurrent exacerbations, suggesting common mechanisms. The airway epithelium plays a crucial role in maintaining normal airway functions. Major molecular and morphologic changes occur in the airway epithelium in both CF and COPD, and growing evidence suggests that airway epithelial dysfunction is involved in disease initiation and progression in both diseases. Structural and functional abnormalities in both airway and alveolar epithelium have a relevant impact on alteration of host defences, immune/inflammatory response, and the repair process leading to progressive lung damage and impaired lung function. In this review, we address the evidence for a critical role of dysfunctional airway epithelial cells in chronic airway inflammation and remodelling in CF and COPD, highlighting the common mechanisms involved in the epithelial dysfunction as well as the similarities and differences of the two diseases.

Airway inflammation is now recognized as a major factor in the pathogenesis of lung disease in cystic fibrosis (CF). Its most characteristic feature is a marked and persistent influx into the airways of neutrophils, which damage the lung by releasing noxious mediators, such as reactive oxygen species and proteolytic enzymes.Recent studies suggest that inflammation occurs very early and may even happen in the absence of infection. Furthermore, links between CF transmembrane conductance regulator dysfunction and both infection and inflammation are postulated; dysregulation of cytokine production and abnormal epithelial host defences have been regarded as causes of sustained inflammation.Bronchoalveolar lavage and the evaluation of neutrophils and inflammatory mediators provide the most accurate picture of airway inflammation. Routine bronchoscopy with bronchoalveolar lavage, however, is unpleasant for the patient and usually is of no immediate benefit to the management of individual cases.Therefore, surrogate markers collected by noninvasive procedures would be of great assistance in the follow-up of cystic fibrosis patients. Several markers have been evaluated in the sputum, serum and urine of cystic fibrosis patients and related to the degree of airway inflammation. Long-term studies are needed to confirm their potential clinical utility and specificity, and to determine which can be used clinically to monitor disease outcome and efficacy of treatment.

Obstructive lung disease is the major cause of morbidity and mortality in cystic fibrosis (CF). To identify risk factors contributing to FEV(1) decline in CF patients, we carried out a retrospective analysis of clinical and pulmonary function data in a population of CF patients followed up for 5 years and studied the correlation between clinical data and FEV(1) decline. Fifty-one adult CF patients were studied. The FEV(1) decline was related to the following clinical characteristics: CFTR genotype, age, gender, weight, height, age at diagnosis, baseline FEV(1), pancreatic function, presence of airway infection, pancreatic insufficiency and diabetes, number of exacerbations/year and intravenous (i.v.) antibiotic courses/year. Both the number of exacerbations/year and the number of i.v. antibiotic courses/year were strongly related to the FEV(1) decline. Patients with airway infection or with diabetes had significantly lower FEV(1) values during the study as compared with non-infected patients or patients without diabetes; however, both the presence of airway infection or diabetes did not affect the FEV(1) decline. These results suggest that the aggressive treatment of disease exacerbations is crucial for delaying lung function decline in CF.