Related Articles

Current approaches to tuberculosis in the United States.

JAMA. 2012 Jul 18;308(3):283-9

Authors: Gordin FM, Masur H

Abstract
Tuberculosis is a major threat to global health, infecting a third of the world's population. In the United States, however, control of tuberculosis has been increasingly successful. Only 3.2% of the US population is estimated to have latent tuberculosis and there are only 11,000 cases annually of active disease. More than half the cases in this country occur in individuals born outside the United States. Human immunodeficiency virus coinfection is not a major factor in the United States, since only approximately 10% of cases are coinfected. Drug resistance is also uncommon in this country. Because the United States has more resources for the diagnosis, therapy, and public health control of tuberculosis than many regions of the world, and because many hospitals have more cases of clinically significant nontuberculous mycobacteria than tuberculosis, the management approaches to tuberculosis need to be quite different in this country than in other regions. The resurgence in interest in developing new tools and the investment in public health infrastructure will hopefully be sustained in the United States so that the effect of tuberculosis on the US population will continue to diminish, and these new tools and approaches can be adapted to both high and low prevalence areas to meet the global challenge.

PMID: 22797646 [PubMed - indexed for MEDLINE]

Respiratory Infection and the Impact of Pulmonary Immunity on Lung Health and Disease.

Am J Respir Crit Care Med. 2012 Jul 12;

Authors: Mizgerd JP

Abstract
Acute lower respiratory tract infection is responsible for an inordinate disease burden. Pulmonary immunity determines the outcomes of these infections. The innate and adaptive immune responses to microbes in the lung are critical to maintaining a healthy respiratory system and to preventing pulmonary disease. In addition to balancing antimicrobial defense against the risk of lung injury during the immediate infection, the shaping of pulmonary immunity by respiratory infection contributes to the pathophysiology of many and even perhaps most chronic pulmonary diseases. This Perspective aims to communicate 2 inter-connected points. First, tremendous morbidity and mortality result from inadequate, misguided, or excessive pulmonary immunity. Second, our understanding of pulmonary immunity is at an exciting stage of rapid developments and discoveries, but many questions remain. Further advances in pulmonary immunity and elucidation of the cellular and molecular responses to microbes in the lung are needed in order to develop novel approaches to predicting, preventing, and curing respiratory disease.

PMID: 22798317 [PubMed - as supplied by publisher]

Related Articles

The genetic and environmental causes of pulmonary fibrosis.

Proc Am Thorac Soc. 2012 Jul;9(3):120-5

Authors: Macneal K, Schwartz DA

Abstract
Although substantial progress has been made in understanding the clinical, radiological, and pathological manifestations of fibrosing interstitial lung diseases (ILD), it remains difficult for the clinician to predict the clinical course or the response to therapy for the subtypes of ILD, even from individual to individual with the same diagnosis. This article reviews the genetic and environmental causes of pulmonary fibrosis, specifically focusing on genetic and epigenetic variants of MUC5B and several types of ILD, to discuss why only some individuals with the MUC5B promoter polymorphism develop pulmonary fibrosis. Once we discover how these genetic and epigenetic risks lead to the development of ILD, we and others can apply these discoveries to: (1) identify individuals at risk of developing ILD, (2) diagnose the condition at an earlier stage, (3) identify novel mechanisms that cause ILD, and (4) eventually develop personalized therapeutic strategies for intervention.

PMID: 22802285 [PubMed - in process]

Related Articles

Stem cells and pulmonary fibrosis: cause or cure?

Proc Am Thorac Soc. 2012 Jul;9(3):164-71

Authors: McNulty K, Janes SM

Abstract
Pulmonary fibrosis is a feature of a number of important lung diseases, and alveolar epithelial injury plays a key role in their pathogenesis. Traditionally, type II alveolar epithelial cells have been viewed as the progenitor cells of the alveolar epithelium; however, recent studies have identified a number of other progenitor and stem cell populations that may participate in alveolar epithelial repair. These studies suggest that the injury microenvironment plays a role in regulation of progenitor cell populations. In human idiopathic pulmonary fibrosis, epithelial abnormalities including altered cell cycling characteristics, hyperplasia, and metaplasia are observed, suggesting that dysregulation of epithelial progenitor cells contributes to the characteristic aberrant repair process. Reactivation of developmental signaling pathways such as the Wnt-β-catenin pathway is implicated in the dysregulation of these cells, and targeting these pathways may provide opportunities for therapeutic intervention. There has been a great deal of interest in the delivery of exogenous stem cells as a therapeutic strategy, and various stem and progenitor cell populations have improved outcomes in animal lung fibrosis models. The contributions of these cells to alveolar epithelial regeneration have been variable, and secretion of soluble mediators has been implicated in the beneficial effects. It remains to be seen whether the promising results seen in the preclinical studies will translate to human disease, and the first studies using mesenchymal stem cells in clinical trials for fibrotic lung disease are underway. Strategies using other stem cell populations hold promise, but currently these are a lot further from the bedside.

PMID: 22802292 [PubMed - in process]