Gammaherpesviruses and Pulmonary Fibrosis

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Progressive lung fibrosis in humans, typified by idiopathic pulmonary fibrosis (IPF), is a serious cause of morbidity and mortality in people. Similar diseases have been described in dogs, cats, and horses. The cause and pathogenesis of such diseases in all species is poorly understood. There is growing evidence in human medicine that IPF is a manifestation of abnormal wound repair in response to epithelial injury. Because viruses can contribute to epithelial injury, there is increasing interest in a possible role of viruses, particularly gammaherpesviruses, in the pathogenesis of pulmonary fibrosis. This review provides background information on progressive fibrosing lung disease in human and veterinary medicine and summarizes the evidence for an association between gammaherpesvirus infection and pulmonary fibrosis, especially Epstein-Barr virus in human pulmonary fibrosis, and equine herpesvirus 5 in equine multinodular pulmonary fibrosis. Data derived from experimental lung infection in mice with the gammaherpesvirus murine herpesvirus are presented, emphasizing the host and viral factors that may contribute to lung fibrosis. The experimental data are considered in the context of the pathogenesis of naturally occurring pulmonary fibrosis in humans and horses.

Related collections

Most cited references 77

Record: found
Abstract: not found
Article: not found

Fibrotic disease and the T(H)1/T(H)2 paradigm.

Thomas Wynn (2004)

0 comments Cited 487 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Idiopathic pulmonary fibrosis: prevailing and evolving hypotheses about its pathogenesis and implications for therapy.

M. Selman, T E King, A. Pardo (2001)

Idiopathic pulmonary fibrosis is a progressive and usually fatal lung disease characterized by fibroblast proliferation and extracellular matrix remodeling, which result in irreversible distortion of the lung's architecture. Although the pathogenetic mechanisms remain to be determined, the prevailing hypothesis holds that fibrosis is preceded and provoked by a chronic inflammatory process that injures the lung and modulates lung fibrogenesis, leading to the end-stage fibrotic scar. However, there is little evidence that inflammation is prominent in early disease, and it is unclear whether inflammation is relevant to the development of the fibrotic process. Evidence suggests that inflammation does not play a pivotal role. Inflammation is not a prominent histopathologic finding, and epithelial injury in the absence of ongoing inflammation is sufficient to stimulate the development of fibrosis. In addition, the inflammatory response to a lung fibrogenic insult is not necessarily related to the fibrotic response. Clinical measurements of inflammation fail to correlate with stage or outcome, and potent anti-inflammatory therapy does not improve outcome. This review presents a growing body of evidence suggesting that idiopathic pulmonary fibrosis involves abnormal wound healing in response to multiple, microscopic sites of ongoing alveolar epithelial injury and activation associated with the formation of patchy fibroblast-myofibroblast foci, which evolve to fibrosis. Progress in understanding the fibrogenic mechanisms in the lung is likely to yield more effective therapies.

0 comments Cited 394 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Macrophages and tissue injury: agents of defense or destruction?

Jeffrey D. Laskin, Jessica C. Gardner, Debra L. Laskin … (2010)

The past several years have seen the accumulation of evidence demonstrating that tissue injury induced by diverse toxicants is due not only to their direct effects on target tissues but also indirectly to the actions of resident and infiltrating macrophages. These cells release an array of mediators with cytotoxic, pro- and anti-inflammatory, angiogenic, fibrogenic, and mitogenic activity, which function to fight infections, limit tissue injury, and promote wound healing. However, following exposure to toxicants, macrophages can become hyperresponsive, resulting in uncontrolled or dysregulated release of mediators that exacerbate acute tissue injury and/or promote the development of chronic diseases such as fibrosis and cancer. Evidence suggests that the diverse activity of macrophages is mediated by distinct subpopulations that develop in response to signals within their microenvironment. Understanding the precise roles of these different macrophage populations in the pathogenic response to toxicants is key to designing effective treatments for minimizing tissue damage and chronic disease and for facilitating wound repair.