Activation of Lymphocytes in the Pulmonary Inflammatory Response to Silica

Abstract

Lymphocytes were separated from the parenchymal lung tissue of mice administered either silica or titanium dioxide particles by intratracheal injection. There was an approximately 10-fold increase in the number of T-lymphocytes recovered from silica-treated animals at 2 weeks after injection. This was accompanied by an increase in the percentage of separated cells expressing the interleukin-2 receptor and by enhanced spontaneous DNA synthesis in serum-free culture. No such changes were demonstrable in cells obtained from animals administered titanium dioxide. These results confirm that an influx of T-lymphocytes occurs as part of the early pulmonary inflammatory response to silica particles. Furthermore, lymphocytes in the lung are functionally activated by at least two criteria. Activated T-lymphocytes may play a role in the induction of fibroblast proliferation and collagen synthesis that occurs in silicotic lung disease.

Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis

“…Silica-induced immunostimulation is an intriguing phenomenon that has been previously described (11,12). Massive increase in lymph node size (13) and sustained activation of distinct T lymphocyte populations (13)(14)(15) suggest that silica is mitogenic for T lymphocytes.…”

“…In experimental models, the lung response to silica deposition recruits host T lymphocytes, as well as macrophages and neutrophils (11,12), and induces marked enlargement of draining lymph nodes (13), with increased production of type 1 cytokine interferon-␥ in both thoracic lymph nodes (13,14) and intrapulmonary lymphocytes (15). Therefore, exposure to silica stimulates lymphocyte populations and phagocytic leukocytes in a sustained manner.…”

Role of p53–fibrinolytic system cross-talk in the regulation of quartz-induced lung injury

“…c o m / l o c a t e / y t a a p . cytokines (Davis et al, 2001;Suzuki et al, 1996;Kumar et al, 1990;Arras et al, 2006) and development of lung fibrosis. In addition, literature survey suggests that apoptosis plays a crucial role in the development of silicosis (Iyer et al, 1996;Lim et al, 1999;Borges et al, 2002).…”

Immunostimulatory Effects of the Anionic Alkali Mineral Complex BARODON on Equine Lymphocytes

“…Subchronic and short-term exposure to silica was shown to enhance respiratory defense mechanisms by increasing the proportions of neutrophils, T lymphocytes, and NK cells and by activating phagocytes to release more reactive oxygen species, which have been known to help in the pulmonary clearance of infectious agents in lungs (3,4,33). More specifically, in the thoracic lymph nodes of rats with subchronic silicosis, a significantly higher percentage of CD8 ϩ T cells and, to a lesser degree, CD4 ϩ T cells was proliferated and activated, with the expression of IL-2R and intercellular adhesion molecule 1 and enhanced expression of IFN-␥ mRNA, which may be an important priming cytokine for a systemic preactivation not only of alveolar macrophages but also of peritoneal macrophages that have experienced no direct contact with silica particles (8,23,34,40).…”