7). even at the two-week time point after contamination. Even though antibody response and viral titers did not appear to be affected by either radiation modality, there was a slight increase in monocyte chemo-attractant protein (MCP)-1 expression in the lungs of externally irradiated animals 14 days after Gracillin influenza contamination, with increased cellular infiltration present. Notably, an increase in the number of regulatory T cells was seen in the mediastinal lymph nodes of irradiated mice relative to uninfected mice. These data confirm the hypothesis that early-life irradiation may have long-term effects around the immune system, leading to an altered antiviral response. INTRODUCTION The events at Fukushima Daiichi continue to raise general public concern about exposure to low-dose radiation. It is certainly true that exposure to high-dose radiation remains a significant health hazard as it can lead to Gracillin damaging effects on precursor cell populations. Potential sources of irradiation include areas with high levels of naturally radioactive rocks and salts, medical therapeutic devices, nuclear power herb accidents and terrorist attacks. Exposure can also occur from either external or internal sources, the latter through inhalation or ingestion (1). However, the complexity and range of pathogenic outcomes related to Gracillin radiation exposure have made it hard to ascribe specific long-term effects from such exposures to later life morbidities in human populations. Thus, there is a need to develop animal models for risk assessment, as well as to enable the development of countermeasures against radiological damage (1, 2). It is widely acknowledged that children are especially vulnerable to exposures from a variety of harmful insults as their organs and tissues are still developing (3, 4). Indeed, studies conducted on survivors of fallout from atomic bombs in Japan have revealed a chronic dysregulation in immune function (5). Our group has focused its recent research efforts on identifying the late effects of external irradiation around the adult and neonate lung and, specifically, the irradiated lungs response to delayed immune challenge (6C8). We have shown that external radiation exposure of the adult lung alone prospects to impaired lung function and increased susceptibility to influenza contamination long after radiation exposure and that club cells, a putative stem cell populace, are particularly affected in this model (7, 9, 10). Furthermore, data CD247 suggest that club cell secretory protein (CCSP) plays a role in recovery from such injury in later life (8). We have also reported that total-body irradiation of neonatal mice where all organ systems including the lung and hematopoietic systems are uncovered, leads to increased morbidity and altered pulmonary immune response to later life contamination with influenza computer virus (6). Given that regenerative cell populations, such as club cells, promulgate tissue repair, it is critical for us to understand how they are affected by radiation damage, especially during early development. In the data reported here, we have extended our studies of neonatal animals to mice that were irradiated at day 14 of life, and describe morbidity results after influenza contamination at 26 weeks after exposure. Of notice, postnatal day 14 in mice corresponds to the timeframe of 6C8 years old in human development (11). In addition, since internal irradiation is usually of concern in areas where nuclear power herb disasters have led to inhalation or ingestion of contaminated foods, we also examined the effects of early internal radiation contamination around the late response to contamination. We confirmed that external irradiation during the juvenile period has long-lasting implications for later life.