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W K Ashe

Publications and source records attributed to W K Ashe.

13 recordsLinked to original sources
PubMed1997

Gestational exposure to loud noise alters the development and postnatal responsiveness of humoral and cellular components of the immune system in offspring.

Gestational exposure of the female to environmental toxins can alter immune function in the offspring. We have recently shown that prenatal maternal stress, that is, stress applied to or induced in the female during pregnancy, can also alter the development of humoral immunocompetence in the offspring and their hormonal and immunologic responses to postnatal stress. This report presents data from two experiments on the effects of prenatal exposure to loud noise-prenatal sound stress (PSS)-on the development and responsiveness of in vitro and in vivo humoral and cellular immune function in the offspring. Pregnant rats were exposed daily from Day 15 to Day 21 of gestation to an inescapable loud noise (an 85- to 90-decibel fire alarm bell) delivered randomly for 1 hr. In developing offspring, PSS produced age-dependent and mitogen-specific alterations in lymphoproliferative activity and reduced immunoglobulin G levels at Postnatal Day 21. Antibody titers to herpes simplex virus type 1 were also reduced. Exposure to loud noise before or after infection produced an additional reduction in titers in these offspring. Arthus skin reaction (AR) to old tuberculin was reduced by PSS. Combined prenatal/postnatal sound stress further reduced this response and the AR to bovine serum albumin (BSA). Delayed hypersensitivity reaction to BSA was reduced in PSS offspring; postnatal sound stress enhanced the reaction to both antigens, but only in males. Antibody titers to BSA were increased by PSS; adjuvant-induced inflammation was attenuated by postnatal sound stress. These data suggest that in utero exposure to loud noise, which can occur in the workplace, is toxic to the developing immune system.

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PubMed1990

Neurobehavioral and immunological effects of prenatal cocaine exposure in rat.

Time-pregnant Sprague-Dawley rats were injected subcutaneously with 20 mg/kg of cocaine HCl or 0.9% saline daily from gestation days 15 through 21. Maternal plasma levels of approximately 720 ng/ml of cocaine did not alter maternal weight gain during treatment, duration of pregnancy, any of the litter variables or several indices of maternal behavior. Offsprings' body weight from birth to 30 days of age and physical maturation were not generally affected by prenatal cocaine exposure. While the development of surface righting, cliff avoidance, and the startle response was accelerated in cocaine-exposed offspring, acquisition of a preference for a social odor was unaltered. Prenatal cocaine also attenuated the locomotor response of the offspring to d-amphetamine and cocaine at PND 15; at PND 30 both of these catecholaminergic agonists increased activity in prenatal saline and prenatal cocaine offspring. However, the difference in plasma levels of cocaine at PND 30 suggests a possible down-regulation of adrenergic receptors following prenatal cocaine exposure. Decreased thymus/body weight ratios and splenomegaly were observed in prenatal cocaine animals at 55 days of age. Although complete neutralization of herpes simplex virus-type 1 was not observed, sera from prenatal cocaine offspring showed an increased rate of appearance of cytopathic effect, while sera from animals given cocaine postnatally showed a reduction in the rate at which viral infectivity was expressed in culture. These results indicate that prenatal cocaine exposure can alter neurobehavioral ontogeny and humoral immune responsitivity in the offspring.

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PubMed1971

Interaction of rheumatoid factor with infectious herpes simplex virus-antibody complexes.

Rheumatoid factor, a human immunoglobulin of the IgM class, failed to attach to herpes simplex virus but did attach to infectious complexes composed of herpes simplex virus and antibody to herpes simplex virus. These newly formed complexes of infectious virus, antiviral antibody, and rheumatoid factor could be neutralized by complement or by antibody to human IgM. The ability of rheumatoid factor to enhance virus neutralization in the presence of complement represents a hitherto unrecognized biological role for rheumatoid factor.

Animals↗
PubMed1965

Previously unrecognized virus from submaxillary glands of gnotobiotic and conventional rats.

Ashe, Warren K. (National Institute of Dental Research, Bethesda, Md.), Henry W. Scherp, and Robert J. Fitzgerald. Previously unrecognized virus from submaxillary glands of gnotobiotic and conventional rats. J. Bacteriol. 90:1719-1729. 1965.-A serially transmissible cytopathic agent was isolated from histologically normal submaxillary glands, but not from various other tissues or specimens, from 74 of 97 gnotobiotic and conventional rats. Triturates of the glands or subsequent culture supernatant fluids induced specific cytopathic effects (CPE) in monolayer cultures of primary rabbit kidney cells (14 passages), a line of human skin cells (8 passages), and HeLa cells (17 passages). Transfer of supernatant fluids containing infected cells enhanced transmissibility. Neutralization of the CPE was demonstrated with sera of gnotobiotic and conventional rats and with homologous rabbit antiserum. A cold hemagglutinin specific for rabbit erythrocytes is associated with, but separable from, the infectious particle. Cultures of the agent induced no discernible effect on inoculation by various routes into suckling, weanling, or adult conventional mice, rats, and hamsters. Weanling and adult rabbits were also unaffected. Cultures for bacteria in gland extracts and infected cell supernatant fluids were uniformly negative. Negative cultures on PPLO media and negative arginine deiminase tests indicated that this agent is not a Mycoplasma. The data indicate that it is a virus whose biological and physical properties distinguish it from the known cytomegaloviruses. Because it has been found so far only in rat submaxillary glands, this agent is designated provisionally as RSMG virus.

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