Faculty Bibliography

This study examined the effects of nitrogen dioxide (NO(2)) exposure on airway inflammation, blood cells, and antiviral respiratory defense. Twenty-one healthy volunteers were exposed on separate occasions to air and 0.6 and 1.5 ppm NO(2) for 3 h with intermittent moderate exercise. Phlebotomy and bronchoscopy were performed 3.5 h after each exposure, and recovered cells were challenged with respiratory viruses in vitro. Blood studies revealed a 4.1% NO(2) dose-related decrease in hematocrit (P = 0.003). Circulating total lymphocytes (P = 0.024) and T lymphocytes (P = 0.049) decreased with NO(2) exposure. Exposure to NO(2) increased the blood lymphocyte CD4(+)-to-CD8(+) ratio from 1.74 +/- 0.11 to 1.85 +/- 0.12 in males but decreased it from 1.88 +/- 0.19 to 1.78 +/- 0.19 in females (P < 0.001 for gender difference). Polymorphonuclear leukocytes in bronchial lavage increased with NO(2) exposure (P = 0.003). Bronchial epithelial cells obtained after exposure to 1.5 ppm NO(2) released 40% more lactate dehydrogenase after challenge with respiratory syncytial virus than with air exposure (P = 0.024). In healthy subjects, exposures to NO(2) at levels found indoors cause mild airway inflammation, effects on blood cells, and increased susceptibility of airway epithelial cells to injury from respiratory viruses.

Detection of human immunodeficiency virus-type 1 (HIV-1) on only one or a few occasions in infants born to infected mothers has been interpreted to indicate that infection may be transient rather than persistent. Forty-two cases of suspected transient HIV-1 viremia among 1562 perinatally exposed seroreverting infants and one mother were reanalyzed. HIV-1 env sequences were not found in specimens from 20; in specimens from 6, somatic genetic analysis revealed that specimens were mistakenly attributed to an infant; and in specimens from 17, phylogenetic analysis failed to demonstrate the expected linkage between the infant's and the mother's virus. These findings argue that transient HIV-1 infection, if it exists, will only rarely be satisfactorily documented.

It has recently been demonstrated that fever, or hyperthermia, results in enhanced survival of lizards infected by Aeromonas hydrophila. In the present study, the effects of hyperthermia on certain immune functions were assayed in vitro with purified human leukocytes. Lymphocyte transformation responses to the mitogen phytohemagglutinin and the common antigen streptokinase-streptodornase were enhanced at 38.5 degrees C relative to 37 degrees C whether analyzed according to absolute counts per minute of incorporated tritiated thymidine or according to stimulation indexes. Enhancement of response was not accompanied by acceleration of response. Augmentation of transformation response was generally not seen at 40 degrees C; incubation at that temperature was associated with decreased cellular viability. Significant, though small, increases of the bactericidal capacity of polymorphonuclear leukocytes at 40 degrees C relative to 37 degrees C were shown at 1 h with Escherichia coli, Salmonella typhimurium, and Listeria monocytogenes, but not with Staphylococcus aureus. Mononuclear phagocytes did not show enhanced bactericidal capacity at the elevated temperature with any of these organisms in this in vitro system. Hyperthermia may enhance certain host defense mechanisms and warrants further study.