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Cell-mediated immunity (CMI) is critical for the prevention and control of varicella-zoster virus (VZV)-related disease.To assess CMI to VZV, a varicella skin test and interferon-γ enzyme-linked immunospot (ELISPOT) assay were both performed in healthy volunteers, and the results were compared. A total of 151 subjects were examined: 16 aged 20-29 years, 26 aged 30-39 years, 18 aged 40-49 years, 73 aged 50-59 years, and 18 aged 60-69 years. All were seropositive by a glycoprotein antigen- based enzyme-linked immunosorbent assay (gpELISA). Skin test reactivity was significantly correlated with the ELISPOT count, and both decreased with increasing age, indicating an age-dependent decline in CMI to VZV. In contrast, the antibody titer obtained by the gpELISA did not correlate with skin test reactivity. The results suggest that the skin test and ELISPOT assay are both reliable for assessing CMI to VZV and can easily be applied to screen individuals susceptible to the development of herpes zoster. [ABSTRACT FROM AUTHOR]

Inhibitory responses of slowly adapting pulmonary stretch receptor (SAR) activity to CO2 inhalation (maximal tracheal CO2 concentration ranging from 9.5 to 12.5%) for ∼60 s were examined before and after administration of acetazolamide (a carbonic anhydrase inhibitor) or 4-aminopyridine (4-AP, a K+ channel blocker). The experiments were performed in 35 anesthetized, artifically ventilated rats after unilateral vagotomy. Sixty-eight of eighty-four SARs were inhibited by CO2 inhalation. The SAR inhibition was attenuated by pretreatment with either acetazolamide (20 mg/kg, n = 10) or 4-AP (0.7 and 2.0 mg/kg, n = 10). In other series of experiments, stainings to show the existence of carbonic anhydrase (CA) enzymatic reaction were not found in the smooth muscle of either extrapulmonary or intrapulmonary bronchi. Protein gene product 9.5 (PGP 9.5)-immunoreactive SAR terminals to form leaflike extensions were found in the bronchioles at different diameters and were smooth-muscle-related receptors. But in the same sections, CA isozyme II-like (erythrocyte CA) immunoreactive SAR terminals were not identified. These results suggest that CO2-induced inhibition of SARs may be involved in the CA-dependent CO2 hydration in addition to the activation of 4-AP sensitive K+ currents. [ABSTRACT FROM AUTHOR]