The aim of this study was to determine the relationship between the radiological pattern of Mycoplasma pneumoniae and the level of cell-mediated immunity of the host.Computed tomographic (CT) scans of the chest and the results of the purified protein derivative (PPD) test were studied during the acute stage of infection in 54 patients with M. pneumoniae pneumonia. The CT findings were used to divide the patients into two groups: one group had a predominance of nodular opacities with a centrilobular distribution (Group N; n=29); and the other showed a predominance of an airspace consolidation (Group C; n=25).Forty out of 54 subjects had negative tuberculin skin tests (<10 mm induration). The positive rate of PPD reaction was higher in Group N (13 out of 29) compared to Group C (1 out of 25) (p=0.0005); whilst pleural effusion appeared more frequently in Group C (10 out of 25) than in Group N (3 out of 29) (p=0.023). There was no significant difference between Groups N and C in white blood cell and lymphocyte counts, level of antibodies to M. pneumoniae in sera, and severity of the disease.These findings suggest that the characteristics of the host cell-mediated immunity might influence the pattern of pulmonary lesions in M. pneumoniae infection. Eur Respir J., 1996, 9, 669-672. The cell-mediated immunity (CMI) of the host plays an important role in the development of Mycoplasma pneumoniae pneumonia (MP) [1,2]. MIZUTANI et al. [3] reported that the delayed hypersensitivity skin reactions to M. pneumoniae antigen appeared to correlate with severity of pneumonia in human MP. FOY et al. [4] reported that MP infection in patients with immunodeficiency syndrome had a lack of radiological chest findings. PUTMAN et al. [5] reported a bilateral reticulonodular pattern when MP was associated with sarcoidosis. These manifestations suggest that pulmonary infiltrates of MP might be a result of the immunological reaction of the host.The purified protein derivative (PPD) reaction is used to confirm past infection by Mycobacterium tuberculosis, and to determine the CMI of the host. In Japan, most individuals have CMI to PPD due to the nearly universal bacille Calmette-Guérin (BCG) vaccination in childhood. Transient tuberculin anergy has been observed (57-61%) [6,7] during the early stage of MP. TSUNEKAWA et al. [7] reported that blastogenic lymphocyte response to PPD and PPD-induced gamma-interferon (IFN-γ) production were significantly reduced in tuberculin-negative patients with MP. However, the relationship between the pattern of pulmonary lesions and host CMI level in MP has not been evaluated.The findings of chest radiography of MP are varied; CLYDE [8] noted four frequent patterns suggesting MP: bronchopneumonia; nodular infiltration; plate-like atelectasis; and hilar adenopathy. Bronchopneumonia of MP is accompanied by thickening of bronchi, streaks of interstitial infiltration, and small areas of subsegmental atelectasis. The changes are produced by the presence of peribronchial inflammatory cell infiltrati...

The aim of this study was to elucidate the adverse respiratory effects of naturally occurring acid fog. In total, 102 adult asthmatic patients (44 nonatopic and 58 atopic) were studied for a 2 yr period (January 1992 to December 1993) in Kushiro, a city with only a small industrial area, located in the northern-most island in Japan. Fog occurred on 378 out of 731 days, and the acidity of the fog ranged from pH 3.32 to 6.91 (mean pH 4.95). The association between hospital visits for asthma and meteorological factors or air pollutants was investigated. In nonatopic patients, fog, high ozone and water vapour pressure, low day-to-day temperature differences, low concentrations of atmospheric NO and NO2 contributed significantly (p<0.05) to increasing hospital visits. In atopic subjects, fog, high water vapour pressure, low levels of atmospheric NO2 and SO2 contributed significantly to hospital visits (p<0.05). In Poisson regression analysis the remaining factors of significance (p<0.01) for nonatopic asthma were fog and low NO and for atopic asthma were high water vapour pressure and low SO2 (p<0.05). A weak but significant correlation was observed between the number of hospital visits and the mean pH of the foggy day (r=-0.38, p<0.05) in nonatopic asthmatic patients, not in atopic asthma. On foggy days, gaseous air pollutant levels were significantly (p<0.01) lower than on fog-free days. It was concluded that, naturally occurring acid fog may have a weak bronchoconstrictive effect which appears to be more influential in nonatopic asthmatic subjects than in atopic subjects.

To elucidate the immunopathologic mechanisms of Mycoplasma pneumonia, the effects of interleukin-2 (IL-2) and cyclosporin A (CYA) on Mycoplasma pneumonia in mice were investigated. Mice were intranasally inoculated with Mycoplasma pulmonis (M. pul) and treated with IL-2, CYA, or minocycline (MINO) every day between Days 3 and 9. They were killed at Days 7, 14, or 21 after the inoculation. Cell-mediated immunity (CMI) of the host was assessed by delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC). Peribronchial and perivascular lymphocyte cuffing and the accumulation of macrophages at the ends of bronchioles were exacerbated (p < 0.05) in IL-2-treated mice at Day 14 and reduced (p < 0.05) in CYA-treated mice at Day 7. Although the DTH responses to SRBC of saline-inoculated, IL-2-treated mice were increased at Days 7 (p < 0.01) and 14 (p < 0.05), those of M. pul-inoculated, IL-2-treated mice at Day 7 could not recover to the control level. The CMI levels of M. pul-inoculated, CYA-treated mice were decreased at Days 7, 14 (p < 0.05), and 21 (p < 0.01). Mycoplasma organisms in the lung showed the greatest decrease (p < 0.05) in MINO- and IL-2-treated mice, but increased at Day 21 (p < 0.05) in mice treated with IL-2 alone. These results suggest that the pathologic features of Mycoplasma pneumonia could be modified by the degree of host CMI.

Floating fog occurs every summer in Kushiro City in Japan, and the annual average of fog water pH in the past 4 years has been under 5.0. We previously reported that epidemiologically fog was the most important positive factor contributing to increased hospital visits of asthmatic patients compared with other meteorological values and air pollutants. This study aimed to investigate the mechanism of the effects of naturally-occurring acid fog on asthmatic patients. We compared pulmonary functions and inflammatory mediators in induced sputum between the foggy (July 1995) and the non-foggy (May 1996) season, and assessed airway responsiveness to hypo-osmolar aerosol. Forty-four out of 118 asthmatic patients of Kushiro City residents participated, pulmonary function tests were completed in 36 patients, and sputum data were available in 26 patients in both seasons. Percent forced expiratory volume in 1 sec (FEV1) was significantly (P< 0.05) decreased, and % peak expiratory flow rate (PEFR) had a trend to decrease in the foggy season more than in the non-foggy, and sputum eosinophil cationic protein (ECP) and interleukin (IL)-8 were higher in the foggy season but not significantly. A moderate inverse correlation was revealed between sputum ECP and %PEFR in the foggy season (r= -0.55, P<0.005). Subjects were divided into two groups according to the best PEFR; one had >10% lower PEFR levels in the foggy season than in the non-foggy season (Group A, n = 7), the remainder did not (Group B, n = 19). In group A, sputum ECP was significantly increased (P< 0.01) in the foggy season, but there were no changes in IL-8 and prostaglandin D2. Ultrasonic nebulized distilled water provocation test revealed no differences between group A and B. These results suggested that eosinophilic inflammation rather than hypo-osmolar effect of fog might contribute to respiratory deterioration by inhalation of naturally-occurring acid fog.

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