[The effects of adenovirus 5 latent infection on pulmonary inflammation caused by biomass fumes in guinea pigs].
OBJECTIVE
To explore the effects of adenovirus 5 (Ad5) latent infection on oxidized injury and inflammation of the lungs caused by exposure to biomass fumes in guinea pigs.


METHODS
Forty-six albino guinea pigs were randomly divided into 2 groups. One group (n = 26) was infected intranasally with Ad5, and the other group (n = 20) was sham-infected with sterile PBS as control. After 22 days, the living animals (n = 20 each) were randomly divided into 2 subgroups. One subgroup was exposed to biomass fumes for 3 weeks, and the other subgroup was exposed to room air. At the end of the experiment, all animals were sacrificed and their lung tissues were examined histopathologically. The levels of interleukin (IL)-8, IL-6, and cell adhesion molecule-1 (CAM-1) in bronchoalveolar lavage fluid (BALF) were measured. The results were analyzed using a two-way analysis of variance (ANOVA) with two crossed factors. The level of significance was P < 0.05.


RESULTS
The exposure to biomass fumes and the latent infection of Ad5 were associated with a significant increase in the total number of airway inflammatory cells in the BALF [(37.1 +/- 5.5) x 10(6)/L and (16.8 +/- 2.3) x 10(6)/L], F = 208.947, 22.687, all P < 0.01). The exposure to biomass fumes was associated with a significant increase in the concentration of IL-8, IL-6, and CAM-1 in the BALF [(0.38 +/- 0.06), (0.188 +/- 0.021) and (6.5 +/- 1.6) mg/kg], F = 13.525 - 69.021, all P < 0.01). The latent infection of Ad5 was associated with a significant increase in the concentration of IL-8, and CAM-1 in the BALF [(0.37 +/- 0.05) and (8.2 +/- 2.1) mg/kg] (F = 11.964, 57.162, all P < 0.01). Ad5 infection had a synergistic effect on the IL-8 and CAM-1 production caused by biomass fume exposure.


CONCLUSIONS
Biomass fumes caused severe histopathological changes and inflammation in lungs of guinea pigs, and Ad5 latent infection aggravated these changes. Increased production of inflammatory cytokines may play an important role in this process.
Shi
Zhe
Z
The State Key Lab of Respiratory Disease, Guangzhou Institute of Respiratory Diseases, the First Affiliated Hospital of Guangzhou Medical College, Guangzhou 510120, China.
Hu
Guo-Ping
GP
Li
Bing
B
Ran
Pi-Xin
PX
D000256:Adenoviridae; D000257:Adenoviridae Infections; D000818:Animals; D005260:Female; D006168:Guinea Pigs; D007249:Inflammation; D011014:Pneumonia / Q000209:etiology; D015208:Smoke Inhalation Injury / Q000821:virology*