Key words: H. influenzae, S. pneumoniae, intranasal infection. mechanism

Transcription

1 Key words: H. influenzae, S. pneumoniae, intranasal infection. mechanism

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3 312 Fig. 1 Viable cells in lungs or tracheas of normal mice after i.n. infection with S. pneumoniae or H. influenzae a) S. pneumoniae TMS3 b) H. influenzae K-14

4 Fig. 2 Total cells and population of lavaged cells in bronchoalveolar lavage fluids of normal mice after i.n. inoculation with S. pneumoniae or H. influenzae a) S. pneumoniae TMS3 b) H. inf K-14

5 314 Fig. 3 In vitro phagocytosis mouse PMN and killing of S. pneumoniae or H. influenzae by a) S. pneumoniae TMS3 b) H. influenzae K-14 Fig. 4 Viable cells in lungs or tracheas of cyclophosphamide i.n. infection with S. pneumoniae or H. influenzae treated mice after a) S. pneumoniae TMS3 b) H. influenzae K-14

6 Fig. 5 Viable cells in lungs or tracheas of formalin-treated mice after i.n. infection with H. influenzae K : Trachea, \ œ \: Lung Fig. 6 Viable cells in lungs or tracheas of cyclophosphamide-and formalin-treated mice after i.n. infection with H. influenzae K-14 Trachea, \ œ \: Lung :

7 1) Aly, R., Straus, W. G. & Maibach, H. I.: Bacterial adherence to nasal mucosal cells. Infect. Immun., 17: , ) Pennington, J. E.: Respiratory tract infectin: Intrinsic risc factors. Am. J. Med., 15: 34-41, ) Johanson, W. G., Woods, D. E. & Chaudhuri, T.: Association of respiratory tract colonization with adherence of gram-negative bacilli to epithelial cells. J. Infect. Dis., 139: , ) Woods, D. E., Straus, P. C., Johanson, W. G. & Bass, J. A.: Role of salivary portease activity in adherence of gram-regative bacilli to mam- buccal epithelial cells in vivo. J. malian Clin. Invest., 18: , ) Sprunt, K. & Redman, W.: Evidence suggesting importance of role of interacterial inhibi- in maintaining balance of normal tion flora.

8 Ann. Inst. Med., 68: , ) Stanley, R. R., Gross, G. N. & Pierce, A. K.: Early bacterial clearance from murine lungs. J. Clin. Invest., 66: , perimental mouse pneumonia following lung injury with one percent formaldehyde. Kawasaki Med. J., 4: 35-39, ) Johanson, W. G. & Pierce, A. K.: Nosoccomi- cal respiratory infections with gram-negative bacilli. The significance of colonization of the respiratory tract. Am. Inst. Med., 77: , ) Quie, P. G., White, J. G., Holmer, B. & Good, R. A.: In vitro bactericidal capacity of human polymorphonuclear leukocytes: Diminised activity in chronic gramulomatous diseases of 13) Matsushima, T., Niki, Y. & Soejima, R.: Ex- 15) Wayne, C. V., Galen, B., Toews, A. & Pierce, K.: Early pulmonary granulocyte recruitment in response to Streptococcus pneumoniae. Am. Rev. Respir. Dis., 129: 87-91, ) Denny, F. W.: Effect of a toxin produced by Haemophilus influenzae on ciliated respiratory epithelium. J. infect. Dis., 129: 93-97, ) Plaut, A. G.: The IgAl protease of pathogenic bacteria. Ann. Rev. Microbiol., 37: , ) Lampe, R. M., Mason, E. D., Kaplan, S. L., Umstead, C. L., Yow, M. D. & Feigin, R. D.: Adherence of Haemophilue influenzae to buccal epithelial cells. Infect. Immun., 35: , children. J. Clin. Invest., 46: , ) Michael, A. A., Shero, M., Dudas, K. C., Stack, R. R., Klohs, W., LaScolea, L. J., Muphy, T. F. & Mylotte, J. M.: Fibriation of Haemophilus species isolated from the respiratory tract of adults. J. Infect. Dis., 150: 40-43, Mechanism of Respiratory Infection due to Streptococcus pneumoniae or Haemophilus influenzae in Mice Shuichi MIYAZAKI, Akira OHNO, Susumu KITAYA, Shinya KUSACHI & Sachiko GOTO Department of Microbiology, School of Medicine, Toho University The sites of Streptococcus pneumoniae and Haemophilus influenzae infection differ in patients with respiratory infection. We investigated the in vivo mechanism of respiratory infection due to these organisms in mice, using an intranasal infection model. Growth factors such as hemin and NAD in the tracheal tissues and a growth inhibitor in the lung tissues were clearly involved in the development of H. influenzae infection. Chronic bronchial infection was caused by imparied mechanical clearance as well as by changes in the quantitative and qualitative function of neutrophilis. In S. pneumoniae infection, the decrease in the functional level of neutrophils was one of the factors in causing respiratory infection.