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BASIC REVIEW

Pathogenesis of Bacterial Exacerbations of COPD

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Pages 109-115 | Published online: 02 Jul 2009

Figures & data

Figure 1. Proposed model of bacterial infection in COPD.

Figure 1. Proposed model of bacterial infection in COPD.

Figure 2. Time lines and molecular typing for patients with COPD. The horizontal line is a time line, with each number indicating a clinic visit. The arrows indicate exacerbations. Isolates of H. influenzae and M. catarrhalis were assigned types based on sodium dodecyl sulfate-polyacrylamide gel and pulsed-field gel electrophoresis respectively. The types are indicated by letters A to E. Molecular mass standards are noted on the left of the gels. Reproduced with permission from Sethi et al. (Citation[20]).

Figure 2. Time lines and molecular typing for patients with COPD. The horizontal line is a time line, with each number indicating a clinic visit. The arrows indicate exacerbations. Isolates of H. influenzae and M. catarrhalis were assigned types based on sodium dodecyl sulfate-polyacrylamide gel and pulsed-field gel electrophoresis respectively. The types are indicated by letters A to E. Molecular mass standards are noted on the left of the gels. Reproduced with permission from Sethi et al. (Citation[20]).

Table 1. Isolation of a new strain of a bacterial pathogen and increases the risk of exacerbation of COPD

Figure 3. Comparison of H. influenzae exacerbation (Exac) and colonization (Col) strains. *denotes p < 0.05. Reproduced with permission from Chin et al. (Citation[22]). (A) Neutophils in bronchoalveolar lavage (BAL) in response to mouse airway infection with bacterial strains. (B) Adherence of bacterial strains to tracheobronchial epithelial cells in culture. (C) Production of interleukin-8 (IL-8) by tracheobronchial epithelial cells in culture on exposure to bacterial strains.

Figure 3. Comparison of H. influenzae exacerbation (Exac) and colonization (Col) strains. *denotes p < 0.05. Reproduced with permission from Chin et al. (Citation[22]). (A) Neutophils in bronchoalveolar lavage (BAL) in response to mouse airway infection with bacterial strains. (B) Adherence of bacterial strains to tracheobronchial epithelial cells in culture. (C) Production of interleukin-8 (IL-8) by tracheobronchial epithelial cells in culture on exposure to bacterial strains.

Figure 4. Comparison of serum IgG and sputum IgA antibody response to homologous strains of M. catarrhalis following colonization or exacerbation. Based on data from Murphy et al. (Citation[25]). (A) Percent of episodes of colonization or exacerbation that were associated with an antibody response. (B) Intensity of antibody response as a percent change from baseline level of antibody. Median values are shown.

Figure 4. Comparison of serum IgG and sputum IgA antibody response to homologous strains of M. catarrhalis following colonization or exacerbation. Based on data from Murphy et al. (Citation[25]). (A) Percent of episodes of colonization or exacerbation that were associated with an antibody response. (B) Intensity of antibody response as a percent change from baseline level of antibody. Median values are shown.

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