Table 2. Effect of infection and route of infection on porcine surfactant protein D (pSP-D) immunoreactivity in the lungs.
| Route of infection | Type of pneumonia | Age of lesions | Infection type | No. of animals | Bacteria | pSP-D upregulation* | pSP-D present in DCs in BALT |
|---|---|---|---|---|---|---|---|
| Aerogeneous | Bronchopneu. | Acute | Experimental | 3 | A. pleuropn. | + | + |
| Chronic | Natural | 7 | A. pleuropn. | + | + | ||
| 1 | Staph. aureus | + | + | ||||
| Haematogenous | Embolic | Chronic | Natural | 2 | Staph. aureus | + | − |
| 3 | Staph. aureus | − | − | ||||
| 3 | Ar. pyogenes | − | − | ||||
| Interstitial† | Acute | Experimental | 4 | Strep. suis | − | ||
| Uninfected controls | 6 | − | − |
*
The extent of the pSP-D immunoreactivity in the surfactant in pulmonary lesions was compared to the extent in normal lung tissue from the same animal, or to the extent in uninfected controls, to determine the degree of up-regulation.
†
Systemic infection induced aerogeneously with the tonsils as entrance portal.25
A. pleuropneumoniae, Actinobacillus pleuropneumoniae; Ar. pyogenes, Arcanobacterium pyogenes; BALT, bronchus-associated lymphoid tissue; Bronchopneu., Bronchopneumonia; DCs, dendritic cells; Staph. aureus, Staphylococcus aureus; Strep. suis, Streptococcus suis.