Table 3.

Analysis of Survival Cohorts of Wild-Type, G−/−, GM−/−, and G−/−GM−/− Mice

GenotypeNo. of DeathsMean Age at Death (wk)3-152Apparent Primary CauseInfections EncounteredOther Findings
(no. examined)3-150of Death (no. of mice)(% animals affected)
Wild-type 8 (4) 44 ± 20 Bowel tumor (2) None evident  
   Renal cyst (1)   
   No cause evident (1)   
G−/− 31 (24) 53 ± 16 Infection and amyloid (10) Any infection (63%) No pulmonary infections found 
   Infection alone (5) Superficial cellulitis (38%) Amyloidosis in 54% 
   No cause evident (4) Abscess formation (hepatic, intraabdominal, or perianal) (25%) Thickening of alveolar septae in 79% 
   Tumors (lymphoma, soft-tissue, pancreatic) (3) Bacterial isolates: S aureus × 1, P mirabilis × 1, Pasturella haemolytica × 1, Enterococci × 1  
   Amyloid without infection (2)   
GM−/− 29 (19) 66 ± 12 Proteinosis and lung infection (8) Any infection (84%) All animals had lung proteinosis3-151 
   Extrapulmonary infection (7) Pulmonary infection (53%) Amyloidosis in 16% 
   Lung proteinosis alone (3) Soft-tissue infections (42%)  
   Tumor (uterine) (1) Bacterial isolates: S aureus × 1, Pasturella pneumotropica × 3, Streptococcus sp. × 2  
G−/−GM−/− 43 (25) 49 ± 19 Extrapulmonary infection (8) Any infection (64%) All animals had lung proteinosis; lymphoid accumulation more severe and widespread than in GM−/− 3-151 
   Proteinosis and lung infection (7) Pulmonary infection (36%) Thickening of alveolar septae in 33% 
   Lung proteinosis alone (6) Soft-tissue infection (36%) Amyloidosis in 25% 
   No cause evident (3) Bacterial isolates: S aureus × 1  
   Tumor (lung) (1)   
GenotypeNo. of DeathsMean Age at Death (wk)3-152Apparent Primary CauseInfections EncounteredOther Findings
(no. examined)3-150of Death (no. of mice)(% animals affected)
Wild-type 8 (4) 44 ± 20 Bowel tumor (2) None evident  
   Renal cyst (1)   
   No cause evident (1)   
G−/− 31 (24) 53 ± 16 Infection and amyloid (10) Any infection (63%) No pulmonary infections found 
   Infection alone (5) Superficial cellulitis (38%) Amyloidosis in 54% 
   No cause evident (4) Abscess formation (hepatic, intraabdominal, or perianal) (25%) Thickening of alveolar septae in 79% 
   Tumors (lymphoma, soft-tissue, pancreatic) (3) Bacterial isolates: S aureus × 1, P mirabilis × 1, Pasturella haemolytica × 1, Enterococci × 1  
   Amyloid without infection (2)   
GM−/− 29 (19) 66 ± 12 Proteinosis and lung infection (8) Any infection (84%) All animals had lung proteinosis3-151 
   Extrapulmonary infection (7) Pulmonary infection (53%) Amyloidosis in 16% 
   Lung proteinosis alone (3) Soft-tissue infections (42%)  
   Tumor (uterine) (1) Bacterial isolates: S aureus × 1, Pasturella pneumotropica × 3, Streptococcus sp. × 2  
G−/−GM−/− 43 (25) 49 ± 19 Extrapulmonary infection (8) Any infection (64%) All animals had lung proteinosis; lymphoid accumulation more severe and widespread than in GM−/− 3-151 
   Proteinosis and lung infection (7) Pulmonary infection (36%) Thickening of alveolar septae in 33% 
   Lung proteinosis alone (6) Soft-tissue infection (36%) Amyloidosis in 25% 
   No cause evident (3) Bacterial isolates: S aureus × 1  
   Tumor (lung) (1)   
F3-150

Animals found dead were not subject to histologic or microbiologic analysis.

F3-151

Both the mean severity and extent of lymphoid perivascular accumulation were greater in G−/−GM−/− mice than in GM−/− mice (3.0 v 2.1 and 79% v 44%, respectively, both P ≤ .0004), whereas the mean severity and extent of surfactant accumulation were not significantly different in G−/−GM−/− and GM−/− animals at the time of death (2.7 v 2.7 and 73% v 83%, respectively, both P > .1).

F3-152

Mean age ± 1 SD of all animals dying, regardless of whether found dead or killed.

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