Mouse Genome Informatics
hm
    Tlr4tm1Aki/Tlr4tm1Aki
B6.129P2-Tlr4tm1Aki
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
mortality/aging
• mice are resistant to lethal shock induced by a synthetic lipopeptide analogue (Myr3CSK4)

respiratory system
N
• no significant increase in inflammatory cells in the lungs over time (J:114985)
• increased apoptosis in lungs
• significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months
• enlarged air spaces distal to the terminal bronchioles
• destruction of normal alveolar structures
• elastin fibers are thin and fragmented in the lung parenchyma
• reduced elastase inhibitory activity in serum and in bronchoalveolar lavage fluid
• bronchoalveolar protein levels are increased by ozone exposure
• ozone induced increase in bronchoalveolar cell counts is less than in controls at 3 hours but not 24 hours
• ozone exposure does not lead to hyperresponsiveness
• increased lung compliance

homeostasis/metabolism
• azoxymethane and dextran sodium sulfate treatment to induce tumor formation
• no visible polyploid lesions are seen in the intestine as they are in controls
• only 5 of 18 mice have 1-2 small, flat dysplastic lesions compared to all controls having from 1 to 17 lesions, half of which are polyploid
• reduced ischemia/reperfusion injury as indicated by a lower rise in serum urea and creatinine 1 day after injury

tumorigenesis
• azoxymethane and dextran sodium sulfate treatment to induce tumor formation
• no visible polyploid lesions are seen in the intestine as they are in controls
• only 5 of 18 mice have 1-2 small, flat dysplastic lesions compared to all controls having from 1 to 17 lesions, half of which are polyploid

digestive/alimentary system
N
• level of colitis developed after azoxymethane and dextran sodium sulfate treatment is similar to controls (J:135620)

renal/urinary system
• reduced ischemia/reperfusion injury as indicated by a lower rise in serum urea and creatinine 1 day after injury
• fewer apoptotic tubular epithelial cells after ischemia/reperfusion injury as compared to controls except at 5 days after injury when apoptosis is elevated
• tubular epithelial cell proliferation is reduced 10 days after injury relative to controls
• less brush border loss after ischemia/reperfusion injury as compared to controls
• reduced tubular necrosis after ischemia/reperfusion injury as compared to controls
• less cast formation after ischemia/reperfusion injury as compared to controls

Mouse Models of Human Disease
OMIM IDRef(s)
Emphysema, Hereditary Pulmonary 130700 J:114985