Phenotypes associated with this allele

• Allele Symbol: Alox5^tm1Bhk
• Allele Name: targeted mutation 1, Beverly Koller
• Allele ID: MGI:1933120
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Alox5^tm1Bhk/Alox5^tm1Bhk	either: (involves: 129P2/OlaHsd * C57BL/6) or (involves: 129P2/OlaHsd * C57BL/6 * DBA/2)	MGI:3589443

Genotype
MGI:3589443

hm1

• Allelic Composition: Alox5^tm1Bhk/Alox5^tm1Bhk
• Genetic Background: either: (involves: 129P2/OlaHsd * C57BL/6) or (involves: 129P2/OlaHsd * C57BL/6 * DBA/2)

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

immune system

abnormal neutrophil physiology ( J:68714 )

impaired neutrophil chemotaxis ( J:68714 )

• treatment with indomethacin (a potent cyclooxygenase inhibitor) prior to AA application significantly reduces neutrophil migration in homozygous mutants relative to wild-type mice

impaired neutrophil recruitment ( J:68714 )

• 24 hrs after topical arachidonic acid (AA) application, ear biopsies from mutant mice show significantly decreased MPO levels, reflecting reduced recruitment of neutrophils to the inflammed site

abnormal inflammatory response ( J:68714 )

decreased acute inflammation ( J:68714 )

• surprisingly, homozygotes show a relatively normal acute inflammatory response to topical arachidonic acid (AA)

• however, treatment of homozygotes with indomethacin (a potent cyclooxygenase inhibitor) prior to AA application, results in reduced ear edema and decreased vascular permeability and extravasation of serum proteins relative to either wild-type or untreated mutant mice

decreased susceptibility to type I hypersensitivity reaction ( J:68714 )

• homozygotes are resistant to platelet-activating factor-induced anaphylaxis, with ~50% of mutants (versus 0% of wild-type mice) surviving the lethal shock

hematopoietic system

hematopoietic system phenotype ( J:68714 )

N • homozygotes are viable, fertile and display no significant differences in growth, size, lymphoid organ histology or development of myeloid and lymphoid populations relative to wild-type mice

abnormal neutrophil physiology ( J:68714 )

impaired neutrophil chemotaxis ( J:68714 )

• treatment with indomethacin (a potent cyclooxygenase inhibitor) prior to AA application significantly reduces neutrophil migration in homozygous mutants relative to wild-type mice

impaired neutrophil recruitment ( J:68714 )

• 24 hrs after topical arachidonic acid (AA) application, ear biopsies from mutant mice show significantly decreased MPO levels, reflecting reduced recruitment of neutrophils to the inflammed site

homeostasis/metabolism

decreased leukotriene level ( J:68714 )

• in culture, mutant peritoneal macrophages fail to produce detectable LTC4 levels following Ca²⁺-ionophore stimulation

increased prostaglandin level ( J:68714 )

• in culture, mutant peritoneal macrophages produce significantly increased prostaglandin E2 levels following Ca²⁺-ionophore stimulation

abnormal thromboxane level ( J:68714 )

• in culture, mutant peritoneal macrophages produce significantly increased TXB2 levels following Ca²⁺-ionophore stimulation

cellular

impaired neutrophil chemotaxis ( J:68714 )

• treatment with indomethacin (a potent cyclooxygenase inhibitor) prior to AA application significantly reduces neutrophil migration in homozygous mutants relative to wild-type mice