Mmp9<tm1Tvu> Targeted Allele Detail MGI Mouse (MGI:1932294)

Mmp9^tm1Tvu
Targeted Allele Detail

Nomenclature

Symbol:	Mmp9^tm1Tvu
Name:	matrix metallopeptidase 9; targeted mutation 1, Thiennu H Vu
MGI ID:	MGI:1932294
Synonyms:	Gelatinase B-Null, GelB^-, MMP-9 KO, MMP-9-, MMP-9KO, Mmp9-
Gene:	Mmp9 Location: Chr2:164766280-164781350 bp, + strand Genetic Position: Chr2, 96.0 cM, cytoband H1-H2

Mutation
origin

Germline Transmission:	Earliest citation of germline transmission: J:47297
Parent Cell Line:	Other (see notes) (ES Cell)
Strain of Origin:	129S6/SvEvTac

Mutation
description

Allele Type:	Targeted (knock-out)
Mutations:	Insertion, Intragenic deletion
	Part of exon 2 and all of intron 2 were replaced with a cassette containing the neomycin resistance gene driven by a PGK promoter. (J:47297)

Find Mice (IMSR)

Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)

Carrying this Mutation:	Mouse Strains: 2 strains available Cell Lines: 0 lines available
Carrying any Mmp9 Mutation:	7 strains or lines available

Phenotype
summary

Phenotype Summary by Mammalian Phenotype terms

(show or hide all annotated terms)

Genotypes are listed in the next section.

Key:

hm	homozygous	ht	heterozygous
cn	conditional genotype	cx	complex: > 1 genome feature
tg	involves transgenes	ot	other: hemizygous, indeterminate,...
N	normal phenotype		expected model not found

Affected Systems

Genotypes:

behavior/neurological

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cardiovascular system

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cellular

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digestive/alimentary system

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growth/size

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hematopoietic system

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homeostasis/metabolism

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immune system

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life span/aging

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limbs/digits/tail

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muscle

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nervous system

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renal/urinary system

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respiratory system

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skeleton

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skin/coat/nails

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touch/vibrissae

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tumorigenesis

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vision/eye

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Disease Models

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Phenotypic
data by
genotype

Phenotypic Data by Genotype

(show or hide all phenotypic details)

Genotype	Allelic Composition	Genetic Background
hm1	Mmp9^tm1Tvu/Mmp9^tm1Tvu	129S6/SvEvTac-Mmp9^tm1Tvu
immune system immune system phenotype (J:113463) mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis
Genotype	Allelic Composition	Genetic Background
hm2	Mmp9^tm1Tvu/Mmp9^tm1Tvu	B6.129S6-Mmp9^tm1Tvu
tumorigenesis decreased tumor incidence (J:105098) mice injected with Lewis lung carcinoma or A549 cells exhibit a decrease in tumors compared with similarly treated wild-type mice altered tumor morphology (J:105098) injected A549 cells exhibit an increase in early apoptosis compared to in wild-type mice
Genotype	Allelic Composition	Genetic Background
hm3	Mmp9^tm1Tvu/Mmp9^tm1Tvu	C3N.129S6-Mmp9^tm1Tvu
immune system decreased susceptibility to induced arthritis (J:150311) B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice however, spirochete numbers in the joint are normal joint inflammation (J:150311) in B. burgdorferi-infected mice compared with similarly treated wild-type mice decreased susceptibility to bacterial infection (J:150311) mice infected with Borrelia burgdorferi exhibit less ankle swelling, joint inflammation, and arthritis than similarly treated wild-type mice however, mice exhibit normal development of carditis when infected with B. burgdorferi skeleton decreased susceptibility to induced arthritis (J:150311) B. burgdorferi-infected mice exhibit reduced arthritis compared with similarly treated wild-type mice however, spirochete numbers in the joint are normal joint inflammation (J:150311) in B. burgdorferi-infected mice compared with similarly treated wild-type mice joint swelling (J:150311) in B. burgdorferi-infected mice compared with similarly treated wild-type mice
Genotype	Allelic Composition	Genetic Background
hm4	Mmp9^tm1Tvu/Mmp9^tm1Tvu	either: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)
skeleton abnormal long bone epiphyseal plate morphology (J:47297) abnormal growth plate development, however after 3 weeks of age, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance except for the shorter long bones abnormal long bone hypertrophic chondrocyte zone (J:47297) ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age apoptosis of hypertrophic chondrocytes is delayed by 3 weeks of age, when the hypertrophic zone is lengthened, aberrant apoptosis begins in the middle of the hypertrophic cartilage and is seen around the areas of ossification throughout the hypertrophic zone at 4 weeks increased width of hypertrophic chondrocyte zone (J:47297) exhibit lengthened zone of hypertrophic cartilage with no difference in the reserve or proliferating zones decreased length of long bones (J:47297) long bones are about 10% shorter than in wild-type short femur (J:47297) short tibia (J:47297) abnormal metatarsal bone morphology (J:47297) hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long abnormal cancellous bone morphology (J:47297) area of metaphyseal trabecular bone is shorter osteopetrosis (J:47297) ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age and the ectopic ossification proceeds rapidly so that in some bones the entire zone of hypertrophic cartilage is ossified, leading to a large area of trabecular bone, however this is resolved with subsequent remodeling so that by 8 weeks, bones appear normal delayed bone ossification (J:47297) secondary (epiphyseal) ossification sites are delayed until 2.5 weeks of age, however, by 3 weeks of age, these sites are completely ossified as in wild-type limbs/digits/tail abnormal long bone epiphyseal plate morphology (J:47297) abnormal growth plate development, however after 3 weeks of age, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance except for the shorter long bones abnormal long bone hypertrophic chondrocyte zone (J:47297) ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age apoptosis of hypertrophic chondrocytes is delayed by 3 weeks of age, when the hypertrophic zone is lengthened, aberrant apoptosis begins in the middle of the hypertrophic cartilage and is seen around the areas of ossification throughout the hypertrophic zone at 4 weeks increased width of hypertrophic chondrocyte zone (J:47297) exhibit lengthened zone of hypertrophic cartilage with no difference in the reserve or proliferating zones decreased length of long bones (J:47297) long bones are about 10% shorter than in wild-type short femur (J:47297) short tibia (J:47297) abnormal metatarsal bone morphology (J:47297) hypertrophic cartilage zone in the metatarsals is about twice that of wild-type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long
Genotype	Allelic Composition	Genetic Background
hm5	Mmp9^tm1Tvu/Mmp9^tm1Tvu	either: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)
cardiovascular system abnormal angiogenesis (J:95880) exhibit reduced angiogenic response to peripheral leg ischemia; do not observe an increase in capillary density and see reduced capillary perfusion capacity and fewer points of capillary intersections (decreased branching) after ischemia
Genotype	Allelic Composition	Genetic Background
hm6	Mmp9^tm1Tvu/Mmp9^tm1Tvu	either: FVB.129S6-Mmp9^tm1Tvu or (involves: 129S6/SvEvTac)
cardiovascular system altered response to myocardial infarction (J:68211) exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type homeostasis/metabolism altered response to myocardial infarction (J:68211) exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild-type
Genotype	Allelic Composition	Genetic Background
hm7	Mmp9^tm1Tvu/Mmp9^tm1Tvu	FVB.129S6-Mmp9^tm1Tvu
life span/aging decreased sensitivity to xenobiotic induced morbidity/mortality (J:104644) DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis cardiovascular system abnormal physiological neovascularization (J:104786) exhibit increased neovascularization post myocardial infarction, as shown by increased total vessel density and normalized vessel distribution between subendo- and epicardial regions relative to wild-type after coronary artery ligation increased angiogenesis (J:104786) exhibit an increased angiogenic potential after myocardial infarction, as shown by the presence of newly formed vessels in the infarct region increased ventricle muscle contractility (J:104786) exhibit higher end-systolic pressure and dP/dt_max than wild-type after myocardial infarction, despite similar infarct sizes altered response to myocardial infarction (J:104786) exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction immune system immune system phenotype (J:104644) decreased susceptibility to induced colitis (J:104644) DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type mice mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice abnormal neutrophil physiology (J:104644) neutrophil chemotatic response to fMLP is greater than for wild-type cells polymononuclear cell migration through Matri-gel-coated membrane in response to fMLP is greater compared with similarly treated wild-type cells homeostasis/metabolism altered response to myocardial infarction (J:104786) exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild-type after myocardial infarction decreased sensitivity to xenobiotic induced morbidity/mortality (J:104644) DSS-treated mice exhibit no mortality unlike similarly treated wild-type mice however, mice exhibit normal mortality in response to Salmonella typhimurium-induced systemic sepsis muscle increased ventricle muscle contractility (J:104786) exhibit higher end-systolic pressure and dP/dt_max than wild-type after myocardial infarction, despite similar infarct sizes digestive/alimentary system decreased susceptibility to induced colitis (J:104644) DSS-treated mice exhibit no weight loss, mortality or lymphocyte accumulation in the colon, reduced neutrophil accumulation, colon shortening, intestinal inflammation, and intestinal injury, and fewer incidence of diarrhea and bleeding compared with similarly treated wild-type mice mice treated orally with Salmonella typhimurium to induce colitis exhibit reduced weight loss and destruction of crypt architecture compared with similarly treated wild-type mice
Genotype	Allelic Composition	Genetic Background
hm8	Mmp9^tm1Tvu/Mmp9^tm1Tvu	FVB.Cg-Mmp9^tm1Tvu/J
life span/aging decreased susceptibility to viral infection induced morbidity/mortality (J:153406) mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice however, mice exhibit a normal survival when injected intracerebrally with West Nile virus immune system decreased susceptibility to viral infection (J:153406) mice infected with West Nile virus exhibit decreased mortality, brain viral load, CD45+ leukocyte infiltration into brain tissue, and blood brain barrier permeability compared with similarly treated wild-type mice however, mice exhibit a normal response to West Nile virus infection when injected intracerebrally with the virus decreased susceptibility to viral infection induced morbidity/mortality (J:153406) mice infected with West Nile virus exhibit decreased mortality compared with similarly treated wild-type mice however, mice exhibit a normal survival when injected intracerebrally with West Nile virus digestive/alimentary system abnormal intestinal goblet cells (J:128322) mice exhibit an increased in the number of intestinal goblet cells compared to in wild-type mice however, the number of goblet cells per crypt is normal behavior/neurological hypoalgesia (J:133660) 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation homeostasis/metabolism abnormal response/metabolism to endogenous compounds (J:147593) mice treated with tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12) exhibit increased body and muscle weight, intact basement membrane, and reduced myopathy, clustering of inflammatory cells, and number of necrotic fibers in the muscle compared with similarly treated wild-type mice decreased susceptibility to injury (J:133660, J:148923) 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice (J:133660) following hepatic ischemia and reperfusion, hepatic apoptosis is decreased compared to in similarly treated wild-type mice (J:148923) however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation (J:133660) touch/vibrissae hypoalgesia (J:133660) 3 days after spinal nerve ligation, mice exhibit less spontaneous pain and early phase mechanical allodynia compared with similarly treated wild-type mice however, mice exhibit normal neuropathic pain by 10 days following spinal nerve ligation cardiovascular system abnormal blood-brain barrier function (J:153406) mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice nervous system abnormal blood-brain barrier function (J:153406) mice infected with West Nile virus exhibit decreased blood brain barrier permeability compared with similarly treated wild-type mice growth/size increased body weight (J:147593) in tumor necrosis factor-related weak inducer of apoptosis (TWEAK or Tnfsf12)-treated mice compared with similarly treated wild-type mice muscle increased muscle weight (J:147593) the weight of the tibialis anterior in mice treated with Tnfsf12-treated mice is greater than in similarly treated wild-type mice
Genotype	Allelic Composition	Genetic Background
hm9	Mmp9^tm1Tvu/Mmp9^tm1Tvu	involves: 129/Sv * 129S6/SvEvTac
homeostasis/metabolism decreased circulating interleukin-10 level (J:55723) DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure immune system decreased circulating interleukin-10 level (J:55723) DNFB-sensitized and challenged mice have lower IL10 levels compared with similarly treated wild-type mice despite normal capacity of spleen cells to produce IL10 after LPS exposure increased susceptibility to type IV hypersensitivity reaction (J:55723) DNFB-sensitized and challenged mice exhibit a prolonged response and delayed resolution of inflammation compared with similarly treated wild-type mice however, resolution of phenol elicited inflammation is normal
Genotype	Allelic Composition	Genetic Background
hm10	Mmp9^tm1Tvu/Mmp9^tm1Tvu	involves: 129S6/SvEvTac
homeostasis/metabolism abnormal blood vessel healing (J:109006) exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen increased circulating interferon-beta level (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice increased circulating interferon-gamma level (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice abnormal chemokine level (J:84293) ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice decreased physiological sensitivity to xenobiotics (J:84293) mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice decreased susceptibility to injury (J:91478, J:79422, J:62760, J:114188) mice are resistant to the pathogenic activity of anti-mBP180 (Col17a1) antibodies that induce subepidermal blistering in wild-type mice (J:91478) mice are resistant to traumatic brain injury compared with similarly treated wild-type mice with smaller traumatic lesion volumes (J:79422) following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice (J:62760) following IgG-induction of acute lung injury, mice exhibit reduced lung injury, decreased BALF protein leakage, and perivascular edema compared with similarly treated wild-type mice (J:114188) however, mice reconstituted with wild-type neutrophils exhibit normal response to anti-Col17a1 antibodies (J:91478) however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms (J:62760) however, the number of macrophages and neutrophils recruited to the lungs is normal in mice with IgG-induced acute lung injury (J:114188) immune system myocarditis (J:148442) CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice decreased dendritic cell number (J:84293) following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice increased circulating interferon-beta level (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice increased circulating interferon-gamma level (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice abnormal chemokine level (J:84293) ovalbumin sensitized and exposed mice exhibit reduced CCL17 protein levels in the bronchoalveolar lavage fluid compared with similarly treated wild-type mice decreased IgE level (J:84293) mice sensitized and exposed to ovalbumin exhibit impaired ovalbumin-IgE production compared with similarly treated wild-type mice abnormal dendritic cell physiology (J:84293) in vitro, chemotaxis of dendritic cells in response to CCL5 (RANTES) and CCL20 (MIP-3alpha) is impaired compared with similarly treated wild-type cells however, homing of dendritic cells from airways to lymph nodes in mice is normal abnormal Langerhans cell physiology (J:76157) migration of Langerhans cells is impaired compared to in wild-type mice however, maturation of Langerhans cells is normal decreased inflammatory response (J:84293) mice sensitized and exposed to ovalbumin fail to exhibit the airway inflammation observed in similarly treated wild-type mice increased susceptibility to viral infection (J:148442) Coxsackievirus B3 (CVB3)-infected mice exhibit increased morbidity, viral load, serum IFN-gamma and IFN-beta, left ventricular posterior wall and interventricular septum thickness, and cardiac injury as determined by increased myocytolysis, calcification, and cellular infiltrate and decreased ejection fraction and E wave compared with similarly treated wild-type mice increased susceptibility to viral infection induced morbidity/mortality (J:148442) CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice cardiovascular system aortic aneurysm (J:62760) following induction of aortic aneurysm with elastase, mice develop fewer aneurysms with less of an increase in aortic diameter compared with similarly treated wild-type mice however, mice reconstituted with wild-type bone marrow exhibit normal susceptibility to elastase-induced aortic aneurysms abnormal induced retinal neovascularization (J:113620) mice exhibit 45% less ischemia-induced retinal neovascularization compared with similarly treated wild-type mice abnormal ventricular septum morphology (J:148442) CVB3-infected mice exhibit increased interventricular septum thickness compared with similarly treated wild-type mice thick ventricular wall (J:148442) CVB3-infected mice exhibit increased left ventricular posterior wall thickness compared with similarly treated wild-type mice cardiac fibrosis (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice abnormal blood vessel healing (J:109006) exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild-type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen abnormal vascular smooth muscle physiology (J:109006) isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro decreased cardiac muscle contractility (J:148442) on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice abnormal impulse conducting system conduction (J:148442) on days 3 and 9, CVB3-infected mice exhibit decreased E wave compared with similarly treated wild-type mice abnormal myocardial fiber physiology (J:148442) myocytolysis is increased in CVB3-infected mice compared to in similarly treated wild-type mice increased susceptibility to dystrophic cardiac calcinosis (J:148442) in CVB3-infected mice compared to in similarly treated wild-type mice myocarditis (J:148442) CVB3-infected mice exhibit an increase in T cell infiltration in the heart compared with similarly treated wild-type mice nervous system abnormal oligodendrocyte morphology (J:105765) exhibit a decrease in the number of mature oligondendrocytes at P10, however no differences in oligodendrocyte precursor cell numbers abnormal myelination (J:105765) exhibit decreased myelination in the corpus callosum at P7 and P10, but not at P14, as evidenced by decreased MBP expression muscle abnormal vascular smooth muscle physiology (J:109006) isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro decreased cardiac muscle contractility (J:148442) on day 9 post-infection in CVB3-infected mice compared to in similarly treated wild-type mice hematopoietic system decreased dendritic cell number (J:84293) following ovalbumin treatment, the numbers of dendritic cell in the bronchoalveolar lavage fluid and airway walls does not increase as much as in similarly treated wild-type mice life span/aging increased susceptibility to viral infection induced morbidity/mortality (J:148442) CVB3-infected mice exhibit increased morbidity compared with similarly treated wild-type mice
Genotype	Allelic Composition	Genetic Background
hm11	Mmp9^tm1Tvu/Mmp9^tm1Tvu	involves: 129S6/SvEvTac * C57BL/6
immune system abnormal leukocyte morphology (J:88065) increased lymphocyte cell number (J:88065) ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue lymphocyte numbers compared with similarly treated wild-type mice increased T-helper 2 cell number (J:88065) on day 24, ovalbumin-treated mice exhibit an increased in Th2 helper cells in the bronchoalveolar lavage compared with similarly treated wild-type mice increased eosinophil cell number (J:88065) on days 24 and 30, ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue eosinophil numbers compared with similarly treated wild-type mice increased macrophage cell number (J:88065) ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue macrophage cell numbers compared with similarly treated wild-type mice increased monocyte cell number (J:88065) ovalbumin-treated mice exhibit an increase in the bronchoalveolar lavage and lung tissue monocyte numbers compared with similarly treated wild-type mice increased T cell proliferation (J:88065) on day 24 hours in ovalbumin-treated wild-type mice compared with similarly treated wild-type mice abnormal chemokine level (J:88065) on day 24, alum treated mice exhibit an increase in CCL22 in lung tissue compared with similarly treated wild-type mice on days 24 and 30, ovalbumin-treated mice exhibit increased CCL11 in the bronchoalveolar lavage compared with similarly treated wild-type mice on day 24, ovalbumin-treated mice exhibit an increase in bronchoalveolar lavage CCL22 compared with similarly treated wild-type mice on day 30, ovalbumin-treated mice exhibit an increase in lung tissue CCL22 compared with similarly treated wild-type mice however, mice exhibit normal levels of CCL2, CCL3, and CCL5 following ovalbumin treatment increased IgE level (J:88065) ovalbumin-treated mice exhibit increased ovalbumin-IgE compared with similarly treated wild-type mice abnormal cytokine secretion (J:88065) decreased interferon-gamma secretion (J:88065) ovalbumin-treated mice exhibit decreased IFN-gamma in bronchoalveolar lavage compared with similarly treated wild-type mice increased interferon-gamma secretion (J:88065) on day 24, T cells from alum-treated mice exhibit increased IFN-gamma secretion compared with cells from similarly treated wild-type mice increased interleukin-13 secretion (J:88065) ovalbumin-treated mice exhibit increased IL13 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice increased interleukin-4 secretion (J:88065) ovalbumin-treated mice exhibit increased IL4 in bronchoalveolar lavage and lung tissue compared with similarly treated wild-type mice on day 24, T cells from ovalbumin-treated mice exhibit increased IL4 secretion compared with cells from similarly treated wild-type mice increased interleukin-5 secretion (J:88065) ovalbumin-treated mice exhibit increased IL5 in lung tissue compared with similarly treated wild-type mice lung inflammation (J:88065) ovalbumin-treated mice exhibit increased lung inflammation with increased total cells, eosinophils, macrophages, lymphocytes, and monocytes in bronchoalveolar lavage and lung tissue compared with similarly treate