Phenotypes Associated with This Genotype

Genotype
MGI:5297164

hm2

• Allelic Composition: Pglyrp4^tm1Rdz/Pglyrp4^tm1Rdz
• Genetic Background: involves: 129S6/SvEvTac * BALB/c

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

cardiovascular system

gastrointestinal hemorrhage ( J:178053 )

• severe in DSS-treated mice

digestive/alimentary system

gastrointestinal hemorrhage ( J:178053 )

• severe in DSS-treated mice

abnormal intestinal epithelium morphology ( J:178053 )

• DSS-treated mice exhibit extremely severe intestinal bleeding with mild hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration compared with similarly treated wild-type mice

abnormal intestinal mucosa morphology ( J:178053 )

• DSS-treated mice exhibit thickened submucosa compared with similarly treated wild-type mice

abnormal intestinal goblet cell morphology ( J:178053 )

• decreased in DSS-treated mice compared with similarly treated wild-type mice

abnormal crypts of Lieberkuhn morphology ( J:178053 )

• DSS-treated mice exhibit loss of morphology and crypt architecture compared with similarly treated wild-type mice

intestinal ulcer ( J:178053 )

• in DSS-treated mice

abnormal gut flora balance ( J:178053 )

• reduced Lactobacillus/Lactococcus and segmented filamentous bacteria groups

• increased Bacteroides group

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with mild hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration; accelerated and increased weight loss; and accelerated and higher mortality compared with similarly treated wild-type mice

• less severe than in Pglyrp1^tm1Rdz, Pglyrp2^tm1Rdz, or Pglyrp3^tm1Rdz homozygotes

• mice exhibit increased sensitivity to DSS-induced colitis at 3% or 5% DSS compared with wild-type mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:178053 )

• DSS-treated mice exhibit loss of morphology and crypt architecture compared with similarly treated wild-type mice

growth/size/body

weight loss ( J:178053 )

• severe in DSS-treated mice

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:178053 )

• in DSS-treated mice

immune system

increased susceptibility to induced colitis ( J:178053 )

• DDS-treated mice exhibit extremely severe intestinal bleeding with mild hyperplasia of the lamina propria, thickened submucosa, loss of morphology and crypt architecture, progressive complete loss of colonic epithelial layer, decrease in goblet cells, and severe ulceration; accelerated and increased weight loss; and accelerated and higher mortality compared with similarly treated wild-type mice

• less severe than in Pglyrp1^tm1Rdz, Pglyrp2^tm1Rdz, or Pglyrp3^tm1Rdz homozygotes

• mice exhibit increased sensitivity to DSS-induced colitis at 3% or 5% DSS compared with wild-type mice

abnormal chemokine secretion ( J:178053 )

• induced mouse embryonic fibroblasts and peritoneal macrophage exhibit increased CXCL1 production compared with wild-type cells

increased interleukin-6 secretion ( J:178053 )

• in induced mouse embryonic fibroblasts and peritoneal macrophage

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:178053 )

• in DSS-treated mice

cellular

abnormal intestinal goblet cell morphology ( J:178053 )

• decreased in DSS-treated mice compared with similarly treated wild-type mice