title: Mesenteric fat - control site for bacterial translocation in colitis?
abstract: In Crohn's disease bacteria could be detected in the adjacent mesenteric fat characterized by hypertrophy of unknown function. This study aimed to define effector responses of this compartment induced by bacterial translocation during intestinal inflammation. Dextran sulfate sodium-induced colitis served as a model of intestinal inflammation. Translocation of peptides and bacteria into mesenteric fat was evaluated. Innate functions of mesenteric fat and epithelium were characterized at whole tissue, cellular, and effector molecule levels. Orally applied peptides translocated in healthy wild-type (WT) mice. Bacterial translocation was not detected in healthy and acute but increased in chronic colitis. Mesenteric fat from colitic mice released elevated levels of cytokines and was infiltrated by immune cells. In MyD88(-/-) mice bacterial translocation occurred in health and increased in colitis. The exaggerated cytokine production in mesenteric fat accompanying colonic inflammation in WT mice was less distinct in MyD88(-/-) mice. In vitro studies revealed that fat not only increases cytokine production following contact with bacterial products, but also that preadipocytes are potent phagocytes. Colonic inflammation is accompanied by massive cytokine production and immune cell infiltration in adjacent adipose tissue. These effects can be considered as protective mechanisms of the mesenteric fat in the defense of bacterial translocation.
authors.affiliation: Medical department I, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Batra
authors.forename: M M
authors.initials: MM
authors.lastname: Heimesaat
authors.forename: S
authors.initials: S
authors.lastname: Bereswill
authors.forename: A
authors.initials: A
authors.lastname: Fischer
authors.forename: R
authors.initials: R
authors.lastname: Glauben
authors.forename: D
authors.initials: D
authors.lastname: Kunkel
authors.forename: A
authors.initials: A
authors.lastname: Scheffold
authors.forename: U
authors.initials: U
authors.lastname: Erben
authors.forename: A
authors.initials: A
authors.lastname: Kühl
authors.forename: C
authors.initials: C
authors.lastname: Loddenkemper
authors.forename: H-A
authors.initials: HA
authors.lastname: Lehr
authors.forename: M
authors.initials: M
authors.lastname: Schumann
authors.forename: J-D
authors.initials: JD
authors.lastname: Schulzke
authors.forename: M
authors.initials: M
authors.lastname: Zeitz
authors.forename: B
authors.initials: B
authors.lastname: Siegmund
mesh_terms: D017667:Adipocytes / Q000276:immunology; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D018988:Bacterial Translocation; D002465:Cell Movement; D002478:Cells, Cultured; D003092:Colitis / Q000139:chemically induced / Q000276:immunology* / Q000382:microbiology; D003424:Crohn Disease / Q000276:immunology* / Q000382:microbiology; D016264:Dextran Sulfate / Q000008:administration & dosage; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D050152:Intra-Abdominal Fat / Q000276:immunology*; D008643:Mesentery / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000378:metabolism; D010446:Peptide Fragments / Q000008:administration & dosage; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D053594:Myeloid Differentiation Factor 88; D010446:Peptide Fragments; D016264:Dextran Sulfate