title: The Role of CHI3L1 (Chitinase-3-Like-1) in the Pathogenesis of Infections in Burns in a Mouse Model.
abstract: In severe burn injury the unique setting of a depleted, dysfunctional immune system along with a loss of barrier function commonly results in opportunistic infections that eventually proof fatal. Unfortunately, the dynamic sequence of bacterial contamination, colonization and eventually septic invasion with bacteria such as Pseudomonas species is still poorly understood although a limiting factor in clinical decision making. Increasing evidence supports the notion that inhibition of bacterial translocation into the wound site may be an effective alternative to prevent infection. In this context we investigated the role of the mammalian Chitinase-3-Like-1 (CHI3L1) non-enyzmatic protein predominately expressed on epithelial as well as innate immune cells as a potential bacterial-translocation-mediating factor. We show a strong trend that a modulation of chitinase expression is likely to be effective in reducing mortality rates in a mouse model of burn injury with superinfection with the opportunistic PA14 Pseudomonas strain, thus demonstrating possible clinical leverage.
authors.affiliation: Center for Engineering in Medicine, Shriners Hospitals for Children and Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America; Department Plastic and Hand Surgery-Burn Center, UKA University Clinics RWTH, Aachen, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Bohr
authors.affiliation: Center for Engineering in Medicine, Shriners Hospitals for Children and Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America.
authors.forename: Suraj J
authors.initials: SJ
authors.lastname: Patel
authors.affiliation: Department of Medicine, New York Medical College, Valhalla, NY, United States of America; Department of Nephrology & Rheumatology, UMG University Clinics, Goettingen, Germany.
authors.forename: Radovan
authors.initials: R
authors.lastname: Vasko
authors.affiliation: Center for Engineering in Medicine, Shriners Hospitals for Children and Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America.
authors.forename: Keyue
authors.initials: K
authors.lastname: Shen
authors.affiliation: Center for Engineering in Medicine, Shriners Hospitals for Children and Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America; Porter School of Environmental Studies, Tel Aviv University, Tel Aviv, Israel.
authors.forename: Alexander
authors.initials: A
authors.lastname: Golberg
authors.affiliation: Department of Biomedical Engineering, Rutgers University, New Brunswick, NJ, United States of America.
authors.forename: Francois
authors.initials: F
authors.lastname: Berthiaume
authors.affiliation: Center for Engineering in Medicine, Shriners Hospitals for Children and Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States of America; Department of Biomedical Engineering, Rutgers University, New Brunswick, NJ, United States of America.
authors.forename: Martin L
authors.initials: ML
authors.lastname: Yarmush
mesh_terms: D000818:Animals; D002056:Burns / Q000235:genetics / Q000382:microbiology* / Q000473:pathology*; D000071451:Chitinase-3-Like Protein 1; D004195:Disease Models, Animal; D006023:Glycoproteins / Q000235:genetics*; D051379:Mice; D008810:Mice, Inbred C57BL; D011550:Pseudomonas aeruginosa / Q000472:pathogenicity*; D018805:Sepsis / Q000276:immunology / Q000382:microbiology*; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000473:pathology
chemical_list: C509289:Chil1 protein, mouse; D000071451:Chitinase-3-Like Protein 1; D006023:Glycoproteins