Local and remote tissue injury upon intestinal ischemia and reperfusion depends on the TLR/MyD88 signaling pathway

Autor: Bernardo Boris Vargaftig, Thomas Secher, Ricardo Martins Oliveira-Filho, Tatiana Victoni, René Moser, Mamdouh A. Kamal, Andressa de Freitas, Gregoire Lauvaux, Wothan Tavares-de-Lima, Bernhard Ryffel, Alexandre Learth Soares, Fernando Rodrigues Coelho, Rodrigo Guabiraba, François Erard
Přispěvatelé: Immunologie et Embryologie Moléculaires (IEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), Fondation pour la Recherche Medicale (F.R.M., France), the European Community, EC (TB REACT Contract n° 028190), Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (02/06606-3, 04/14128-0), Conselho Nacional de Pesquisa (CNPq)
Jazyk: angličtina
Rok vydání: 2010
Předmět:
Lung Diseases
Male
MESH: Histocytochemistry
Neutrophils
Interleukin-1beta
Vascular permeability
Bacteremia
MESH: Neutrophils
MESH: Intestinal Diseases
My D88
MESH: Mice
Knockout
Mice
MESH: Lung Diseases
0302 clinical medicine
Ischemia
MESH: Interleukin-1beta
Immunology and Allergy
MESH: Animals
Receptor
MESH: Bacteremia
Lung
Mice
Knockout
0303 health sciences
Mice
Inbred BALB C
Microscopy
Histocytochemistry
Toll-Like Receptors
General Medicine
3. Good health
Intestines
Reperfusion Injury
MESH: Survival Analysis
[SDV.IMM]Life Sciences [q-bio]/Immunology
Tumor necrosis factor alpha
medicine.symptom
MESH: Toll-Like Receptors
MESH: Myeloid Differentiation Factor 88
MESH: Intestines
Microbiology (medical)
MESH: Microscopy
Immunology
Bacterial Toxins
MESH: Mice
Inbred BALB C
Inflammation
Lung injury
Biology
Capillary Permeability
03 medical and health sciences
TLR
medicine
Animals
MESH: Lung
MESH: Mice
030304 developmental biology
Innate immune system
Bacteria
Tumor Necrosis Factor-alpha
lung inflammation
MESH: Capillary Permeability
medicine.disease
Survival Analysis
MESH: Male
Intestinal Diseases
MESH: Bacteria
MESH: Bacterial Toxins
intestinal ischemia
MESH: Tumor Necrosis Factor-alpha
Myeloid Differentiation Factor 88
MESH: Reperfusion Injury
MESH: Ischemia
Reperfusion injury
030215 immunology
Zdroj: Medical Microbiology and Immunology
Medical Microbiology and Immunology, Springer Verlag, 2010, 199 (1), pp.35-42. ⟨10.1007/s00430-009-0134-5⟩
ISSN: 0300-8584
1432-1831
Popis: Victoni, Tatiana Coelho, Fernando Rodrigues Soares, Alexandre Learth de Freitas, Andressa Secher, Thomas Guabiraba, Rodrigo Erard, Francois de Oliveira-Filho, Ricardo Martins Vargaftig, B Boris Lauvaux, Gregoire Kamal, Mamdouh A Ryffel, Bernhard Moser, Rene Tavares-de-Lima, Wothan Germany Med Microbiol Immunol. 2010 Feb;199(1):35-42. doi: 10.1007/s00430-009-0134-5. Epub 2009 Nov 26.; International audience; Innate immune responses against microorganisms may be mediated by Toll-like receptors (TLRs). Intestinal ischemia-reperfusion (i-I/R) leads to the translocation of bacteria and/or bacterial products such as endotoxin, which activate TLRs leading to acute intestinal and lung injury and inflammation observed upon gut trauma. Here, we investigated the role of TLR activation by using mice deficient for the common TLR adaptor protein myeloid differentiation factor 88 (MyD88) on local and remote inflammation following intestinal ischemia. Balb/c and MyD88(-/-) mice were subjected to occlusion of the superior mesenteric artery (45 min) followed by intestinal reperfusion (4 h). Acute neutrophil recruitment into the intestinal wall and the lung was significantly diminished in MyD88(-/-) after i-I/R, which was confirmed microscopically. Diminished neutrophil recruitment was accompanied with reduced concentration of TNF-alpha and IL-1beta level. Furthermore, diminished microvascular leak and bacteremia were associated with enhanced survival of MyD88(-/-) mice. However, neither TNF-alpha nor IL-1beta neutralization prevented neutrophil recruitment into the lung but attenuated intestinal inflammation upon i-I/R. In conclusion, our data demonstrate that disruption of the TLR/MyD88 pathway in mice attenuates acute intestinal and lung injury, inflammation, and endothelial damage allowing enhanced survival.
Databáze: OpenAIRE
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