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RESEARCH PRODUCT
Mechanical ventilation alters the development of staphylococcus aureus pneumonia in rabbit
Delphine CroisierLaure Anne PauchardRémi BruyèreJérôme PuginCaroline BruillardPierre Emmanuel CharlesSaber Davide BarbarDavy Hayezsubject
0301 basic medicinePulmonologyPhysiologyStaphylococcusmedicine.medical_treatment[SDV]Life Sciences [q-bio]lcsh:MedicinePharmacologyPathology and Laboratory Medicinemedicine.disease_causeStaphylococcal/immunology/pathologyImmune ReceptorsBiochemistry0302 clinical medicineImmune PhysiologyPneumonia StaphylococcalMedicine and Health SciencesMedicineStaphylococcus Aureuslcsh:ScienceImmune ResponseToll-like ReceptorsMammalsddc:616Innate Immune SystemImmune System ProteinsMultidisciplinaryddc:617RespirationPneumonia Ventilator-AssociatedInterleukinAnimal ModelsHematologyBacterial PathogensBody Fluids3. Good healthBloodmedicine.anatomical_structureMedical MicrobiologyStaphylococcus aureusVertebratesArtificialCytokinesRabbitsPathogensAnatomymedicine.symptomStaphylococcus aureus/immunologyResearch ArticleSignal TransductionToll-Like Receptor 2/immunologyImmunologyInflammationLung injuryResearch and Analysis MethodsMicrobiology03 medical and health sciencesModel OrganismsSigns and SymptomsDiagnostic MedicineAnimalsMicrobial PathogensInflammationMechanical ventilationInterleukin-8/immunologyLung[ SDV ] Life Sciences [q-bio]BacteriaTumor Necrosis Factor-alphabusiness.industrylcsh:RInterleukin-8OrganismsBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyPneumoniaMolecular Developmentmedicine.diseaseTumor Necrosis Factor-alpha/immunologyRespiration ArtificialToll-Like Receptor 2Pneumonia030104 developmental biologyVentilator-Associated/immunology/microbiology/pathologyImmune SystemAmniotesImmunologylcsh:QbusinessSpleenEx vivoDevelopmental Biologydescription
Ventilator-associated pneumonia (VAP) is common during mechanical ventilation (MV). Beside obvious deleterious effects on muco-ciliary clearance, MV could adversely shift the host immune response towards a pro-inflammatory pattern through toll-like receptor (TLRs) up-regulation. We tested this hypothesis in a rabbit model of Staphylococcus aureus VAP. Pneumonia was caused by airway challenge with S. aureus, in either spontaneously breathing (SB) or MV rabbits (n = 13 and 17, respectively). Pneumonia assessment regarding pulmonary and systemic bacterial burden, as well as inflammatory response was done 8 and 24 hours after S. aureus challenge. In addition, ex vivo stimulations of whole blood taken from SB or MV rabbits (n = 7 and 5, respectively) with TLR2 agonist or heat-killed S. aureus were performed. Data were expressed as mean +/- standard deviation. After 8 hours of infection, lung injury was more severe in MV animals (1.40 +/- 0.33 versus [vs] 2.40 +/- 0.55, p = 0.007), along with greater bacterial concentrations (6.13 +/- 0.63 vs. 4.96 +/- 1.31 colony forming units/gram, p = 0.002). Interleukin (IL)-8 and tumor necrosis factor (TNF)-alpha serum concentrations reached higher levels in MV animals (p = 0.010). Whole blood obtained from MV animals released larger amounts of cytokines if stimulated with TLR2 agonist or heat-killed S. aureus (e.g., TNF-alpha: 1656 +/- 166 vs. 1005 +/- 89; p = 0.014). Moreover, MV induced TLR2 overexpression in both lung and spleen tissue. MV hastened tissue injury, impaired lung bacterial clearance, and promoted a systemic inflammatory response, maybe through TLR2 overexpression.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2016-01-01 |