title: Dexamethazone protects against Escherichia coli induced sickness behavior in rats.
abstract: Systemic bacterial infection results in systemic inflammatory response syndrome due to the release of lipopolysaccharide (LPS) in blood that can lead to multiple organ failure, shock, and potentially death. Other impact, LPS exposure produces robust increase in anxiety-like behavior, suppression of locomotor, exploratory activity, and reduced social behavior. The therapeutic use of glucocorticoids in septic shock remains one of the first-aid approaches for their anti-inflammatory properties. The aim of this study was to evaluate the possible protective effect of dexamethazone (DEX), the most commonly used corticosteroid, against Escherichia coli (E. coli) immunohistochemical changes and neurobehavioral dysfunction. To this end, male Sprague-Dawley rats were divided into four groups; (1) Control group (2) E. coli infected group, where animals received 0.2 ml of 24 h growth of E. coli suspension in nutrient broth containing approximately 1.8×10(8) cfu/ml i.p for once, 48 h before sacrificing (3) DEX (20 mg/kg, i.p, 3 days) treated group (4) DEX and E. coli treated group. The results revealed that DEX significantly protected animals against most E. coli-induced behavioral deficits, reduced signs of cognitive impairment. DEX also reduced the LPS-evoked rise in C-reactive protein (CRP), Interferon gamma (IFγ), as well as, expression of Caspase-3. In conclusion, DEX provides neuroprotection against E. coli-associated neurobehavioral and immunological changes via its anti-inflammatory and immunomodulatory effects.
authors.affiliation: Department of Pharmacology, National Organization of Drug Control and Research (NODCAR), Giza, Egypt.
authors.forename: A
authors.initials: A
authors.lastname: Hanaa-Mansour
authors.affiliation: Department of Pharmacology, National Organization of Drug Control and Research (NODCAR), Giza, Egypt. Electronic address: wedad.abdallah@yahoo.com.
authors.forename: Wedad A
authors.initials: WA
authors.lastname: Hassan
authors.affiliation: Department of Pharmacology, National Organization of Drug Control and Research (NODCAR), Giza, Egypt.
authors.forename: Gehan S
authors.initials: GS
authors.lastname: Georgy
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D004195:Disease Models, Animal; D004926:Escherichia coli; D004927:Escherichia coli Infections / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D055809:Illness Behavior / Q000187:drug effects*; D007150:Immunohistochemistry; D007371:Interferon-gamma / Q000378:metabolism; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley
chemical_list: D000893:Anti-Inflammatory Agents; D018696:Neuroprotective Agents; D003907:Dexamethasone; D007371:Interferon-gamma; D002097:C-Reactive Protein; C505410:Casp3 protein, rat; D053148:Caspase 3
keywords: Escherichia coliDexamethasone; Inflammation; Lipopolysaccharide; Neurobehavior