title: Increased resistance of immobilized-stressed mice to infection: correlation with behavioral alterations.
abstract: Immobilization is an easy and convenient method to induce both psychological and physical stress resulting in restricted motility and aggression and is believed to be the most severe type of stress in rodent models. Although it has been generally accepted that chronic stress often results in immunosuppression while acute stress has been shown to enhance immune responses, the effects of IS on the host resistance to Escherichia coli (E. coli) infection and associated behavioral changes are still not clear. In a series of experiments aimed at determining the level of hypothalamic COX-2, HSP-90, HSP-70, SOD-1 and plasma level of corticosterone, cytokine, antibody titer and their association with behavioral activities, mice were infected with viable E. coli during acute and chronic IS by taping their paws. In this study we show that acute and chronic IS enhances the resistance of mice to E. coli infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and by improving the exploratory behavior. Altogether, our findings support the notion that cytokines released during immune activation and under the influence of corticosterone can modulate the open field behavior both in terms of locomotor activity as well as exploration. One of the features observed with chronic stressor was a lower ability to resist bacterial infection, although in case of acute stress, a better clearance of bacterial infection was observed in vivo with improvement of exploratory behavior and cognitive functions.
authors.affiliation: Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, 92 APC Road, Calcutta 700009, West Bengal, India.
authors.forename: Sayantika
authors.initials: S
authors.lastname: Mahanti
authors.forename: Arnab
authors.initials: A
authors.lastname: Majhi
authors.forename: Sharmalika
authors.initials: S
authors.lastname: Chongdar
authors.forename: Kiran
authors.initials: K
authors.lastname: Kundu
authors.forename: Kallol
authors.initials: K
authors.lastname: Dutta
authors.forename: Anirban
authors.initials: A
authors.lastname: Basu
authors.forename: Biswadev
authors.initials: B
authors.lastname: Bishayi
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D001424:Bacterial Infections / Q000276:immunology* / Q000503:physiopathology / Q000523:psychology; D003345:Corticosterone / Q000097:blood / Q000502:physiology; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000502:physiology; D016207:Cytokines / Q000097:blood / Q000502:physiology; D060467:Disease Resistance / Q000276:immunology* / Q000502:physiology; D018841:HSP90 Heat-Shock Proteins / Q000032:analysis / Q000502:physiology; D007031:Hypothalamus / Q000737:chemistry / Q000503:physiopathology; D007103:Immobilization / Q000502:physiology* / Q000523:psychology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013315:Stress, Psychological / Q000503:physiopathology* / Q000523:psychology; D013482:Superoxide Dismutase / Q000032:analysis / Q000502:physiology; D000072105:Superoxide Dismutase-1
chemical_list: D000907:Antibodies, Bacterial; D016207:Cytokines; D018841:HSP90 Heat-Shock Proteins; D051546:Cyclooxygenase 2; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D003345:Corticosterone