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Exogenous oxytocin (OT) ameliorates pulmonary damage caused by Escherichia coli (E. coli) infection in chronically stressed rats
Author(s) -
Stadnikov Alexander A,
Kozlova Ali,
Klimushkin Aleksey V
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.999.4
Subject(s) - oxytocin , escherichia coli , endocrinology , medicine , lung , saline , hypothalamus , endogeny , immunohistochemistry , escherichia coli infection , apoptosis , lipopolysaccharide , neuropeptide , andrology , chemistry , biochemistry , receptor , gene
This study examines the hypothesis that exogenous OT will reduce pulmonary damage caused by E. coli infection in stressed rats. Four groups of male albino rats were used as follows: 1) rats received an intratracheal ( i.t. ) injection of 0.2 mL E. coli suspension containing 1·10 9 bacteria/mL in saline; 2) rats were subjected to footshock (FS) stress for 1–11 days; 3) rats were subjected to FS stress for 7 days and then received an i.t. injection of E. coli; 4) rats subjected to FS stress had concurrently received i.m. injections of OT (0,02 IU/mL) for 7 days and then were injected with E. coli. The lungs, hypothalamus, and neurohypophysis were analyzed by light and electron microscopy, immunohistochemistry on days 1 to 11 (groups: 1–2) and days 8 to 11 (groups: 3–4). We found that an E. coli infection in chronically stressed rats caused a greater inflammatory response, cell death and fibrosis than were seen in non‐FS animals. The detrimental changes in the former coincided with increased inhibition of OT release from neurohypophysial terminals. The injections of OT reduced the number of apoptotic cells (~40%) and production of MMP‐9 (~75%), while it stimulated the expression of Bcl‐2, Clara cell protein (CC‐16), and lactoferrin in the lungs. Thus, we concluded that exogenous OT shows a therapeutic effect against E. coli‐induced lung injury under condition of chronic stress, when the release of endogenous neuropeptide is impaired.