PMID- 29145213 OWN - NLM STAT- MEDLINE DCOM- 20190121 LR - 20190121 IS - 1423-0216 (Electronic) IS - 1021-7401 (Linking) VI - 24 IP - 4-5 DP - 2017 TI - Depressed Immune Responses and Accelerated Splenic Apoptosis due to Experience of Food Deprivation and Inequality but not Unstable Social Status in Balb/c Mice. PG - 200-210 LID - 10.1159/000480732 [doi] AB - OBJECTIVE(S): We aimed to show that the immune system is sensitive to the detrimental effects of inequality and social injustice, and splenic vulnerability to apoptosis may also increase. METHODS: In order of better determination of immune responses to chronic social stress, we implemented food deprivation, food intake inequality, and unstable social status (a change of cage-mate every 3 days) for a period of 14 days in 60 male Balb/c mice. At the end of this stress period, nitric oxide (NO) production by peritoneal adherent cells and the serum concentration of corticosterone were measured. Moreover, the viability of peritoneal adherent cells and spleen lymphocytes was evaluated by MTT assay. The terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay was done to reveal the TUNEL-reactive apoptotic bodies in the spleen. RESULTS: Our results showed that food deprivation and inequality caused significant changes in the apoptosis of splenic cells in comparison with the control group (p < 0.05). Moreover, the vital activities of lymphocytes and peritoneal adherent cells, as well as NO production by the latter, increased significantly (p < 0.05). However, the experience of unstable social status did not cause a further increase in the viability of lymphocytes and peritoneal adherent cells, or NO production in animals that were food-deprived or experienced inequality. Serum concentration of corticosterone in all experimental groups, except for animals that experienced unstable social status only, significantly decreased versus the control group (p < 0.05). CONCLUSIONS: The results suggest that poverty and social inequality, but not unstable social status, affect immune responses and are likely involved in the induction of splenic apoptosis in mice. CI - (c) 2017 S. Karger AG, Basel. FAU - Aghajani, Marjan AU - Aghajani M AD - Department of Physiology, Medical Faculty, Tehran University of Medical Sciences, Tehran, Iran. FAU - Vaez Mahdavi, Mohammad Reza AU - Vaez Mahdavi MR FAU - Najafabadi, Mohsen Khalili AU - Najafabadi MK FAU - Ghazanfari, Tooba AU - Ghazanfari T FAU - Moradi, Fatemeh AU - Moradi F FAU - Golchoobian, Ravieh AU - Golchoobian R FAU - Askari, Hasan AU - Askari H FAU - Sanadgol, Nima AU - Sanadgol N FAU - Moghaddam, Ehsan Kazemi AU - Moghaddam EK LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20171117 PL - Switzerland TA - Neuroimmunomodulation JT - Neuroimmunomodulation JID - 9422763 SB - IM MH - Animals MH - Apoptosis/*immunology MH - Cells, Cultured MH - Food Deprivation/*physiology MH - Immunity, Cellular/*immunology MH - Male MH - Mice MH - Mice, Inbred BALB C MH - *Social Behavior MH - Socioeconomic Factors MH - Spleen/*immunology/pathology OTO - NOTNLM OT - Apoptosis OT - Food deprivation OT - Lymphocyte viability OT - Macrophages OT - Nitric oxide OT - Social inequality OT - Unstable social status EDAT- 2017/11/18 06:00 MHDA- 2019/01/22 06:00 CRDT- 2017/11/18 06:00 PHST- 2017/04/06 00:00 [received] PHST- 2017/08/28 00:00 [accepted] PHST- 2017/11/18 06:00 [pubmed] PHST- 2019/01/22 06:00 [medline] PHST- 2017/11/18 06:00 [entrez] AID - 000480732 [pii] AID - 10.1159/000480732 [doi] PST - ppublish SO - Neuroimmunomodulation. 2017;24(4-5):200-210. doi: 10.1159/000480732. Epub 2017 Nov 17.