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Effect of Age on Sympathetic Nerve Discharge (SND) and Splenic Cytokine Gene Expression Responses to Hypothermia
Author(s) -
Ganta Chanran Kumar,
Blecha Frank,
Ganta Roman R,
Helwig Bryan G,
Kenney Michael J
Publication year - 2006
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.20.5.a1421-c
The sympathetic nervous system plays an important role in mediating neural‐immune interactions and activation of central sympathetic nerve outflow alters splenic cytokine gene expression. Aging modifies sympathetic nervous system and immune system regulation under basal conditions and in response to acute stress; however, the influence of age on sympathetic‐immune interactions is not well understood. In the present study, we determined splenic SND and splenic cytokine gene expression under basal conditions and in response to acute hypothermia (internal body temperature reduced from 38 to 30°C) in young (3–5‐months‐old) and aged (24‐months‐old) F344 rats. Gene expression analysis was performed using a cDNA microarray containing 96 genes representing inflammatory cytokines, chemokines, and cytokine/chemokine receptors. A subset of genes was verified by real‐time RT‐PCR analysis. Expression of selected splenic cytokines/chemokines under euthermic conditions appears to be similar in young and aged rats. Splenic SND was decreased during acute cold stress in young but not in aged rats. Hypothermia increased the expression of selected splenic cytokines (IL‐1α, IL‐1β, IL‐6) and chemokines (CCL2, CCL20, CXCL2, CXCL10) in young and aged splenic‐intact and splenic‐denervated rats. These initial results suggest that aging modifies splenic sympathetic nerve activity but not splenic cytokine gene expression responses to acute cooling. (Supported by NIH HL‐65346 and HL‐69755).