PMID- 8642417
OWN - NLM
STAT- MEDLINE
DCOM- 19960712
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 16
IP  - 11
DP  - 1996 Jun 1
TI  - Endogenous substance P mediates cold water stress-induced increase in 
      interleukin-6 secretion from peritoneal macrophages.
PG  - 3745-52
AB  - Previous studies from this laboratory had shown that exposure of mice to cold 
      water stress leads to an increase in the secretion of interleukin-1 (IL-1) and 
      tumor necrosis factor-alpha (TNF alpha) from their peritoneal macrophages. We now 
      report that the secretion of IL-6 from peritoneal macrophages is also increased 
      after cold water stress and that the peptide substance P (SP) participates in 
      this stress-induced response. The stress paradigm involved subjecting male 
      C57BL/6J mice to 5 min swim tests in 10 +/- 2 degrees C water twice daily for 4 
      d. Cold water stress augments the lipopolysaccharide-induced IL-6 secretion from 
      peritoneal macrophages, elevates immunoreactive SP (iSP) in the peritoneal wash 
      fluid, and reduces iSP in certain peritoneum-containing tissues or organs (i.e., 
      diaphragm, abdominal wall, ileum, and rectum). The 10 d stress time studies 
      indicate that increased IL-6 secretion is positively related to elevated iSP in 
      the peritoneal wash fluid and inversely related to reduced iSP in certain 
      peritoneum-containing tissues. Pretreatment with capsaicin, which depletes SP in 
      the sensory nerve endings, eliminates stress-control differences in the 
      peritoneal wash fluid and in certain peritoneal tissues. Moreover, RP67,580, a 
      specific SP antagonist, eliminates the cold water stress-induced augmentation of 
      IL-6 secretion from peritoneal macrophages. These results suggest that cold water 
      stress promotes the release of SP from peritoneal tissues into the peritoneal 
      cavity, where it participates in the cold water stress-induced macrophage 
      functional alterations.
FAU - Zhu, G F
AU  - Zhu GF
AD  - Department of Microbiology, Boston University School of Medicine, Massachusetts 
      02118, USA.
FAU - Chancellor-Freeland, C
AU  - Chancellor-Freeland C
FAU - Berman, A S
AU  - Berman AS
FAU - Kage, R
AU  - Kage R
FAU - Leeman, S E
AU  - Leeman SE
FAU - Beller, D I
AU  - Beller DI
FAU - Black, P H
AU  - Black PH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Analgesics)
RN  - 0 (Indoles)
RN  - 0 (Interleukin-6)
RN  - 0 (Isoindoles)
RN  - 0 (Lipopolysaccharides)
RN  - 059QF0KO0R (Water)
RN  - 135911-02-3 
      (7,7-diphenyl-2-(1-imino-2-(2-methoxyphenyl)ethyl)perhydroisoindol-4-one)
RN  - 33507-63-0 (Substance P)
RN  - S07O44R1ZM (Capsaicin)
SB  - IM
MH  - Analgesics/pharmacology
MH  - Animals
MH  - Ascitic Fluid/chemistry/cytology
MH  - Capsaicin/pharmacology
MH  - Cold Temperature
MH  - Indoles/pharmacology
MH  - Interleukin-6/*metabolism
MH  - Isoindoles
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages, Peritoneal/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nerve Endings/drug effects/metabolism
MH  - Peritoneum/drug effects/innervation/metabolism
MH  - Stress, Physiological/*immunology/physiopathology
MH  - Substance P/antagonists & inhibitors/*physiology
MH  - Water
PMC - PMC6578844
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
PMCR- 1996/12/01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
PHST- 1996/12/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.16-11-03745.1996 [doi]
PST - ppublish
SO  - J Neurosci. 1996 Jun 1;16(11):3745-52. doi: 10.1523/JNEUROSCI.16-11-03745.1996.