Known and plausible modulators of depressed immune functions following spinal cord injuries

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.

Original languageEnglish
Pages (from-to)111-120
Number of pages10
JournalJournal of Spinal Cord Medicine
Volume23
Issue number2
StatePublished - Dec 1 2000

Fingerprint

Spinal Cord Injuries
Interleukin Receptors
Diet
Disease Resistance
Macrophage Activation
Autonomic Nervous System
Opportunistic Infections
Methylprednisolone
Politics
Urinary Tract
Phagocytosis
Natural Killer Cells
Interleukin-2
Interleukin-6
Cell Count
Fats
Morbidity
T-Lymphocytes
Lung
Skin

Keywords

  • Autonomic nervous system
  • Diet
  • Drugs
  • Exercise
  • Immune system
  • Spinal cord injury

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Known and plausible modulators of depressed immune functions following spinal cord injuries. / Nash, Mark S.

In: Journal of Spinal Cord Medicine, Vol. 23, No. 2, 01.12.2000, p. 111-120.

Research output: Contribution to journalArticle

@article{0d26d85ee4584d698a279db26c3bbb55,
title = "Known and plausible modulators of depressed immune functions following spinal cord injuries",
abstract = "Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.",
keywords = "Autonomic nervous system, Diet, Drugs, Exercise, Immune system, Spinal cord injury",
author = "Nash, {Mark S}",
year = "2000",
month = "12",
day = "1",
language = "English",
volume = "23",
pages = "111--120",
journal = "Journal of Spinal Cord Medicine",
issn = "1079-0268",
publisher = "Maney Publishing",
number = "2",

}

TY - JOUR

T1 - Known and plausible modulators of depressed immune functions following spinal cord injuries

AU - Nash, Mark S

PY - 2000/12/1

Y1 - 2000/12/1

N2 - Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.

AB - Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.

KW - Autonomic nervous system

KW - Diet

KW - Drugs

KW - Exercise

KW - Immune system

KW - Spinal cord injury

UR - http://www.scopus.com/inward/record.url?scp=0034203788&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034203788&partnerID=8YFLogxK

M3 - Article

C2 - 10914352

AN - SCOPUS:0034203788

VL - 23

SP - 111

EP - 120

JO - Journal of Spinal Cord Medicine

JF - Journal of Spinal Cord Medicine

SN - 1079-0268

IS - 2

ER -