3 recent abstracts

[Guest guest]

a.. Role of trophic factors on neuroimmunity in neurodegenerative infectious

diseases.

b.. Neural immunity: Friend or foe?

c.. Antidepressant drugs and cytokines in mood disorders.

J Neurovirol 2002 Dec;8(6):625-38

Role of trophic factors on neuroimmunity in neurodegenerative infectious

diseases.

Langford D, Masliah E.

Department of Pathology, University of California, San Diego, La Jolla,

California, USA.

Viral infection of the central nervous system elicits a myriad of cellular,

vascular, and neuroimmune factors that contribute to acute, subacute, and

chronic damage to the brain. In response to cellular damage, the host is capable

of producing trophic factors that may protect neuronal, glial, and endothelial

cell populations. Both neurotrophic and angiotrophic factors can also operate by

modulating the neuroimmune response, which plays a central role in the

pathogenesis of the neurodegenerative process. In this regard, crosstalk

signaling among host cells, components of the neuroimmune response, and virus

could influence cell fate by production of trophic factors that protect or

rescue neurons vulnerable to viral damage. In this context, the main objective

of this review is to provide an overview of evidence in support of the role of

trophic factors in regulating the neuroimmune response in chronic viral

infections of the central nervous system. Special emphasis is placed on the

interaction of the human immunodeficiency virus (HIV) Tat protein with

endothelial, astroglial, microglial, and neuronal cells, resulting in altered

expression of vascular endothelial growth factor, fibroblast growth factor,

interleukin-8, and regulation of calcium flux via CXCR2, which directly

influences neuronal cell fitness.

PMID: 12476355 [PubMed - in process]

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J Neurovirol 2002 Dec;8(6):474-9

Neural immunity: Friend or foe?

Gendelman HE.

The Center for Neurovirology and Neurodegenerative Disorders, The Departments of

Pathology and Microbiology, Internal Medicine and Psychiatry, University of

Nebraska Medical Center, Omaha, Nebraska, USA.

The articles compiled in this special edition of Journal of NeuroVirology target

a developing field of investigation seeking to uncover how the immune system

affects both the pathogenic process and protection against the ravages of

neurodegenerative processes. Whether caused by a microbe, trauma, toxic

metabolite, autoimmunity, or part of a wide degenerative process, immune

dysfunction commonly affects central nervous system (CNS) disease. All together,

the work presented here proved to be a unique undertaking with contributing

scientists outside the field of neurovirology. Indeed, multiple disciplines

including molecular neuroscience, neuroimmunology, virology, cellular

immunology, receptor pharmacology, neuronal electrophysiology, neurochemistry,

clinical neurology, and development neurobiology were joined. The basis of this

work rests with the hypothesis that brain mononuclear phagocytes (MP;

perivascular and brain macrophages and microglia) act as inducers of disease by

engaging the immune system to protect, defend, or induce neural injury. Indeed,

it is the brain MP that act as scavengers killing microblial pathogens, regulate

immune responses through antigen presentation and mobilization of adaptive

immune activities, and affect the production of neurotrophic or toxic secretory

factors that incite disease processes. For many years, these responses were

thought to be reactive to ongoing disease mechanisms with little effects on

disease itself, let alone repair. The works compiled in this issue demonstrate

quite clearly this is no longer true. Immune responses cannot be directed only

against a microbe but also against self-antigens that are expressed in damaged

CNS, leading to innate neurotoxic or adaptive anti-self immunity that commonly

follow viral infections. Importantly, therapeutic modalities may take advantage

of CNS immune responses through vaccination generating neuroprotection.

Together, these articles serve to bring together common neuroimmune links

between highly divergent diseases (for example, Parkinson's and Alzheimer's

disease and human immunodeficiency virus type-one dementia). In the end, I hope

this work will serve as discussion points for future collaborations and began to

break down the barriers of disease, enabling targeted research activities toward

what we have in common.

PMID: 12476342 [PubMed - in process]

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Int Immunopharmacol 2002 Nov;2(12):1619-26

Antidepressant drugs and cytokines in mood disorders.

Nishida A, Hisaoka K, Zensho H, Uchitomi Y, Morinobu S, Yamawaki S.

anishida@...

This article reviews recent developments in cytokine research that pertain to

pharmacological treatment of mood disorders such as antidepressants and lithium.

We review the possible involvement of cytokines in mood disorders and their role

in the therapeutic effects of antidepressant drugs. Growing evidence suggests

that specific cytokines signal the brain to generate neurochemical, neuroimmune,

neuroendocrine and behavior changes. An imbalance of cytokines within the

central nervous system (CNS), or even systemically, may play a role in the

pathophysiology of mood disorders. Modulation of these cytokines by chronic

antidepressant treatment may result in restored balance. However, the effect of

antidepressants on cytokines is still unclear both in clinical and preclinical

research due to limited data. Further research is needed to clarify the

involvement of cytokines in mood disorders. Understanding this relationship may

lead to rational, therapeutic improvements in antidepressant and mood

stabilizing drugs.

PMID: 12469936 [PubMed - in process]

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