Neural immunoregulation: emerging roles for nerves in immune homeostasis and disease

Downing, J. E. G.; Miyan, Jaleel

doi:10.1016/s0167-5699(00)01635-2

Cited by 216 publications

(102 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recent evidence shows that the autonomic nervous system significantly modulates processes implicated in cellular and humoral immunity as a consequence of the close anatomical and functional relationship between this system and the immune system 88 . This finding raises the possibility that the autonomic dysfunction associated with chagasic infection could be an influential or determining cause of immunological alterations contributing to the development and maintenance of chronic Chagas chronic infection.…”

Section: Other Possible Effects Of Autonomic Dysfunctionmentioning

confidence: 99%

Insights into the clinical and functional significance of cardiac autonomic dysfunction in Chagas disease

Junqueira Junior

2012

Rev. Soc. Bras. Med. Trop.

View full text Add to dashboard Cite

INTRODUCTION: Exclusive or associated lesions in various structures of the autonomic nervous system occur in the chronic forms of Chagas disease. In the indeterminate form, the lesions are absent or mild, whereas in the exclusive or combined heart and digestive disease forms, they are often more pronounced. Depending on their severity these lesions can result mainly in cardiac parasympathetic dysfunction but also in sympathetic dysfunction of variable degrees. Despite the key autonomic effect on cardiovascular functioning, the pathophysiological and clinical significance of the cardiac autonomic dysfunction in Chagas disease remains unknown. METHODS: Review of data on the cardiac autonomic dysfunction in Chagas disease and their potential consequences, and considerations supporting the possible relationship between this disturbance and general or cardiovascular clinical and functional adverse outcomes. RESULTS: We hypothesise that possible consequences that cardiac dysautonomia might variably occasion or predispose in Chagas disease include: transient or sustained arrhythmias, sudden cardiac death, adverse overall and cardiovascular prognosis with enhanced morbidity and mortality, an inability of the cardiovascular system to adjust to functional demands and/or respond to internal or external stimuli by adjusting heart rate and other hemodynamic variables, and immunomodulatory and cognitive disturbances. CONCLUSIONS: Impaired cardiac autonomic modulation in Chagas disease might not be a mere epiphenomenon without significance. Indirect evidences point for a likely important role of this alteration as a primary predisposing or triggering cause or mediator favouring the development of subtle or evident secondary cardiovascular functional disturbances and clinical consequences, and influencing adverse outcomes.

show abstract

Section: Other Possible Effects Of Autonomic Dysfunctionmentioning

confidence: 99%

Insights into the clinical and functional significance of cardiac autonomic dysfunction in Chagas disease

Junqueira Junior

2012

Rev. Soc. Bras. Med. Trop.

View full text Add to dashboard Cite

show abstract

“…Stress can affect inflammatory diseases (see Black, 2002(Black, 2002a for review), in part mediated by the effect of stress hormones on leukocyte function (Bierhaus et al, 2006;Bilbo et al, 2002;Dhabhar, 2002;Landmann et al, 1984;O'Leary et al, 1996;Shephard, 2003), and catecholamines mediate interactions between the sympathetic and the immune systems, to alter immune cell activity (Benschop et al, 1997;Downing and Miyan, 2000;Elenkov et al, 2000;Oberbeck, 2006;Straub et al, 1998). Norepinephrine, released from sympathetic nerve terminals, and epinephrine, released from the adrenal medulla (Elenkov et al, 2000), act primarily on α 2 and β 2 adrenergic receptors expressed on most resting and activated immune cells (Barnes, 1995;Barnes, 1999;Kin and Sanders, 2006;Maestroni, 2006;Wahle et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Coupade¹,

Brown²,

Dazin

et al. 2007

Journal of Neuroimmunology

View full text Add to dashboard Cite

In wild-type FVB mice, leukocyte recruitment to lipopolysaccharide was sexually dimorphic, with a greater number of leukocytes recruited in females. In male β 2 -adrenergic receptor knock out mice (bred on a congenic FVB background) the number leukocytes recruited was increased ~4-fold, while in females there was no change, eliminating sexual dimorphism in leukocyte migration. While there were significantly fewer recruited CD62L + and CD11a + leukocytes in wild-type males, only in male β 2 -adrenergic receptor knock out mice was there an increase in the number of recruited CD11a + leukocytes, again eliminating sexual dimorphism. Thus, leukocyte migration and CD11a + adhesion molecule expression in male, but not in female, leukocytes is β 2 -adrenergic receptor-dependent. Our findings provide support for a role of β 2 -adrenergic receptor mechanisms in the inflammatory response, and suggest that β 2 -adrenergic receptor on male leukocytes contributes to sexual dimorphism in the effect of stress on inflammatory diseases.

show abstract

“…Associations between stress and HIV-1 disease progression suggest that neural activity might play a role in modulating lentiviral replication (2). Neurons from the sympathetic division of the autonomic nervous system (ANS) terminate in the parenchyma of all primary and secondary lymphoid organs and release micromolar concentrations of norepinephrine into T cell-rich compartments (3,4). Norepinephrine ligation of cellular ␤ 2 adrenoreceptors modulates leukocyte activation, localization, and cytokine production via G ␣S protein-mediated induction of cAMP͞protein kinase A (PKA) signaling (5)(6)(7).…”

mentioning

confidence: 99%

Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity

Cole

Naliboff²,

Kemeny³

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

124

View full text Add to dashboard Cite

Neurotransmitters can accelerate HIV-1 replication in vitro, leading us to examine whether differences in autonomic nervous system (ANS) activity might promote residual HIV-1 replication in patients treated with highly active antiretroviral therapy. Patients who showed constitutively high levels of ANS activity before highly active antiretroviral therapy experienced poorer suppression of plasma viral load and poorer CD4 ؉ T cell recovery over 3-11 months of therapy. ANS activity was not related to demographic or behavioral characteristics that might influence pathogenesis. However, the ANS neurotransmitter norepinephrine enhanced replication of both CCR5-and CXCR4-tropic strains of HIV-1 in vitro via chemokine receptor up-regulation and enhanced viral gene expression, suggesting that neural activity may directly promote residual viral replication.

show abstract

Neural immunoregulation: emerging roles for nerves in immune homeostasis and disease

Cited by 216 publications

References 50 publications

Insights into the clinical and functional significance of cardiac autonomic dysfunction in Chagas disease

Insights into the clinical and functional significance of cardiac autonomic dysfunction in Chagas disease

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity

Contact Info

Product

Resources

About