Integrated evolutionary, immunological, and neuroendocrine framework for the pathogenesis of chronic disabling inflammatory diseases

@article{Straub2003IntegratedEI,
  title={Integrated evolutionary, immunological, and neuroendocrine framework for the pathogenesis of chronic disabling inflammatory diseases},
  author={Rainer H. Straub and Hugo Oscar Besedovsky},
  journal={The FASEB Journal},
  year={2003},
  volume={17},
  pages={2176 - 2183}
}
The pathogenesis of chronic disabling inflammatory diseases (CDIDs) is poorly understood. Current concepts that focus on abnormalities of the immune system are, in our view, incomplete. Here we propose that chronic disruption of homeostasis through abnormal neuronal and endocrine host re‐ sponses to transient inflammatory reactions contributes to the appearance of CDIDs. Coordinated reactions of the supersystems (immune, nervous, endocrine, and reproductive) that maintain homeostasis have been… Expand
Chronic inflammatory systemic diseases
TLDR
Considering evolved energy trade-offs helps to understand how an energy imbalance can lead to the disease sequelae of CIDs and clinicians must translate this knowledge into early diagnosis and symptomatic treatment in CIDs. Expand
Concepts of evolutionary medicine and energy regulation contribute to the etiology of systemic chronic inflammatory diseases
  • R. Straub
  • Medicine
  • Brain, Behavior, and Immunity
  • 2011
TLDR
The present review suggests that Selye's alarm reaction of the 1930s, which is necessary to re-allocate energy-rich fuels to the body, should be called "energy appeal reaction". Expand
Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology
  • R. Straub
  • Medicine
  • Journal of Molecular Medicine
  • 2012
TLDR
The revised theory addresses the mechanisms of essential hypertension since, on the basis of water loss, acute inflammatory diseases can stimulate water retention using a positively selected water retention system (identical to the energy provision system), while in chronic smoldering inflammation, there is no increased water loss. Expand
Neuroendocrine Immunoregulation in Multiple Sclerosis
TLDR
An overview of the complex system of crosstalk between the neuroendocrine and immune system as well as reported dysfunctions involved in the pathogenesis of autoimmunity, including MS are provided. Expand
Adverse neuro-immune–endocrine interactions in patients with active tuberculosis
TLDR
Collectively, immune-endocrine disturbances of TB patients are involved in critical components of disease pathology with implications in the impaired clinical status and unfavorable disease outcome. Expand
Systemic disease sequelae in chronic inflammatory diseases and chronic psychological stress: comparison and pathophysiological model
  • R. Straub
  • Medicine
  • Annals of the New York Academy of Sciences
  • 2014
TLDR
A new pathophysiological theory is presented that places inflammation and stress axes in the middle and explains the behavior of body weight in CIDs versus loss or gain in stress. Expand
Immune-Neuroendocrine Interactions and Autoimmune Diseases
TLDR
There is evidence that hormonal changes may appear before the symptomatic phase of the disease, and it is possible that a pro-inflammatory hormone favors the rupture of tolerance, which is a key feature of autoimmune diseases. Expand
[Neuroendocrine immunology: new pathogenetic aspects and clinical application].
  • R. Straub
  • Medicine
  • Zeitschrift fur Rheumatologie
  • 2011
TLDR
The networks of energy regulation and energy allocation have been evolutionarily positively selected for transient inflammatory episodes but long-standing use of these adaptive programs for CID support systemic disease sequelae, and considerations might help to deviate focus from pure anti-inflammatory treatment to adequate diagnosis and therapy of systemic disease sequelsae. Expand
Pathogenesis and Neuroendocrine Immunology
TLDR
This chapter delineates the recent findings on mitochondrial abnormalities in adrenocortical cells of chronically inflamed animals and describes the excessive conversion of anti-inflammatory androgens to downstream proinflammatory estrogens in inflamed tissue. Expand
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