A simple systems approach to neural-immune communication

Clatworthy, Andrea L.

doi:10.1016/0300-9629(95)02130-2

Cited by 15 publications

(17 citation statements)

References 53 publications

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“…Even in the most primitive organisms such as molluscs and sponges, which are incapable of elaborate defence against distal threats, some form of host response against infection and injury can be identified (Beck et al 1994). Moreover, there is evidence that as early in evolution as the molluscs, defence against infection and injury involved pro-inflammatory cytokines in bi-directional communication between immunological and neural structures, as well as the release peptides traditionally viewed as stress hormones (Clatworthy, 1996 ;Maier & Watkins, 1998, for reviews). When the fright-flight response evolved later in more complex organisms, existing mechanisms such as cytokine-based communication networks appear to have been incorporated in this new adaptation (Maier & Watkins, 1998).…”

Section: Links Between Acute Sickness Behaviour and The Stress Responsementioning

confidence: 99%

Acute sickness behaviour: an immune system-to-brain communication?

Vollmer‐Conna¹

2001

Psychol. Med.

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EDITORIALAcute sickness behaviour : an immune system-to-brain communication ?"Over the past 20 years, psychoneuroimmunological research has produced a large body of evidence that challenges the historically dominant view that the immune system operates in an autonomous manner independent of other physiological systems. Today, there is little doubt that the brain and the immune system are intimately linked and capable of reciprocal communication (Ader et al. 1991). Despite the acknowledged bi-directional nature of the brain-immune system connection, the predominant focus of study has been on the effects of psychological and behavioural events (e.g. stress) on immune responses and disease processes, and the mechanisms underlying such effects (see Kusnekov & Rabin, 1994 ;Maier et al. 1994 ;Rozlog et al. 1999). However, considerable interest in the possibilities of immune-system-to-brain communication was initiated by a seminal paper considering the biological basis of behaviour in sick animals (Hart, 1988). Subsequently, the immunological determinants of the behavioural, cognitive and emotional changes associated with acute illness, as well as with more chronic psychopathological states (e.g. depression) have become the subject of rapidly expanding areas of research (e.g. Kent et al. 1992 ;Lloyd et al. 1992 ;Hickie & Lloyd, 1995 ;Rothwell & Hopkins, 1995 ;Dantzer et al. 1996 ;Maier & Watkins, 1998 ;Vollmer-Conna et al. 1998 ;Maes, 1999). The main objective of this editorial is to provide a succinct overview of current knowledge of the normal behavioural correlates of acute infective illness, their adaptive function and underlying mechanisms. Elucidation of the processes involved in the appearance, maintenance and inhibition of ' normal ' sickness behaviour is important if extrapolations from this phenomenon to more chronic psychopathological conditions are to provide more than a new label for poorly understood non-specific symptom clusters. A ROLE FOR SICKNESS BEHAVIOUR IN THE HOST DEFENCE AGAINST INFECTION AND INFLAMMATIONAcute infective illnesses, both in animals and humans, are typically accompanied by a cluster of non-specific symptoms such as fever, an increased need to sleep, hyperalgesia, anorexia, loss of interest in usual activities, decreased social interaction and body care, depression and impaired concentration (Hart, 1988 ;Dantzer et al. 1996). Perhaps because they are prevalent and nonspecific concomitants of infective illnesses, these phenomena are commonly dismissed or relatively ignored by physicians. Yet, it has recently been argued that sickness behaviours constitute a highly organized and evolved strategy to combat infection and injury. Specifically, it has been suggested that the behavioural changes function to conserve energy and, thus, facilitate the role of fever in stimulating immune function and inhibiting the proliferation of thermo-sensitive pathogens (Hart, 1988).The adaptive nature of the fever response is well documented and apparent from numerous demonstrations that inhibition of fev...

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Section: Links Between Acute Sickness Behaviour and The Stress Responsementioning

confidence: 99%

Acute sickness behaviour: an immune system-to-brain communication?

Vollmer‐Conna¹

2001

Psychol. Med.

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“…9B-F). These cells resemble the hemocytes in Aplysia hemolymph that share properties with cells of the vertebrate immune system (Clatworthy, 1996). Hemocytes accumulate at a nerve crush and sites of inflammation in vivo Clatworthy, 1996;Bale et al, 2001) and phagocytose damaged cells.…”

Section: Apfasp and Apbt Proteins Function At Growth Cones In Vitromentioning

confidence: 99%

mRNAs encoding theAplysia homologues of fasciclin-I and β-thymosin are expressed only in the second phase of nerve injury and are differentially segregated in axons regenerating in vitro and in vivo

2005

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Studies using Aplysia californica have demonstrated that transcription after nerve injury occurs during a rapid, transient first phase and a delayed, prolonged second phase. Although the second phase is especially important for regeneration, the mRNAs produced during this phase have not been identified. We characterized two such mRNAs following axotomy. One encodes a novel fasciclin-I homologue, Aplysia fasciclin-like protein (apFasP), and the other encodes Aplysia beta-thymosin (apbetaT). In addition to mRNA synthesis, proteins required for regeneration must be available at the site of growth, and the transport and local translation of certain extrasomatic mRNAs aids in this process. We found apbetaT and apFasP proteins and mRNA at growth cones in vitro. However, only the mRNA for apbetaT was present in regenerating axons in vivo. This implies that the membrane protein apFasP is supplied by rapid transport from the soma, whereas the soluble apbetaT is synthesized locally.

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“…Stress elevates stress-associated signals that increase the synaptic plasticity and growth potential in neurons. The finding that neurons and immune system cells communicate using a conserved chemical language renders gastropod research into the basic mechanisms of neural-immune communication especially significant (Clatworthy, 1996) and unites the field with the studies of neural plasticity (Clatworthy, 1998;.…”

Section: Promotion Of Axonal Regenerationmentioning

confidence: 99%

Regeneration as an application of gastropod neural plasticity

Moffett

2000

Microsc. Res. Tech.

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A simple systems approach to neural-immune communication

Cited by 15 publications

References 53 publications

Acute sickness behaviour: an immune system-to-brain communication?

Acute sickness behaviour: an immune system-to-brain communication?

mRNAs encoding theAplysia homologues of fasciclin-I and β-thymosin are expressed only in the second phase of nerve injury and are differentially segregated in axons regenerating in vitro and in vivo

Regeneration as an application of gastropod neural plasticity

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