Evidence map›Paper›PMID 29541878›Full record

ReviewClinical autonomic research : official journal of the Clinical Autonomic Research Society2018

Neural pathways involved in infection-induced inflammation: recent insights and clinical implications.

Marion Griton, Jan Pieter Konsman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. The effect of adrenalectomy on bleomycin-induced pulmonary fibrosis in mice.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. "Dysautonomia": a plea for precision.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Marion GritonService de Réanimation Anesthésie Neurochirurgicale, Centre Hospitalier Universitaire (CHU) de Bordeaux, Bordeaux, France.
Jan Pieter KonsmanINCIA, Institut de Neurosciences Cognitive et Intégrative d'Aquitaine, UMR 5287, Bordeaux, France. jan-pieter.konsman@u-bordeaux.fr.ORCID 0000-0001-7247-0472
Centre Hospitalier Universitaire de Bordeaux · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the immune and nervous systems have long been considered independent biological systems, they turn out to mingle and interact extensively. The present review summarizes recent insights into the neural pathways activated by and involved in infection-induced inflammation and discusses potential clinical applications. The simplest activation concerns a reflex action within C-fibers leading to neurogenic inflammation. Low concentrations of pro-inflammatory cytokines or bacterial fragments may also act on these afferent nerve fibers to signal the central nervous system and bring about early fever, hyperalgesia and sickness behavior. In the brain, the preoptic area and the paraventricular hypothalamus are part of a neuronal network mediating sympathetic activation underlying fever while brainstem circuits play a role in the reduction of food intake after systemic exposure to bacterial fragments. A vagally-mediated anti-inflammatory reflex mechanism has been proposed and, in turn, questioned because the major immune organs driving inflammation, such as the spleen, are not innervated by vagal efferent fibers. On the contrary, sympathetic nerves do innervate these organs and modulate immune cell responses, production of inflammatory mediators and bacterial dissemination. Noradrenaline, which is both released by these fibers and often administered during sepsis, along with adrenaline, may exert pro-inflammatory actions through the stimulation of β1 adrenergic receptors, as antagonists of this receptor have been shown to exert anti-inflammatory effects in experimental sepsis.

Indexed as

AnimalsAutonomic Nervous System DiseasesCatecholaminesCentral Nervous System InfectionsHumansInfectionsInflammationNervous System DiseasesNeural PathwaysCatecholaminesAutonomic nervous systemCatecholaminesImmune organsSepsisVagus nerve

Identifiers

PMID29541878
OpenAlexW2790770531

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.