galanin-like-peptide and Inflammation

The immune system defends the organism against invading pathogens. In recent decades it became evident that elimination of such pathogens, termination of inflammation, and restoration of host homeostasis all depend on bidirectional crosstalk between the immune system and the neuroendocrine system. This crosstalk is mediated by a complex network of interacting molecules that modulates inflammation and cell growth. Among these mediators are neuropeptides released from neuronal and non-neuronal components of the central and peripheral nervous systems, endocrine tissues, and cells of the immune system. Neuropeptide circuitry controls tissue inflammation and maintenance, and an imbalance of pro- and anti-inflammatory neuropeptides results in loss of host homeostasis and triggers inflammatory diseases. The galanin peptide family is undoubtedly involved in the regulation of inflammatory processes, and the aim of this review is to provide up-to-date knowledge from the literature concerning the regulation of galanin and its receptors in the nervous system and peripheral tissues in experimental models of inflammation. We also highlight the effects of galanin and other members of the galanin peptide family on experimentally induced inflammation and discuss these data in light of an anti-inflammatory role for this family of peptides.

Topics: Animals; Galanin; Galanin-Like Peptide; Humans; Immune System; Inflammation; Neurosecretory Systems; Peptides; Receptors, Galanin; Signal Transduction; Skin

Galanin-like peptide (GALP) is a neuropeptide that is thought to play a role in the regulation of energy balance. However, the effects of GALP on food intake and body weight appear to be complex. In rats, central administration of GALP initially stimulates food intake, an effect that is followed by a reduction in food intake and body weight, whereas in mice, GALP has an anorectic action only. In rats and mice, GALP also causes a prostaglandin-dependent increase in core body temperature. These anorectic effects of GALP are similar to those observed after central administration of the pro-inflammatory cytokine interleukin-1 (IL-1). This review will discuss the evidence for the dichotomous actions of GALP on energy balance, and the potential mechanisms involved. I also describe a role for IL-1 in mediating the anorectic and febrile actions of GALP, and consider the possibility that GALP may act like an inflammatory mediator.

Topics: Animals; Appetite Depressants; Body Temperature; Body Weight; Eating; Energy Metabolism; Galanin-Like Peptide; Inflammation; Interleukin-1; Prostaglandins; Proto-Oncogene Proteins c-fos

Galanin-like peptide (GALP) is a neuropeptide that has been proposed to play a role in the regulation of food intake behaviour and body weight. However, the actions of GALP on energy balance are complex. In rats, it appears to impel both appetite stimulating and suppressing effects, whereas in mice, the only effect is a reduction in food intake. Thus, it is currently unclear whether GALP is important in the homeostatic regulation of energy balance, or if it produces effects on appetite and body weight by non-specific actions. This review discusses current evidence of the role of GALP with respect to energy balance, and the mechanisms involved in its regulation. We describe recent evidence that suggests that GALP may elicit differential effects in different rodent species. Furthermore, we provide an insight into a potential novel role for GALP in inflammation, and discuss how this may relate to the non-homeostatic regulation of energy balance.

Topics: Animals; Brain; Energy Metabolism; Galanin-Like Peptide; Homeostasis; Humans; Inflammation; Mice; Rats

This study reports on changes caused by chemically driven inflammation and axotomy in galanin-like immunoreactive (GAL-LI) nerve structures in the porcine descending colon. The distribution pattern of GAL-LI structures was studied using the immunofluorescence technique in the circular muscle layer, the myenteric (MP), outer submucous (OSP) and inner submucous plexuses (ISP), and also in the mucosal layer. Under physiological conditions GAL-LI perikarya were shown to constitute 3.68 +/- 0.32%, 7.02 +/- 0.93% and 10.99 +/- 0.71% in MP, OSP and ISP, respectively. Both colitis and axotomy caused an increase in GAL-like immunoreactivity, which was different in particular parts of the bowel segment studied. The numbers of GAL-LI perikarya increased to 14.16 +/- 0.49%, 16.78 +/- 1.09% and 37.46 +/- 1.18% during colitis and 7.92 +/- 0.72%, 10.44 +/- 0.71% and 16.20 +/- 0.96% after axotomy in MP, OSP and ISP, respectively. Both these processes caused an increase in the number of GAL-LI nerve fibres in the circular muscle and mucosal layers as well as the appearance of a population of GAL-LI cells in the mucosa.

Topics: Animals; Axotomy; Colitis; Colon, Descending; Female; Galanin-Like Peptide; Inflammation; Swine; Swine Diseases

The cutaneous vasculature plays a key role in the pathophysiology of inflammatory skin diseases. The vascular activity is under the control of the peripheral nervous system that includes locally released neuropeptides. Recently, we detected receptors for the neuropeptide galanin in association with dermal blood vessels, suggesting a role of the galanin-peptide-family in the regulation of the cutaneous microvasculature. Therefore, we have investigated galanin and galanin-like peptide (GALP), a neuropeptide previously only considered to be involved in metabolism and reproduction in the central nervous system, for vaso-modulatory activity in the murine skin in vivo. Picomole amounts of intradermally injected galanin and GALP decreased cutaneous blood flow and inhibited inflammatory edema formation. Both the full-length GALP (1-60) and the putative smaller proteolytic fragment GALP (3-32) showed similar effects. These activities are most likely mediated by galanin receptors galanin receptor subtype 2 (GalR2) and/or galanin receptor subtype 3 (GalR3), because reverse transcription-PCR analysis of murine skin revealed messenger RNA (mRNA) expression of GalR2 and GalR3 but not of galanin receptor subtype 1. The lack of galanin receptor mRNAs in endothelial and smooth muscle cells indicates a neuronal localization of these receptors around the vessels. These results indicate functional activity of GALP in the periphery in vivo and suggest a potential role as an inflammatory modulator.

Topics: Animals; Blood Vessels; Calcitonin Gene-Related Peptide; Edema; Endothelial Cells; Female; Galanin; Galanin-Like Peptide; Inflammation; Mice; Neuropeptides; Peptides; RNA, Messenger; Skin; Vasodilator Agents

Galanin-like peptide (GALP) has been recently isolated from the porcine hypothalamus. The GALP mRNA is restricted to neurons in the hypothalamic arcuate nucleus (Arc) and pituicytes in the posterior pituitary gland (PP), but physiological functions of the GALP remains unclear in both areas. We examined the effects of acute and chronic inflammatory stresses on the GALP mRNA levels in the rat Arc using in situ hybridization histochemistry. Intraperitoneal (i.p.) injection of bacterial endotoxin lipopolysaccharide (LPS) caused a marked increase of the GALP mRNA levels in the Arc. The effects of i.p. injection of LPS on the GALP mRNA levels in the Arc were significantly attenuated by pretreatment with i.p. injection of indomethacin cyclooxygenase inhibitor. Adjuvant arthritis caused by subcutaneous (s.c.) injection of heat-killed Mycobacterium butyricum as chronic inflammatory stress did not affect the GALP mRNA levels in the Arc, though the GALP mRNA levels in the pituicytes of the PP were markedly increased by two peaks at 12 h and 15 days after s.c. injection of heat-killed M. butyricum. Enzymeimmunoassay showed that the plasma concentration of GALP was not affected by these inflammatory stresses. These results suggest that acute inflammatory stress might be a potent stimulant to increase the GALP mRNA levels in the Arc of the rat via synthesis of prostaglandins.

Topics: Analysis of Variance; Animals; Arcuate Nucleus of Hypothalamus; Body Temperature; Cyclooxygenase Inhibitors; Drug Interactions; Enzyme-Linked Immunosorbent Assay; Galanin-Like Peptide; Gene Expression Regulation; In Situ Hybridization; Indomethacin; Inflammation; Lipopolysaccharides; Male; Mycobacterium; Rats; Rats, Inbred Lew; Rats, Wistar; RNA, Messenger; Time Factors