vasoactive-intestinal-peptide and Wounds-and-Injuries

Traumatic injury as a trigger for the subsequent development of psoriatic arthritis (PsA) has been implicated by several case reports and case series. However, it is still unclear whether trauma is the inciting event or just an incidental finding. It is thought that the interplay of genetic, immunologic, and environmental factors, such as trauma, may trigger the development of PsA. At least two hypotheses of how trauma may be linked to the development of PsA have surfaced and involve a "deep Koebner effect," the concept of a synovio-entheseal complex and activation of the innate immune system by biomechanical factors. The role of neuropeptides such as substance P and vasoactive intestinal peptide has been highlighted in the synovium after trauma. Better understanding of this phenomenon would shed light into the pathophysiology of Psa and help the development of preventive and therapeutic strategies.

Topics: Adult; Aged; Arthritis, Psoriatic; Female; Humans; Male; Middle Aged; Neuropeptides; Research Design; Substance P; Synovial Membrane; Vasoactive Intestinal Peptide; Wounds and Injuries; Young Adult

Topics: Animals; Humans; Inflammation; Lung; Lung Injury; Myocardial Reperfusion Injury; Neurons; Nitric Oxide; Vasoactive Intestinal Peptide; Wounds and Injuries

It has been proposed that vasoactive intestinal peptide (VIP) or a very closely related peptide has important actions very early in embryonic development. Recent data supporting this hypothesis are that subnanomolar concentrations of VIP significantly increased the growth rate of cultured embryonic day-9.5 (E9.5) mouse embryos, and that embryos at this and later stages exhibit a high degree of VIP binding in the brain stem and spinal cord. It is not known whether VIP is derived from the fetus, placenta, or mother at these early stages, or whether VIP acts in this culture system in place of a related peptide. The earliest reported expression of VIP in rat embryos is at E13.5, when the peptide and mRNA are expressed transiently in a high percentage of cells in the rat stellate ganglia. The time course of events mapped in other sympathetic ganglia at this stage suggest that transient expression of VIP in the ganglia might function to regulate neuroblast and/or glial cell proliferation, maturation or survival. Tissue culture studies indicate that VIP can support many of these trophic functions at concentrations that are the same or lower than that necessary to increase cAMP levels by way of classical VIP receptors. For example, VIP at 10(-10) M stimulates the release of neurotrophic factors from glial cells and maximally stimulates the proliferation of astrocytes. Two VIP receptors encoded on different genes have now been cloned. Both are members of the seven transmembrane G-protein-coupled receptor family and, when expressed in mammalian cells, mediate an increase in cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Embryo, Mammalian; Embryonic and Fetal Development; Ganglia, Spinal; Ganglia, Sympathetic; Humans; Nerve Growth Factors; Nerve Regeneration; Receptors, Vasoactive Intestinal Peptide; Vasoactive Intestinal Peptide; Wounds and Injuries

Topics: Burns; Humans; Nitric Oxide; Vasoactive Intestinal Peptide; Wounds and Injuries

VIP and NO co-localized in many of the same neurons, are co-released by some of the same physiological stimuli. In this study we seek the divergent roles in relation to tissue injury between the neurotransmitters within 24 h after burn injury. Forty-four subjects were examined. Fourteen were mechanical trauma patients with mean injury severity score (ISS) of 27, 15 burns patients with mean per cent total burn surface area (%TBSA) of 18%, and 15 healthy controls. Patients plasma were withdrawn immediately on admission (OA) and 24 h post-injury (PI). Controls fasted (>10 h) the night before morning sampling. Enzyme-linked immunosorbent assay (ELISA) technique suitable for the measurements of NO and VIP was used. For each comparison between the patients and control groups, NO(2)(-)/NO(3)(-) plasma levels were higher in burn (P<0.001) and trauma (P<0.0005) than controls. VIP was higher in trauma (P<0.05) but not in burns (P=NS). Trauma and human burn injuries are associated with increase levels of NO productions. While VIP rose in trauma, it remained unchanged in burns. The relationship between VIP and NO observed under physiological conditions in thermal and trauma injury may be of importance in wound healing.

Topics: Adult; Aged; Aged, 80 and over; Burns; Enzyme-Linked Immunosorbent Assay; Humans; Male; Middle Aged; Nitric Oxide; Vasoactive Intestinal Peptide; Wounds and Injuries