Katacalcin and calcitonin immunoreactivity in different types of leukocytes indicate intracellular procalcitonin content

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

“…In 1980, it was shown that macrophages and lymphocytes were able to produce adrenocorticotropin and endorphins (Blalock and Smith, 1980;Smith and Blalock, 1981). To date, immune cells produce around 30 neuroendocrine mediators, including growth hormone (Weigent et al, 1988), prolactin (Montgomery et al, 1987), proenkephalin A (Rosen et al, 1989), somatostatin (Fuller and Verity, 1989;, oxytocin-vasopressin (Geenen et al, 1987), atrial natriuretic peptide (Vollmar et al, 1992), substance P (Ho et al, 1997;Lai et al, 1998;Lambrecht et al, 1999), gonadotropin-releasing hormone (Chen et al, 1999), glucocorticoids (Lechner et al, 2000), procalcitonin (Oberhoffer et al, 1999), corticotropin-releasing factor (CRF) (Brouxhon et al, 1998), vasoactive intestinal peptide (VIP; see Section II. ), pituitary adenylate cyclase-activating polypeptide (PACAP) , neuropeptide Y (Schwarz et al, 1994), calcitonin gene-related peptide (CGRP) (Singaram et al, 1991), ␣-melanocyte-stimulating hormone (␣MSH) (Lolait et al, 1986;Rajora et al, 1996), and opioid peptides (Przewlocki et al, 1992).…”

Pituitary Adenylate-Cyclase-Activating Polypeptide Expression in the Immune System

“…In the last 20 years, it has been demonstrated that cells of these three systems synthesize and secrete similar substances, bearing the same receptors for them, thus suppressing the original differences between neurotransmitters, hormones and immune mediators. In this way, the most recent members of the group of mediators traditionally produced by nervous and endocrine systems, and now discovered to be also produced by cells of the immune system are: glucocorticoids synthesized by thymic epithelial cells [1]; procalcitonin produced by various types of human leukocytes [2]; calcitonin-gene-related peptide secreted by T lymphocytes [3], and the hypothalamic deca-peptide gonadotropin-releasing hormone, which has been reported to be endogenously produced by human peripheral lymphocytes [4].…”

Strong Correlation of B2-Microglobulin (B2-m) with Procalcitonin (PCT) in the Serum of Chronic Hemodialysis Patients: A Role for Infections in the Dialysis-Related Amyloidosis?

“…Taking into account that PCT is considered a marker of infection, [7][8][9]16,17,23] the correlation of B 2 -m to PCT is most likely attributed to the expression and production of these two substances from activated cells (i.e., monocytes, macrophages, lymphocytes). [5,17,24,25] This activation can be due to the secretion of cytokines and interferons during the immune response in the setting of pro-inflammatory substances release syndrome. Though this release can be provoked by infections or non-infectious conditions (e.g., contact of blood with bioincompatible membranes), the lack of correlation between B 2 -m to CRP, an accepted marker of systemic inflammatory reaction, [10][11][12] in all time periods points to the simultaneous production and release of B 2 -m and PCT only (or mostly) by infections.…”

“…[1,2] Although DRA has been wellknown for many years, little is known about the rate of B 2 -m production. It is quite reasonable to hypothesize that inflammatory conditions, such as infections, by activating the aforementioned defensive cells can modify (most probably increase) the rate of secretion and the serum levels of B 2 -m. Infections are common and mostly subclinical [3,4] in CHD, and procalcitonin (PCT), a secretory protein released by various types of human cells, [5,6] is considered to be a sensitive and reliable marker for their detection. [7][8][9] Our prospective study aimed to detect any correlation of B 2 -m to PCT (as a marker of infections) in the serum of CHD and to C-reacting protein (CRP), a widely accepted marker of non-specific inflammatory reaction [10][11][12] in a parallel assessment of the influence to B 2 -m serum levels.…”