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J Neuroimmunol. 2002 Sep;130(1-2):100-8.
Novel orphanin FQ/nociceptin transcripts are expressed in human immune cells.

Arjomand J, Cole S, Evans CJ.

Neuroscience Interdepartmental Program, UCLA, Los Angeles, CA, USA.

The opioid-like receptor (NOP) is widely expressed throughout the human immune system. Here, we report that human peripheral blood lymphocytes (PBLs) express transcripts encoding the NOP receptor agonist, orphanin FQ/nociceptin (OFQ/N). OFQ/N transcripts in resting PBLs were restricted to CD19+B cells and contained a novel 5' exon (ImEx2b), replacing exons 1 and 2 found in neuronal transcripts. Translation of ImEx2b-containing transcripts resulted in truncated OFQ/N precursors lacking a classical signal peptide. Mitogen activation of PBLs dramatically up-regulated neuronal-like transcripts, predominantly in CD3+T cells. Overall, this suggests different promoters direct specific OFQ/N transcript expression in immune cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225892&dopt=Abstract

J Neuroimmunol. 2002 Sep;130(1-2):109-16.
Nitric oxide synthase I and VIP-activated signaling are affected in salivary glands of NOD mice.

Rosignoli F, Perez Leiros C.

Departamento de Quimica Biologica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina.

The autoimmune sialadenitis developed by non-obese diabetic (NOD) mice is considered a suitable model to study the ethiopathogenic mechanisms leading to sicca symptoms in Sjogren's syndrome (SS). Evidence supporting a neural rather than immune origin of the secretory dysfunction has been provided. As both nitric oxide and vasoactive intestinal peptide (VIP) are common messengers to nervous and immune systems mediating secretory and inflammatory responses, we examined nitric oxide synthase (NOS) activity with special focus on VIP-mediated effects in salivary glands of NOD mice. We found a decreased NOS activity and expression in major salivary glands of NOD mice with respect to control mice. In addition, there was a deficient VIP-activated signaling associated with a reduced saliva and amylase secretion in response to VIP. Our results support the hypothesis of an impaired balance of neuroimmune interactions in salivary glands as early events to take place in the progressive loss of secretory function of NOD mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225893&dopt=Abstract

J Neuroimmunol. 2002 Sep;130(1-2):140-54.
Differential expression of nicotinic acetylcholine receptor subunits in fetal and neonatal mouse thymus.

Kuo Y, Lucero L, Michaels J, DeLuca D, Lukas RJ.

Division of Neurobiology, Barrow Neurological Institute, 350 West Thomas Road, 85013, Phoenix, AZ, USA. ykuhw.edu

Studies were initiated to identify nicotinic acetylcholine receptor (nAChR) subunits and subtypes expressed in the developing immune system and cell types on which nAChR are expressed. Reported here are reverse transcription-polymerase chain reactions (RT-PCR) studies of nAChR alpha2-alpha7 and beta2-beta4 subunit gene expression using fetal or neonatal regular or scid/scid C57BL/6 mouse thymus. Findings are augmented with studies of murine fetal thymic organ cultures (FOTC) and of human peripheral lymphocytes. Novel partial cDNA sequences were derived for mouse nAChR alpha2, alpha3, beta3 and beta4 subunits, polymorphisms were identified in mouse nAChR alpha4, alpha7 and beta2 subunits, and recently derived sequences for mouse nAChR alpha5 and alpha6 subunits were confirmed. Thymic stromal cells appear to express nAChR alpha2, alpha3, alpha4, alpha7 and beta4 subunits, perhaps in addition to alpha5 and beta2 subunits, in a pattern reminiscent of expression in the developing brain. Immature T cells appear to express alpha3, alpha5, alpha7, beta2 and beta4 subunits, just as do neural crest-derived cells targeted by cholinergic innervation. Peripheral T cells seem to express an unusual profile of alpha2, alpha5 and alpha7 subunits, perhaps indicating that their nAChR express yet-to-be-identified assembly partners or that T cell nicotinic responsiveness occurs through homomeric nAChR composed of alpha7 subunits. Our findings are consistent with published work but show a much wider array of nAChR subunit gene expression in mouse thymic stromal and/or lymphoid cells and evidence for developmental regulation of nAChR subunit expression. These studies suggest important roles for nAChR in immune system development and function and in the neuroimmune network.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12225896&dopt=Abstract

Cas Lek Cesk. 2002 Aug 2;141(15):483-6.
[Analysis of the inflammation reaction and selected indicators of immunity in patients with an infected diabetic ulcer]

[Article in Czech]

Jirkovska A, Fejfarova V, Hosova J, Striz I, Kalanin J, Skibova J.

Centrum diabetologie IKEM, Praha. aljedicon.cz

BACKGROUND: Patients with diabetes represent 50 to 70% of patients who undergo nontraumatic foot or leg amputation, caused mostly by infection and necrosis of soft tissues accompanied with osteomyelitis. Signs and symptoms of infections may often be absent in patients with infected foot ulcers--the syndrome of "diabetic foot" (DF). The course and consequences of the infection may be influenced by the immune system dysfunction. The aim of our study was to assess presence of the chronic inflammation and specific immune responses, both humoral and cellular in patients with diabetic foot infection. METHODS AND RESULTS: 34 patients treated over one month for an infected DF in our foot clinic (mean age 54 +/- 8 years, mean duration of diabetes 20 +/- 9 years, mean HbAlc 8.8 +/- 1.5%), were matched with 27 healthy subjects. All patients were without clinical signs of acute deep foot infection and without critical leg ischemia. The inflammatory response was assessed by white blood cells count and C-reactive protein (CRP), humoral immune response was assessed by immunoglobulins (Ig) and cellular immunity was evaluated by T lymphocytes subpopulations. Patients with DF compared with healthy controls exhibited the laboratory signs of infection--significantly increased white blood cells count (7.6 +/- 2.1 vs. 6.4 +/- 1.3.10(9)/l, p < 0.01) and neutrophil count (4.6 +/- 1.8 vs. 3.8 +/- 0.9.10(9)/l, p < 0.05) and significantly increased CRP (7 +/- 12 vs. 2 +/- 6 mg/l, p < 0.01). Patients with DF had also significantly higher IgA levels (3.5 +/- 1.6 vs. 2.7 +/- 1.1 g/l, p < 0.05) and significantly more CD3+ T cells (76 +/- 8 vs. 71 +/- 10%, p < 0.05) and suppressor/cytotoxic CD8+ T cells (32 +/- 11 vs. 26 +/- 10%, p < 0.05). Other followed parameters IgG, IgM and serum monocyte and lymphocyte counts, CD4+ helper T cells and CD4+/CD8+ T-cell ratio did not differ between patients with DF and healthy controls. CONCLUSIONS: We did not anticipate a severe secondary immunodeficiency in followed cellular and humoral immune parameters in patients with chronic bacterial foot infection. It is necessary to assess the sufficiency of immune system activation with respect to chronic inflammation in next research.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226915&dopt=Abstract

Fiziol Zh. 2002;48(4):63-9.
[Effect of progesterone and 17beta-estradiol on proinflammatory cytokine costimulatory proliferative activity]

[Article in Ukrainian]

Hrekova SP, Vodianyk MO, Chernyshov VP.

Institute of Pediatrics, Obstetrics and Gynecology, Academy of Medical Sciences, Kiev.

The lymphocyte proliferation is multicomponent mechanism of immune system reactivity. Many costimulatory factors take part in this process. Proinflammatory cytokines (TNF, IL-1 alpha and beta) enhance proliferation of activated lymphocytes. Female steroid hormones inhibit proliferation of mitogen and alloantigen-activated lymphocytes. The aim of this study was to investigate the effect of progesterone and 17 beta-estradiol on the costimulatory proliferative activity of proinflammatory cytokines in vitro. Female steroid hormones inhibit lymphocyte response to antiCD3 antibody. Progesterone had a stronger effect than 17 beta-estradiol (64 and 13% of inhibition respectively). 17 beta-estradiol enhanced the TNF costimulatory effect on the lymphocyte proliferation. Progesterone neutralized this TNF-induced effect and reverted it (inhibition of lymphocyte proliferation was enhanced in the presence of TNF). We found dominant inhibitory effect of progesterone on the TNF costimulatory activity when progesterone and estrogen were added simultaneously. Progesterone and 17 beta-estradiol downregulated costimulatory proliferative activity of IL-1 alpha or beta. Thus female steroid hormones had suppressive effect on the antiCD3-stimulated lymphocyte proliferation. They downregulated costimulatory proliferative activity of IL-1 alpha/beta and had opposite effect on TNF costimulatory activity. Our results suggest possible roles female steroid hormones as regulators on activity of proinflammatory cytokines and their functions in lymphocyte proliferation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12226929&dopt=Abstract

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