Immune abnormalities and endotoxemia in patients with ulcerative colitis and in their first degree relatives: attempts at neutralizing endotoxin-mediated effects.

Proinflammatory cytokines released from monocytes/macrophages, in particular tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, IL-6, and IL-8 seem to play an important role in Inflammatory Bowel Disease (ulcerative colitis and Crohn's disease). Endotoxins or lipopolysaccharides, derived from the outer membrane of Gram-negative bacteria interact with CD14 on surface membrane of macrophages, thus triggering a signal cascade, which leads to the production and release of proinflammatory cytokines, particularly TNF-alpha. Therefore, in IBD, lipopolysaccharides could play a pathogenic role. In this respect, plasma endotoxins have been demonstrated in a not negligible percentage of patients with ulcerative colitis and in their unaffected relatives. The presence of circulating endotoxins could be due, at least in part, to the impaired natural immunity in either patients with ulcerative colitis or in their first degree unaffected relatives. Lactoferrin is an iron-binding glycoprotein, which binds to the lipid A region of lipopolysaccharide with a high affinity and this interaction prevents the binding of lipopolysaccharide to CD14, thus inhibiting the release of proinflammatory cytokines. Therefore, based on the possible pathogenic role exerted by endotoxins in ulcerative colitis, lactoferrin may deserve attention as a possible therapeutical agent in experimental models of Inflammatory Bowel Disease.

Biological and clinical significance of endotoxemia in the course of hepatitis C virus infection.

Endotoxins or lipopolysaccharides (LPS), major components of the cell wall of Gram-negative bacteria, once released from the bacterial outer membrane bind to specific receptors and, in particular, to a membrane-bound receptor, the CD14 (mCD14) and the toll-like receptor 4 present on monocytes/ macrophages. In turn, LPS-activated monocytes/ macrophages release in the host tissue an array of so-called proinflammatory cytokines and, among them, Tumor Necrosis Factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8 and IL-12 are the major mediators. Before therapy (To) and at the end of 6-month interferon (IFN)-alpha/Ribavirin (RIB) treatment (T6), circulating endotoxin levels were measured in responder and non responder HCV+ patients. At T0, 57% of the non responders were endotoxin-positive and had, on average, 54 pg/ml of plasma LPS while in 50% of the responder patients endotoxin were found with an average of 29 pg/ml. At T6, in responders LPS were no longer detectable, while in 42% of the non responders LPS were found (average levels 45 pg/ml). In terms of serum cytokine concentration, at T6 IFN-gamma levels when compared to those detected at T0 were increased in both endotoxin-positive and endotoxin-negative patients. However, at T6 IL-10 concentration was significantly increased only in the group of endotoxin-negative subjects (responder patients), in comparison to T0 values. The origin of endotoxemia in HCV+ patients seems to be multifactorial, likely depending on impaired phagocytic functions and reduced T-cell mediated antibacterial activity. In these patients, however, one cannot exclude the passage of LPS from the gut flora to the blood stream, owing a condition of altered intestinal permeability. At the same time, a less efficient detoxification of enteric bacterial antigens at the hepatic level should be taken into consideration. Finally, novel therapeutic attempts aimed to neutralize LPS in the host are discussed.

In vitro effects of naloxone on T-lymphocyte-dependent antibacterial activity in hepatitis C virus (HCV) infected patients and in inflammatory bowel disease (IBD) patients.

Naloxone acts as an opioid antagonist, displacing opioid drugs from cellular receptors. Among opioid substances, beta-endorphins are able to bind to several cell receptors, even including those expressed by immune cells. In this respect, evidence has been provided that in the course of viral infections, as well as in patients with ulcerative colitis high levels of beta-endorphins are detectable. Here, peripheral blood lymphocytes (PBL) from 21 HCV infected patients and 14 patients with IBD, respectively, were incubated with Naloxone and Naloxone + Ca2+ in order to evaluate a putative modulation of PBL-mediated antibacterial activity. In fact, previous studies have demonstrated a reduction of this T-cell activity in HCV and IBD patients. In general terms, the above treatment led to a recovery of the depressed antibacterial activity. In some cases, increase in T lymphocyte function was obtained with Naloxone alone, while in other cases the combination Naloxone + Ca2+ gave rise to a restorative effect. Of note, in some instances, lymphocytes were unresponsive to pharmacological modulation. The overall results suggest that beta-endorphins may down modulate T-cell antibacterial response in HCV and in IBD patients by saturating peripheral receptors on immune cells. Therefore, it is likely that Naloxone and/or Naloxone + Ca2+ may displace opioid drugs, thus antagonizing their effects.

Circulating cytokines and gastrin levels in asymptomatic subjects infected by Helicobacter pylori (H. pylori).

The pathophysiology of hypergastrinemia in H. pylori infection has been largely investigated and different reports clearly show that the infected antrum has a marked inflammatory response with a suggestive local production of cytokines. Notwithstanding, a few data are available on the circulating levels of cytokines and gastrin in the asymptomatic people carrying H. pylori infection. Thus, aim of the study was to evaluate circulating proinflammatory cytokines [Interleukin (IL)-8, Interleukin (IL)-10, Interferon (IFN)-gamma, and Tumor Necrosis Factor (TNF)-alpha] and gastrin levels in H. pylori positive asymptomatic subjects vs. H. pylori negative ones. To this end, thirty healthy volunteers with no digestive symptoms or systemic disease were enrolled and H. pylori infection was identified by a 13C-urea breath test. Plasma levels of gastrin were determined using the RIA kit whereas IL-8, TNF-alpha, IL-10, and IFN-gamma levels in serum were measured with a solid-phase ELISA. Fifteen infected people showed significantly higher gastrin and TNF-alpha levels than uninfected subjects. On the contrary, IL-8 levels were significantly higher in the uninfected subjects than in H. pylori positive ones (P < 0.0422). IFN-gamma and IL-10 circulating levels were not affected by H. pylori presence, being not significantly different in the two groups.

Embryonal cardiotoxicity of the Helicobacter pylori lipopolysaccharide.

Helicobacter (H.) pylori is the causative agent of the peptic ulcer disease and a co-factor in the development of gastric malignancies. Recently, it has been maintained that chronic H. pylori infections in adults are linked to a higher risk of coronary heart diseases. In this respect, the acute toxic effects of the H. pylori lipopolysaccharide (LPS) on embryonal cardiomyocytes at different developmental stages was evaluated. White Leghorn chick embryos and smooth (S)--form NCTC 11637 strain H. pylori organisms were used. Both whole heath-killed H. pylori suspensions (3.10(6) bacteria/egg) and isolated S-LPS (500 ng/egg) or S-Lipid A (500 ng/egg) were non-lethal to 4-day embryos, becoming moderately lethal (5% to 30%) to 6- and 8-day embryos and highly lethal (> 90%) to 10- to 17-day embryos. The contractile activity of isolated atrial fragments from 10-day embryos was completely inhibited, within 5 min, following treatments with heath-killed H. pylori (3 x 10(6)/ml), or S-LPS (500 ng/ml), or S-Lipid A (500 ng/ml); the block determined by S-LPS and S-Lipid A was irreversible, while the block by bacterial suspensions was completely reversible upon withdrawal. Following a 24-hour treatment with S-LPS or S-Lipid A of single-cell cultures of cardiomyocytes (isolated from 10-day embryos) a dose-dependent cell loss was observed, as assessed by total protein dosage and direct counting of adherent cells. Propidium Iodide/Annexin V FACS-analysis confirmed the occurrence of cellular necrosis, but did not show any evidence of apoptotic processes. The release of superoxide anion radicals by cultured cardiomyocytes was as follows: S-Lipid A (25 micrograms/ml) > S-LPS (25 micrograms/ml) > heath killed H. pylori suspensions (3 x 10(6)/ml); control cultures did not release detectable amounts of superoxide anion radicals. Furthermore, cultured cardiomyocytes produced increased amounts of NO (N-monomethylarginine-inhibitable) following stimulation with S-LPS (25 micrograms/ml) or S-Lipid A (25 micrograms/ml) (but not heath killed H. pylori 3 x 10(6)/ml suspensions). Under all the above experimental conditions S-polysaccharide proved to be non-toxic. Concluding, H. pylori LPS is relatively non-toxic to the less differentiated cardiomyocytes; cardiomyocytes which are more advanced in their biochemical differentiation become highly sensitive to LPS and produce ROS and NO. ROS are probably responsible for the early toxic actions, while both ROS and NO are likely to be involved in the later degenerative/necrotic effects.

Helicobacter pylori infection, immune response and vaccination.

It is well known that abnormal immune responses may play a pathogenic role in the H. pylori-related gastropathy. Indeed, as far as humoral immune response is concerned, it is still debated whether specific anti-H. pylori antibodies have a protective or noxious effect in infected hosts. Besides proinflammatory cytokines released from macrophages, such as tumor-necrosis factor-a and interleukin-1beta, and IFN-gamma derived from T-helper 1 lymphocytes, also interleukin-10, a product of T-helper 2 lymphocytes with antiinflammatory properties, seems to be surprisingly involved in the pathogenesis of H. pylori-induced gastritis. In addition, lipopolysaccharide derived from the outher membrane of H. pylori acts as a chemoattractant for monocytes and induces release of free radicals, interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha. On the other hand, H. pylori lipopolysaccharide could be responsible for the increased polyamine concentrations in the gastric mucosa and polyamines, such as putrescine, spermidine and spermine, could be involved in the increased cell proliferation and consequent possible neoplastic transformation of the gastric mucosa. Incubation of peripheral blood mononuclear cells with H. pylori increases significantly the surface expression of CD95 receptor (Fas), thus suggesting that these bacteria are able to induce apoptosis. In animal models, different types of vaccination have been investigated, including stimulation of nasal and rectal lymphoid tissue, as well as adoptive transfer of T cell from donors immunized with H. pylori. However, results obtained are frequently disappointing. In humans, urease of H. pylori was safely used as oral vaccine in the absence or presence of adjuvants with encouraging results. Finally, DNA vaccines could offer in the future advantages for prophylactic H. pylori eradication, especially where population is infected by this microorganism since childhood.

Effects of 17beta-estradiol administration on apoptosis and polyamine content in AGS cell line.

BACKGROUND: Estrogens and polyamines seem to play an important role not only in cell growth and differentiation, but also in programmed cell death. The aim of the present study was to investigate the effects of 17beta-estradiol supplementation on apoptosis as well as on the polyamine content of an ER-positive human gastric cancer cell line (AGS). MATERIALS AND METHODS: Apoptosis was investigated by evaluating DNA fragmentation, using enzyme immunoassay and agarose gel electrophoresis and the phosphatidylserine exposure by flow cytometry analysis. Polyamine levels were evaluated by HPLC. RESULTS: 17Beta-estradiol gave rise to a marked pro-apoptotic effect at concentrations of 16 microM or higher compared to the control. Moreover, the hormone significantly reduced the contents of polyamines compared to control cells. The apoptotic effect of 17beta-estradiol was partially counteracted by exogenous spermine administration. CONCLUSION: 17Beta-estradiol administration induces apoptosis in AGS cells. Further, an increase in cell sensitivity to apoptosis due to a decline in the polyamine content may be suggested.

Phagocytosis, killing, lymphocyte-mediated antibacterial activity, serum autoantibodies, and plasma endotoxins in inflammatory bowel disease.

OBJECTIVE: Alteration of mucosal and systemic immune responses may play an important role in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to evaluate natural immune responses (i.e., phagocytosis, killing, and antibacterial activity), serum autoantibodies (antineutrophil cytoplasmic antibodies [ANCA] and anti-lactoferrin [LF] antibodies), and plasma endotoxins in patients affected by ulcerative colitis (UC) and Crohn's disease (CD). METHODS: Blood samples were obtained from 71 patients with UC, 32 patients with CD, and 32 control subjects. Disease activity was scored using Truelove's criteria in patients with UC and the Crohn's Disease Activity Index (CDAI) in patients with CD. Candida albicans served as a target for evaluation of phagocytosis and killing exerted by polymorphonuclear cells (PMN) and monocytes (MO), whereas Salmonella typhi was used for assessing lymphocyte-mediated antibacterial activity. ANCA were detected by indirect immunofluorescence, whereas anti-LF antibodies were assayed by means of enzyme-linked immunosorbent assay. Plasma endotoxins were measured by Limulus amoebocyte lysate assay. RESULTS: Phagocytosis and killing exerted by PMN and MO, as well as lymphocyte-mediated antibacterial activity, were significantly reduced (p < 0.0001) in patients affected by UC and CD in comparison with controls, irrespective of either disease activity or treatment. Plasma endotoxins were detected in 12/71 (17%) patients with UC, and in 10/32 (31%) patients with CD. ANCA were present in 42/71 (59%) patients with UC and in 3/32 (9%) patients with CD, whereas anti-LF antibodies were detected in 31 (44%) UC patients and in six (19%) CD patients. No significant differences in phagocytosis and killing exerted by PMN were found between ANCA-positive and ANCA-negative UC patients. CONCLUSIONS: Our data demonstrate an impairment of natural immunity exerted by peripheral blood phagocytes and lymphocytes in patients with UC and CD. ANCA and anti-LF antibodies were present mainly in UC patients but their presence did not affect PMN-mediated phagocytosis and killing. Finally, plasma endotoxins may contribute to the chronic inflammatory status, likely by inducing release of proinflammatory mediators.

Helicobacter pylori infection and host cell responses.

It is well known that Helicobacter pylori is able to colonize the gastric mucosa, causing a chronic and persistent infection with complications, such as peptic ulcer and gastric cancer. This review places emphasis on some epidemiological aspects of Helicobacter pylori infection and its mode of transmission. At the same time, invasive and non-invasive methods of diagnosis of Helicobacter pylori infection are illustrated. More space is devoted to the host response following invasion of the stomach. In this respect, the role played by different growth factors and polyamines in the course of Helicobacter pylori disease is discussed also in relation to the result of eradicating treatment. On the other hand, an accurate description of the host immune responses against Helicobacter pylori organism and/or their components (e.g. lipopolysaccharides) is reported. Finally, since Helicobacter pylori has been classified as a class I carcinogen, current researches are focussed on the Helicobacter pylori-induced carcinogenesis.

Relationship among red blood cell polyamine content, phagocytic activities and plasma endotoxins in untreated colorectal cancer patients.

Polyamines are actively involved in immune processes and it is known that patients with cancer often exhibit immune deficits. Twenty-two patients with colorectal cancer were enrolled into this study, before starting conventional treatments. The relationship among the content of polyamines in red blood cells and phagocytosis and killing of monocytes and polymorphonuclear cells, and endotoxemia was investigated. The data show a negative correlation among levels of total polyamines and spermine and monocyte phagocytosis. Higher levels of spermine were present in patients with detectable circulating endotoxins. Our findings suggest a down-modulating effect of polyamines on the monocyte phagocytosis in untreated colorectal cancer patients; this effect could explain the presence of circulating endotoxins in cancer bearing patients.

Immunological disorders in inflammatory bowel disease and immunotherapeutic implications.

Ulcerative colitis and Crohn's disease, also called inflammatory bowel diseases, are characterised by altered mucosal and systemic immune responses. An increase in T helper (h) 1 cytokines, such as interleukin-2 and interferon-gamma, has been found in mucosa from patients affected by Crohn's disease. On the contrary, in patients with ulcerative colitis, mucosal cytokines seem to belong to the Th2 type with an increased release of interleukin-4, and -10. B lymphocytes isolated from lamina propria of patients with ulcerative colitis produce perinuclear anti-neutrophil cytoplasmic antibodies, thus suggesting a status of hyperactivation of these cells in inflammatory bowel diseases, which may lead to autoimmune phenomena. Polymorphonuclear cells and monocytes/macrophages heavily infiltrate the intestinal mucosa and release proinflammatory cytokines, such as interleukin-1, -6, -8 and tumour necrosis factor-alpha. Endotoxins or lipopolysaccharides, major constituents of the gram-negative bacterial cell wall, are present in the circulation of patients with inflammatory bowel diseases and may account for the release of both cytokines and free radicals. Finally, besides immunosuppressive drugs (e.g. cyclosporin A), immunotherapy with neutralising monoclonal antibodies against tumour necrosis factor-alpha has been experimented in Crohn's disease with encouraging results. In addition, novel promising therapeutic approaches in these diseases include the administration of recombinant interleukin-10 or interleukin-11.

[Giant-cell reparative granuloma (GCRG). A review of the literature, the present state of knowledge and therapeutic suggestions]. / Il granuloma riparativo a cellule giganti (GRCG). Review della letteratura, stati attuali delle conoscenze, suggerimenti terapeutici.

In the cranio-facial region the giant-cell reparative granuloma (GCRG) is a typical lesion of the maxillary bones. Because giant-cell reparative granuloma is not strictly a granuloma, clinically and histologically, many authors prefer call it giant-cell lesion (GCL). A review of the literature have along with our experiences is reported. Authors present 17 patients with giant-cell lesion and their results, treated at the Maxillo-Facial Department of Parma. Clinical, radiographic and pathologic features were evaluated and differential diagnosis was considered, showing the real great difficulty in differential diagnosis also and especially for surgical treatment.

Impairment of phagocytic and T-cell-mediated antibacterial activity and plasma endotoxins in patients with untreated gastrointestinal cancer.

BACKGROUND: Cancer patients have multiple immune deficits, and mediators, such as prostaglandins, transforming growth factor-beta, and interleukin (IL)-10, may play a role in the pathogenesis of these immune dysfunctions. METHODS: Fifty-six patients with gastrointestinal cancer (11 gastric cancer, 7 papilla of Vater cancer, and 38 colorectal cancer) were enrolled for this study, before starting conventional treatments. Phagocytosis and killing exerted by polymorphonuclear cells and monocytes, peripheral blood mononuclear cell absolute numbers, T-cell-mediated antibacterial activity, serum levels of IL-10 and interferon (IFN)-gamma, and plasma bacterial endotoxin concentration were evaluated. RESULTS: Data show an impaired phagocytic and T-cell-mediated antibacterial activity in all cancer patients, whereas only in subjects with gastric cancer were IFN-gamma serum levels reduced. Circulating endotoxins were detected in 17 patients. CONCLUSIONS: In untreated gastrointestinal cancer patients the capacity of phagocytes and T-cells to clear pathogens is reduced. This dysfunction may increase the risk of becoming infected and may account for the presence of endotoxin in 30% of patients.

The influence of Helicobacter pylori eradication on the gastric mucosal content of epidermal growth factor, transforming growth factor-alpha, and their common receptor.

BACKGROUND: The relationship between the expression of epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) and that of their receptor (EGF-R) in the Helicobacter pylori-infected gastric mucosa has not been completely elucidated. The aim of this study was to examine the interplay between H. pylori colonization and gastric mucosal growth factor content. METHODS: By means of a solid-phase enzyme-linked immunosorbent assay EGF, TGF-alpha, and EGF-R levels and interleukin-1beta (IL-1beta) content, which is considered a marker of chronic inflammation, were evaluated in the antral mucosa of 24 H. pylori-positive patients before and 8 weeks after eradication therapy. RESULTS: After therapy H. pylori was eradicated in 19 patients. The eradication was accompanied by a significant decrease in IL-1beta content and an increase in EGF and TGF-alpha levels. On the other hand, in the five patients in whom the bacterium was not eradicated EGF, TGF-alpha, and EGF-R levels were quite similar to those assayed before therapy, whereas IL-1beta content was still high. CONCLUSIONS: These results suggest that H. pylori exerts an inhibitory effect on the mucosal expression of EGF and TGF-alpha, which are likely involved in the gastric mucosa repair process.

[Secondary reconstruction, after maxillectomy, using an osteocutaneous flap from the fibula. Report of a case]. / Il lembo rivascolarizzato osteocutaneo di fibula nella ricostruzione secondaria dopo maxillectomia. Caso clinico.

Surgical functional reconstruction after partial maxillectomy with fibula free flap. A bilateral upper alveolar bone, gingival and palatal defect after tumor resection, has various problems originating from reconstruction with prosthesis or temporalis muscle flap. We report a secondary reconstructive procedure using the fibula osteocutaneous free flap. The combined bone segments created the upper alveolar arch, and the skin paddle closed the palatal defect. This procedure restored the patient to masticatory function of the upper jaw, intelligible speech and natural facial appearance. As a result quality of life of patient was extremely improved.

Immunological effects following administration of interferon-alpha in patients with chronic hepatitis C virus (cHCV) infection.

The immunological effects of interferon (IFN)-alpha administration were evaluated in 15 patients with cHCV infection. Individuals were treated with 6 MU of lymphoblastoid IFN-alpha three times a week for 6 months and with 3 MU three times a week for an additional 6 months. Patients were divided into responders (12 subjects) and nonresponders (3 subjects), respectively, according to alanine aminotransferase serum levels at the end of treatment. Before therapy (T0), absolute numbers of CD3+, CD4+, CD8+, CD14+ and CD16+ cells were significantly reduced in both groups when compared to normal values. At the same time, all patients displayed a profound decrease of phagocytosis and killing exerted by both polymorphonuclear cells (PMN) and monocytes (MO). However, MO Killing resulted to be normal in the responder group. With special reference to T cell function, T cell mediated antibacterial activity, using Salmonella typhi as a target, was also significantly reduced. After therapy (T12), in responder patients a significant increase of CD3+, CD4+, CD14+ and CD16+ cell absolute numbers was observed, while phagocytic and T cell functions were still depressed. Among the nonresponders, in two of three patients IFN-alpha administration gave rise to an increase (above normality) of CD3+, CD4+, CD8+, CD14+, CD16+ and CD20+ cell absolute numbers, while in one patient the same markers dramatically dropped below normal range. In two patients, antibacterial activity was significantly augmented by IFN-alpha treatment, whereas in one patient no modification was observed. Finally, in the same patients IFN-alpha did not correct PMN and MO pretreatment deficits.

In vitro effects of 3'-azido-3'-deoxythymidine (AZT) on normal human polymorphonuclear cell and monocyte-macrophage functional capacities.

The in vitro effects of 3'-azido-3'-deoxythymidine (AZT) (at concentrations of 1, 10 and 100 microM, respectively) on normal human polymorphonuclear cell (PMN) and monocyte-macrophage functional capacities were evaluated. Results show that AZT was able to decrease monocyte phagocytosis only, while PMN polarization, phagocytosis and killing were unaffected by drug pretreatment. Quite interestingly, monocyte-derived macrophages maintained their unaltered phagocytic function in spite of the presence of AZT in overnight cultures, thus indicating that monocytes are more susceptible than macrophages to the antiproliferative effects of AZT. Since our data indicate that AZT affects normal human monocyte phagocytosis, it is advisable to evaluate this immune parameter in HIV+ patients administered with this drug.

Evaluation of cellular immune responses and soluble mediators in patients with chronic hepatitis C virus (cHCV) infection.

In 54 patients with cHCV infection, peripheral immune responsiveness and soluble mediator release were evaluated. Results demonstrate that in these patients phagocytosis and killing capacities exerted by polymorphonuclear cells and monocytes were profoundly depressed. At the same time, absolute numbers of CD3+, CD8+ and CD16+ cells were reduced, while the CD4(+)-CD8+ dependent antibacterial activity was also impaired. With special reference to soluble mediators, elevated amounts of both soluble interleukin-2 receptor and soluble intercellular adhesion molecule-1 were detected in sera of patients. By contrast, serum levels of tumor necrosis factor-alpha were within normal ranges, whereas interferon-gamma serum concentrations were decreased. Of note, in 18.5% of cHCV patients circulating levels of bacterial lipopolysaccharides (LPS) were detected by means of Limulus assay. In the Limulus+subset of patients, absolute numbers of CD14+ cells were reduced in a significant manner, this implying a putative monocyte-LPS interaction. In conclusion, the overall results indicate a condition of peripheral immune depression in cHCV patients with an exaggerated shedding of various mediators endowed with noxious effects for the host.

Role of lymphocyte function-associated antigen-1 on the interplay between lipid A-activated monocytes and polymorphonuclear cells.

Previous findings provided evidence that bacterial lipopolysaccharide (LPS)-activated human monocytes are able to upregulate autologous polymorphonuclear (PMN) phagocytic ability via cell-to-cell contact mechanisms mediated by membrane (m)-associated cytokines (CKs), such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-1 beta, IL-6 and IL-8. Consequently, the role of the lymphocyte function-associated antigen (LFA)-1 molecule on the monocyte (Mo)-PMN interplay was evaluated. In the first step, lipid A (LA)-stimulated Mo were pretreated with anti-recombinant human (Rhu) LFA-1 alpha monoclonal antibody (MoAb), and the enhanced phagocytic activity of PMN was abrogated. Pretreatment of unstimulated Mo with the same MoAb led to a reduction of PMN phagocytosis. In the second step, the role of m-LFA-1 on PMN was investigated with regard to Mo modulation. Anti-Rhu LFA-1 alpha MoAb was supplemented to LA-activated and unstimulated PMN, respectively, before coculturing with autologous LA-activated Mo. The addition of anti-Rhu LFA-1 alpha MoAb gave rise to a significant decrease in PMN phagocytosis regardless of PMN activation. These data suggest that, besides m-CKs, LFA-1 present on Mo and PMN might be involved in the mutual interplay between PMN and Mo.

Alexithymia, immunity and cervical intraepithelial neoplasia: a pilot study.

Alexithymia and circulating lymphocyte subsets were studied in 62 women [36 healthy women and 26 women affected by cervical intraepithelial neoplasia (CIN I, II, III) who were not aware of their status] in order to assess a possible relationship between alexithymia, CIN and immunological lymphocytic functions. Alexithymia was estimated by the 20-item Schalling-Sifneos Personality Scale and then correlated with peripheral blood lymphocyte subsets. The results of our study report an association between alexithymia and CIN. Alexithymic women show lower rates of almost all lymphocytic subsets compared to nonalexithymic ones. The difference was also found between alexithymic women affected by CIN and alexithymic women with an unsuspicious Pap smear. On the whole, these preliminary results seem to confirm data reported by other authors who hypothesized that a certain personality trait characterized by emotional inhibition is related to a greater cancer vulnerability. Such relationships might be mediated by certain lymphocytic functions as the result of the alexithymic status. Results reported here need more extensive surveys, in order to control potentially confounding factors related to the personality assessment of the subjects in this study.