European Journal of Inflammation

Hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV) are the leading cause of chronic liver diseases. The aims of the present study are to determine the etiological relationship of HBV and HCV in patients with chronic liver disease in North-Eastern Bulgaria and prevalence of dual and triple infections. A total of 434 patients were investigated for HBsAg, 402 of whom were also tested for anti-HCV. The HBsAg positive subjects were tested for anti-HDV and 32 of them also for HbeAg/anti-Hbe. Separated commercial ELISA kits were used. HBsAg was detected in 132 (30.4%); 10.6% were co-infected with HDV. Anti-HCV was detected in 15.4%. Five of 132 HbsAg positive patients (3.78%) were simultaneously HBV and HCV positive. Two patients out of 132 (1.52%) were positive to HBV, HCV and HDV. Our data indicate that HBV infection was the main cause of chronic liver diseases in North-Eastern Bulgaria, and 10.6% of the patients suffered from severe disease because of co-infection with HDV. HCV plays the same role in 15.4% of the cases. Recently, we observed dually infected (HBV and HCV) and triple infected (HBV, HCV, HDV) patients suffering from severe chronic liver diseases.

The aim of the present study was to assess atypical changes in urothelial cells among petroleum station workers. This is a case control study, investigating 300 participants by cytological methods. Of the 300 participants, 150 were cases (exposed to petroleum products) and 150 were controls (non-exposed). Full voided urine was obtained and was cytologically assessed. Cytological atypia was identified in nine (6%) out of the 150 cases and could not be identified in 141/150 (94%) of the cases, whereas, in the control group, cytological atypia was recognized in four (2.7%) of the 150 controls and could not be identified in 146/150 (97.3%). The risk associated with petroleum product exposure, the odds ratio (OR), and 95% confidence interval (CI) was 2.33 (0.7015–7.7378), P = 0.1673. Exposure of petroleum station workers to petroleum products increases the risk of urothelial atypical changes, which may progress to precancerous and cancerous changes.

Rhino-orbital-cerebral mycosis (ROCM) is a life-threatening fungal disease associated mostly with Mucoralean fungi. The infection presents as headache, vision loss, proptosis, ptosis, painful ophthalmoplegia, and peripheral face palsy, with a high mortality (>80% for infections that spread to the brain) and severe morbidity, such as eyeball exenteration and vision loss. In our hospital, a 61-year-old woman with diabetes was diagnosed with rhino-orbital-cerebral infection caused by Alternaria infectoria. Cavernous sinus thromboses (CST) were seen in surgery, pathology, and MRI. She did not respond to potent antifungal therapy until the adding of anti-thrombosis drugs. By analyzing our case, together with the ones that have been published, we realized that fungal thrombosis in the cavernous sinus is the main pathophysiological problem in ROCM that typically shows mass enhancement within the cavernous sinus in radiographic images, thrombosis with characteristics of ischemia and infarction in pathology. Anticoagulation/antithrombus therapy might be helpful in the management of ROCM if potent antifungal treatment does not have effect.

Arthritis is estimated to affect over 30% of all adults and all the available drugs add considerable morbidity and mortality of their own. A recent therapeutic approach targets the mast cells that are currently considered critical in a variety of inflammatory diseases, especially arthritis. Mast cells could be activated by many immune and neural triggers, as well as by many food substances and drugs leading to secretion of numerous vasoactive and inflammatory molecules. Recent studies have shown that mast cells can be inhibited by certain naturally occurring flavonoids, such as quercetin, and the sulfated proteoglycan chondroitin sulfate. Glucosamine and chondroitin are present in many dietary supplements, but neither the source nor the purity of the active substances is listed; moreover, these formulations do not permit sufficient absorption, due to the high molecular weight and negative charge. Moreover, a common source of chondroitin sulfate is cow trachea with the risk of spongioform encephalopathy (mad cow disease). A new series of dietary supplements (Algonot-Plus®) are based on published scientific evidence and combine quercetin, glucosamine sulfate and chondroitin sulfate of high purity in formulations that include kernel olive oil to increase absorption of the inhibitory substances.

Oral rehabilitation by means dental implants is a surgical procedure with high standards of success. Since very few reports focus on clinical success related to implant site and no report is available on a new type of implants (FMD srl, Rome, Italy), a retrospective study was performed. A total of 390 two-piece implants were inserted, 213 in females and 177 in males. The median age was 59 ± 11 (min-max 24–80 years). Two hundred and five implants were inserted in upper jaw and 185 in mandible. Three implants were lost, survival rate = 99.23%. Among the studies variables immediate loaded implants on single tooth rehabilitations (p=0.047) have a worse clinical outcome. Then peri-implant bone resorption (i.e. delta IAJ) was used to investigate SCR. Among the remaining 387 implants, 47 fixtures have a crestal bone resorption greater than 1.5 mm (SCR = 87.85). Statistical analysis demonstrated that no studied variable has an impact on clinical outcome and thus there are no differences in term of SVR and SCR by sites. In conclusion FMD implants are reliable devices for oral rehabilitation with a very high SCR and SVR.

Inflammation is a critical process in the oral cavity, especially in gingival inflammation and pulpitis, as seen in periodontitis and decayed tooth structure. Nevertheless, the cellular process involved in oral inflammation is not well delineated. Recent evidence from other organs as well as the mouth suggests that neurogenic inflammation involving mast cells (MCs) may be a critical factor. MCs, best known for their role in allergic reactions, are also involved in immunity and inflammation. They are located at strategic points close to small blood vessels and nerve fibers often containing substance P (SP). The pain models of reversible or irreversible pulpitis simply suggest the complexity of neural-inflammatory interactions within the dental pulp. In the pulp and periapical area, neuropeptides and cytokines modulate vascular responses, increase permeability and leukocyte migration. SP-immunoreactive nerve fibers and TNF-positive MCs were found localized around blood vessels in all samples of periapical granulomas. By generating a profound number of potent mediators, MCs may serve as a link between the immune, endocrine and nervous systems in pulp inflammation. This role has been strengthened by recent evidence of MCs involvement in inflammatory conditions.

After microbial invasion and tissue damage, a set of cytokines, including interleukin-1α (IL-1α), IL-1β, IL-6, IL-18 and tumor necrosis factor-α (TNF-α), and microbial and endogenous molecules named pathogen-associated molecular pattern (PAMPs) and damage-associated molecular pattern (DAMPs), are released from activated leukocytes and dead cells and bind to immune receptors to induce the innate and adaptive response. The intracellular signals induced by the multiprotein complex formed by the Toll-like receptors/IL-1 receptors (TLRs), NOD-like receptors (NLRs) and tumor necrosis factor-α receptors (TNFRs) and their ligands and downstream effectors lead to the activation of NF-κB (NFkappaB) and the interferon regulatory factor (IRF) transcription factors and thereby the synthesis of pro- and anti-inflammatory genes as well as pro- and anti-cell death genes. Depending on cell-intrinsic and extrinsic biochemical events elicited by an inflammatory response, the cells die via apoptosis, necrosis, pyroptosis or autophagy cell death program. This article resumes our current understanding of these processes and how they influence inflammation.

The immunology of gluten hypersensitivity and celiac disease has been pursued with significant interest in the past 20 years. For the prevention of systemic diseases, most pathogens that gain entry into our bodies must be met with an effective immune response, yet in the gastrointestinal tract it is equally important that commensal bacteria and a diverse collection of dietary proteins and peptides be recognized without eliciting an active immune response or constant activation of the inflammatory pathway. This phenomenon of hyporesponsiveness to food antigens is known as oral tolerance. This oral tolerance to dietary antigens is maintained by three different mechanisms: anergy, cell deletion and immune suppression. However, in the presence of mechanical/chemical stressors and infections, this tolerance may break down, and gut associated lymphoid tissues (GALT) will react to different luminal antigens. The reaction of GALT to these antigens may lead to the production of pro-inflammatory cytokines, opening of tight junctions, entry of undigested antigens into the circulation, and the subsequent production of IgA, IgG, IgM and IgE antibodies in blood and secretory components. Like any other food hypersensitivity reaction, gluten sensitivity can be divided into immediate and delayed hypersensitivities. In this review an attempt is made first to differentiate immediate hypersensitivity to gliadin, mediated by IgE, from delayed hypersensitivity, which is mediated by IgA and IgG. Furthermore, we attempt to differentiate between gluten hypersensitivity with enteropathy (celiac disease) and gluten hypersensitivity without enteropathy.

Current evidence suggests an increasing role of macrophages in inflammation and tumor progression. Most tumors contain an abundant number of macrophages as a major component of their leukocyte infiltrate, which co-exist with tumor cells at the tumor microenvironment. Upon activation with soluble tumor antigens, macrophages release a distinct repertoire of growth factor, cytokines, chemokines and enzymes that inhibit growth of the tumor. However, the anti-tumor immune response induced by macrophages does not always ensue. Tumor cells themselves are capable of down-regulating macrophage phenotype and functions and anti-tumor immune responses in the tumor-bearing host. The present review aims to elucidate the role of macrophages in tumor growth and progression, invasion, metastasis, and angiogenesis at the site of tumor growth. Moreover, the effect of tumor microenvironment on the phenotype and function of macrophages, which are altered due to the continuous exposure of various soluble and non-soluble tumor promoting factors secreted by tumor cells, and implication of macrophages in cancer immunotherapy have been discussed in detail.

Chemokines and their receptors direct cell migration in homeostatic and inflamed conditions, thus they are major players in key events of immune-mediated disorders. Indeed, much evidence indicates a non-redundant role of the chemokine system in several human diseases, ranging from classical immune-mediated pathologies, such as autoimmune and allergic diseases and transplant rejection, to neoplastic and vascular diseases. Increasing emerging evidence suggests the possible role of chemokines as biomarkers for monitoring disease activity, predicting relapses, monitoring surgical and pharmacological therapy and for providing prognostic indications. Several methods are now available for the detection and measurement of chemokines and their receptors in body fluids and tissues. The advantage of these assays is that they may be used in clinical laboratory and are directly applicable for biomedical diagnosis, representing a powerful tool which could dramatically improve screening, diagnosis and monitoring of diseases in the very near future.

Immune reconstitution inflammatory syndrome (IRIS) is a recently described syndrome among human immunodeficiency virus (HIV)-infected patients attributable to the recovery of the immune system during antiretroviral therapy. A growing number of researches on this syndrome have been conducted in recent years, but IRIS in children has not been widely studied. We report the case of a 4.5 month-old, tuberculosis (TB)-HIV co-infected girl who developed IRIS two months after beginning antiretroviral and anti-TB medications. We moreover review the immunopathogenesis of TB-HIV coinfection and IRIS, with particular regard to TB-related IRIS.

Heat Shock Proteins (HSPs) are a large family of highly conserved proteins involved in assisting protein folding and unfolding in the cells. HSPs are expressed constitutively as well as inducibly and, interacting with antigen presenting cells, induce the expression of various cytokines and chemokines as well as the maturation and migration of dendritic cells, thus acting themselves as cytokines. HSP-chaperoned antigenic peptides are also generated within the tumor cells. Such chaperoned peptides are released in the extra cellular medium with an association of HSPs by cell stress, death or tumor cell lyses. HSP-peptide complexes from extra cellular medium are taken up by antigen presenting cells through CD91 receptor and are represented or cross-presented by their MHC class I molecules for specific anti-tumor immune response. In addition, HSPs expressed on the cell surface of tumor cells stimulate αβ T-cells and γδ T-cells as well as natural killer (NK) cells that are first-line defense mechanisms. In this manner, HSPs have the ability to stimulate both arms of the effecter mechanism of the immune system. These unique immunological attributes of HSPs are presently becoming the basis for tumor immunotherapy. Tumor-derived HSP-peptide complexes have been demonstrated to serve as anti-tumor vaccines. To date various approaches of vaccination using HSPs have been developed and tested clinically. These HSP-based vaccine approaches can be combined with hyperthermia and CTLA-4 blockade to enhance their anti-tumor potentiality.

The aim of this study was to determine gingival crevicular fluid (GCF) expressions of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and tartrate-resistant acid phosphatase (TRAP) 5b in the mechanism of orthodontic tooth movement. Nine adolescents requiring canine distalization participated in the study. A canine undergoing distal movement served as the test tooth, and the contra-lateral canine served as the control. The clinical parameters were recorded and GCF samples were collected from the mesial and distal gingival crevices of teeth at baseline, 1 h, 24 h, 7 days, and 28 days following force application. GCF samples were analyzed using ELISA. The data were analyzed using three-way repeated measures analysis of variance. TNF-α and TRAP5b levels in distal and mesial sites of the test teeth were significantly higher than that at both sites of the controls. When compared with baseline values, increase was prominent at 1 h and 24 h. The IL-10 concentration decreased during experimental period at both sites of the control and test teeth. The results demonstrated that orthodontic forces evoke changes in the levels of TNF-α, IL-10, and TRAP5b during the initial stages of force application. The changes in local host response in periodontal tissues may be one of the triggers in regulating alveolar bone resorption during orthodontic tooth movement.

This study was aimed to investigate the protective effects of caffeic acid phenyl esther (CAPE) and Intralipid (IL) against hepatotoxicity and nephrotoxicity caused by acute intoxication of glyphosate (N-phosphonomethyl)glycine) (GI) in rats. Forty-nine Wistar Albino rats were randomly divided into seven groups as: I, Control; II, Intralipid (IL) (18.6 mL/kg, orally); III, CAPE (10 µmol/kg, intraperitoneally); IV, GI (4 mg/kg/day, intraperitoneally); V, GI + IL; VI, GI+CAPE; and VII, GI + IL + CAPE. Total antioxidant status (TAS) and total oxidant status (TOS) levels were measured in serum samples. Tissues were analyzed with hematoxylin and eosin (H&E) staining protocol. Bcl-2, Bax, and caspase-3 were evaluated by immunohistochemical method. The results revealed that, in hepatic tissues, the TAS levels were lower and the TOS levels were higher in the GI group compared to other groups. In renal tissues, the TAS levels were significantly lower in the GI group than in the control, IL, CAPE, and GI + IL + CAPE groups. The TOS levels were significantly higher in the GI group than in the control group. Moreover, histopathological analysis revealed severe hepatotoxicity in the GI group. In the GI + CAPE + IL group, hepatotoxicity recovered significantly. Nephrotoxicity was also observed in the GI group and moderately reduced in the GI + CAPE group. Biochemical results were confirmed by histopathologic examination. The results also revealed that CAPE and IL, due to their antioxidant effects, have a decreasing effect against both hepatotoxicity and nephrotoxicity caused by GI. Therefore, CAPE and IL may function as potential agents for supportive therapy since they decrease organ damage, or may facilitate the therapeutic effects of the routine treatment of patients with GI poisoning.

Exercise-induced asthma (E.I.A) affects 12–16% of the general population and most of the patients affected by extrinsic or intrinsic asthma. Surprisingly, also a high percentage of professional and Olympic athletes are affected, showing that E.I.A. does not impair physical activity, whereas endurance sports bear a higher risk than the others. The mast cell role, late asthmatic responses, diagnosis, therapy, theories and data about immunological parameters in sports are taken into consideration in this review.

Radical oxygen species (ROS) modulate various cellular processes and are involved in physiologic and pathologic conditions, including inflammation. There is growing evidence that supports the existence of an abnormal redox status in some chronic inflammatory skin diseases, including contact dermatitis, atopic dermatitis and psoriasis. This review introduces some general aspects on the role of oxidative stress in cutaneous inflammation, with special emphasis on urticarias, summarizing recent novel findings derived from the study of physical urticarias and chronic idiopathic urticaria.

Immunosuppressants may be applied topically to mucosal surfaces for treating inflammatory diseases, e.g. vulvar lichen planus and Behçet's disease. The efficacy of the treatment is dependent on the potency of the drug and its penetration into the tissue. In this study the in vitro diffusion characteristics of Tacrolimus (Tac) and Cyclosporin A (CsA) across human vaginal mucosa are investigated and compared. Fresh human vaginal mucosa was snap-frozen in liquid nitrogen and stored at −85 °C. Prior to an experiment, the tissue was defrosted to 20°C in PBS buffer, pH 7.4, and placed in the seven flow cells of a flow-through perfusion apparatus. Either tritiated Tac, or CsA, was then pipetted into the donor chamber of the flow cell. Samples from each flow cell were collected every 2 hours (1.5 ml/h) over a 24-hour period. Statistical analyses were carried out using an F-test. CsA and Tac flux values progressively increased throughout the 24-hour period, and steady state was not reached for either drug. The mean estimated flux values (mean at 16, 20 and 24 h) for Tac (599 ± 44 dpm.cm⁻².min⁻¹) were greater than those for CsA (96 ± 5.0 dpm. cm⁻².min⁻¹). Whole curve comparison indicated statistically significant differences (P = 1.77×10⁻¹⁶³). Both drugs diffuse well across vaginal mucosa. However, mean steady state flux values for Tac were approximately 6 times higher than those for CsA, indicating that human vaginal mucosa is less permeable to CsA than to Tac.

It is generally accepted that the mandible (especially in the interforaminal region) has better bone quality than the maxilla, and this fact is probably the reason why several reports are available regarding implants inserted into the mandible. Since no report is available on a new type of implants, a retrospective study was performed. A total of 185 two-piece implants (FMD srl, Rome, Italy) were inserted in mandible, 102 in female and 83 in males. The median age was 58 ± 13 (min-max 25–80 years). Implants replaced 14 incisors, 7 cuspids, 49 premolars and 115 molars. Implant' length was x ≤ 10 mm, 10,30 ≤ x ≤ 12.30, equal to 13 mm and x ≥14 mm in 80, 90,13 and 2 cases, respectively. Implant' diameter was narrower than 3.5 mm, equal to 3.8 mm and wider than 4.0 mm in 25, 17,143 cases, respectively. There were 36,41,106 and 2 Elisir, I-fix, Shiner, and Storm implant types, respectively. One implant was lost, survival rate = 98.15%. Among the studies variables immediate loaded implants on single tooth rehabilitations (p=0.017) have a worse clinical outcome. Then peri-implant bone resorption (i.e. delta IAJ) was used to investigate SCR. Among the remaining 184 implants, 20 fixtures have a crestal bone resorption greater than 1.5 mm (SCR = 89.13). Statistical analysis demonstrated signifiance only for surgeon (p=0.001). In conclusion FMD implants are reliable devices for oral rehabilitation with a very high SCR and SVR.