37 Supplementation of α-tocopherol in an end-stage kidney disease dialysis population reduced the risk of associated cardiovascular disease, decreased oxidative stress and increased erythrocyte anti-oxidants SOD, Gpx and CAT.60 However, in a meta-analysis by Miller and colleagues,61 based on the combination of several studies, an increase in all-cause mortality was found with high-dose vitamin E (≥400 IU/day) in patients with chronic diseases.62 Furthermore, the SELECT trial demonstrated that dietary supplementation with vitamin E significantly increased the risk of prostate cancer among healthy men.63 Future

trials should determine the cause of these risks as well as focus on γ- and δ-tocopherol

supplementation. Although considered more NVP-LDE225 an anti-inflammatory64 than anti-oxidant selleck products treatment, long chain omega(ω)-3 polyunsaturated fatty acids, including docosahexanoic acid and eicosapentanoic acid, have been investigated in a large range of in vitro and in vivo CKD models. They were found to enhance endogenous anti-oxidant defence systems such as γ-glutamyl-cysteinyl ligase and glutathione reductase.65 In models of progressive renal fibrosis, kidney function and structure were improved using eicosapentanoic acid and docosahexanoic acid supplementation, with reduced oxidative stress, inflammation and tubulointerstitial fibrosis.66 Use of ω-3 polyunsaturated fatty acids in human CKD patients is under multicentre trials and the anti-oxidant status of

the patients will, hopefully, be recorded in these trials. N-acetyl cysteine (NAC) is an essential precursor to many endogenous anti-oxidants involved in the decomposition of peroxides. It attenuates oxidative stress from various underlying causes by replenishing intracellular glutathione stores. The limiting precursor to glutathione biosynthesis is L-cysteine. This amino acid is not readily available in the human diet and this was the primary basis for NAC supplementation – to replenish cysteine levels. However, the sulfhydryl-thiol group of L-cysteine is also able to exert direct anti-oxidant effects by scavenging free radicals. The results U0126 mw of NAC supplementation in kidney disease have been variable. NAC pretreatment reduced endothelial dysfunction caused by uremic toxins by reducing ROS-dependent expression of NF-κB.67 NAC reduced kidney MDA levels in a mouse model of diabetic nephropathy.68 The treatment of CKD patients with NAC has been largely disappointing,69 but in end-stage kidney disease patients receiving either haemodialysis or peritoneal dialysis, NAC reduced serum 8-isoprostane and the inflammatory cytokine IL-6.70,71 Allopurinol and its metabolite, oxypurinol, are xanthine oxidoreductase inhibitors that lower serum uric acid levels.

PMQR genes have also been increasingly reported [5, 6]. To date, at least three types of PMQR determinants, namely qnr families, aac(6′)-Ib-cr and quinolone efflux pump (qepA and oqxAB) have been extensively described in E. coli [3, 5, 6]. In particular, qnr genes have been frequently detected among isolates producing ESBLs [6]. Additionally, a close association between aac(6′)-Ib-cr and CTX-M-15, an ESBL that has emerged worldwide, has been reported by many epidemiological studies

[6]. Recent studies in Egypt have reported a high prevalence of CTX-M-15 encoding genes among different E. coli clones in community and hospital settings [7, 8]. The aim of this study was STA-9090 datasheet to investigate the molecular epidemiology and resistance

determinants pattern of cephalosporin resistant E. coli isolates identified from cancer patients in Cairo, Egypt in 2009–2010. A retrospective analysis of E. coli isolates from clinical samples was performed at the National Cancer Institute, Cairo, Egypt, from January 2009 to June 2010. Identification and antimicrobial susceptibility testing of gram-negative isolates had been performed in the microbiology laboratories PLX3397 datasheet of the hospitals of origin by routine methods. Thirty-two of 73 viable isolates (43.8%) were selected after ESBL production screening according to the following MIC breakpoints: cefotaxime, ≥8 mg/L; ceftazidime, ≥2 mg/L and aztreonam, ≥8 mg/L [9]. Duplicate isolates from the same patient with indistinguishable susceptibility patterns were excluded. Basic demographic and clinical data were

obtained from the databases of the microbiology laboratories. Because the study consisted of a retrospective review of routine microbiological data that were analyzed anonymously, approval by the Ethics Committee and informed consent were not required. buy Paclitaxel Minimum inhibitory concentrations of amoxicillin–clavulanic acid, cefotaxime, ceftazidime, imipenem, meropenem, gentamicin and ciprofloxacin of the 32 selected isolates were assessed by E-test (Biomérieux, Marcy l’Etoile, France). Assignment of E. coli phylogenetic groups was performed by the triplex PCR assay described by Clermont et al. [10]. Clonal relationships were established by rep-PCR amplification using the DiversiLab Escherichia fingerprinting kit (BioMérieux) according to the manufacturer’s instructions [11]. Rep-PCR products were detected and sized using microfluidic LabChips placed on an Agilent 2100 bioanalyzer (Agilent Technologies, Diegem, Belgium). DNA fragment patterns were then analyzed by using Pearson correlation coefficient pairwise pattern matching and the UPGMA clustering algorithm. Representative E. coli isolates of the four rep-PCR clusters, unclustered phylogroup D isolates and two additional isolates of special epidemiological interest were characterized by MLS) using the Achtman typing scheme (mlst.ucc.ie/mlst/dbs/Ecoli) according to the protocols published on the website.

CD4+ T cells (lanes 1 and 2) and Jurkat cells (lanes 3 and 4). Silver staining of immunoprecipitates, CD4+ T cells (lane 1) and Jurkat cells (lane 3). Immunoprecipitates analysed by Western blotting using anti-FcγRIIIA/B, lane 2 (CD4+ T cells) and lane 4 (Jurkat cells). At 29 kD a broad band with another band at 35 kD was observed in CD4+ T cells and a single band at 29 kD in Jurkat cells. Fig. S7. Immunoprecipitates obtained using anti-FcγRIIIA/B Proteasome function monoclonal antibodies. Proteins stained using silver (left) and blots stained with Coomassie Brilliant Blue R250. Untreated cells (lane 1), terminal complement complex

(TCC) (lane 2), TCC and immune complexes (ICs) (lane 3) and IC-treated cells (lane 4). Arrow point to a protein migrating at approximately 72 kD (Syk). Fig. S8. Inhibition of aggregated human γ-globulin (AHG) binding to CD4+ T cells by BMN 673 in vivo anti-FcγRIIIA/B monoclonal antibody. 1 × 106 cells treated with AHG-AlexaFluor®488 (5 µg), control cells treated

with isotype antibody (10 µg, left panel) and monoclonal anti-FcγRIIIA/B (10 µg, right panel). “
“Eotaxin-3/CCL26 is an agonist for chemokine receptor 3 (CCR3) and a natural antagonist for CCR1, CCR2 and CCR5. CCL26 expression by non-haematopoietic cells has been well documented; however, no studies to date have demonstrated CCL26 expression by leucocytes. In this study, we investigated the ability of human monocytic cells to produce CCL26 in response to cytokines. We found that interleukin-4 (IL-4) increased the expression of CCL26 messenger RNA (mRNA) and protein in U937 Tobramycin cells, in human monocytes and in human monocyte-derived macrophages. Tumour necrosis factor-α (TNF-α) and interleukin-1β

(IL-1β) alone did not induce CCL26 expression, yet these pro-inflammatory cytokines synergized with IL-4 to increase CCL26 protein expression. Signal transducer and activator of transcription 6 (STAT6) was not affected by costimulation with TNF-α, suggesting that the synergy between IL-4 and TNF-α occurs at a step downstream of STAT6 activation. Co-incubation of interferon-γ (IFN-γ) with IL-4 had no effect on CCL26 protein release. By contrast, pretreatment with IFN-γ decreased total STAT6 protein, blocked IL-4-mediated STAT6 phosphorylation and decreased IL-4-mediated CCL26 mRNA expression and protein release. These data show that IL-4 and pro-inflammatory cytokines such as TNF-α, IL-1β and IFN-γ regulate CCL26 synthesis in human monocytic cells, which may be important in regulating monocyte inflammatory responses. The eotaxin subfamily of CC chemokines consists of eotaxin/CCL11, eotaxin-2/CCL24 and eotaxin-3/CCL26.1–3 Although they only share 34–39% protein homology, all eotaxins activate cells via CC chemokine receptor 3 (CCR3), which is expressed on several different cell types including eosinophils, basophils, dendritic cells, smooth muscle cells, epithelial cells and fibroblasts (reviewed in Ref. 4). CCL11 and CCL24 are expressed by haematopoietic and non-haematopoietic cells.

The new technique was based on a bi-triangulated preparation of the branching-vessel end, HTS assay resulting in a “fish-mouthed” opening. We performed two different types of end-to-side anastomoses in forty pig coronary arteries and produced one elastic,

true-to-scale silicone rubber model of each anastomosis. Then we installed the transparent models in a circulatory experimental setup that simulated the physiological human blood flow. Flow velocity was measured with the one-component Laser-Doppler-Anemometer system, recording flow axial and perpendicular to the model at four defined cross-sections for seven heart cycles in each model. Maximal and minimal axial velocities ranged in the conventional model between 0.269 and −0.122 m/s and in the experimental model between 0.313 and −0.153 m/s. A less disturbed flow velocity distribution was seen in the experimental model distal to the anastomosis. The OES-technique showed superior flow profiles distal to the anastomosis with

minor tendencies of flow separation and represents a new alternative for end-to-side anastomosis. © 2013 Wiley Periodicals, Inc. Microsurgery 34:28–36, 2014. Free flap transfers have reached a high rate of success and represent the gold standard procedure for defect reconstruction at the head and neck.[1] The essential vascular support can be maintained either by end-to-end or end-to-side anastomosis. AZD1208 mouse The superiority of one technique has been an item of debate for decades.[2-4] Both techniques have their special advantages and disadvantages and the usage of either of them should be based upon clinical circumstances and microsurgeon’s experience.[5-7] In the 1970s and early 1980s, the end-to-side anastomosis was proclaimed as the technique of choice, as it was told Teicoplanin to be associated with some advantages in blood

flow.[2, 8-10] The possibility to vary the fashion of creating a “side window” (vesselotomy) of the main vessel, the preparation of the branching vessels’ end and the angle of the branching vessel fed the search for the perfect technique. Following, numerousness variations of the end-to-side technique have been published.[5, 11-13] But rheological changes in the range of the transitional flow, have not been investigated.[14, 15] Flow patterns and hemodynamic forces, especially in branches and curvatures, are able to sustain molecular signalling of pro-inflammatory and proliferative pathways.[16] Since flow separation distal to bifurcations is inter alia strongly dependent on the geometry (physiologically or surgically induced), branch-to-trunk flow rate ratio, pulsatility, elasticity of the vessel wall, and special flow pattern of blood,[17-19] every surgeon dealing with vessels should have basic knowledge of blood flow. Nowadays, microsurgical researcher have access to different simulative models, whether in vivo or in vitro models.

In 2 of the 4 studies, there was

a statistically significant increase in albuminuria of about 50 mg/24 hours compared with controls, at a mean of 14 years post-donation.10,17 In the 2 studies that examined the risk of developing microalbuminuria in a total of 67 donors and 51 controls, there was a 3.9-fold increased relative risk of microalbuminuria with donation.7,17,18 There is only one study that has been published (in abstract form only) that examines the long-term outcomes of living kidney donors with elevated levels of proteinuria prior to donation.12 This study prospectively examined 8 donors who pre-donation had a spot urine albumin to creatinine concentration over 10 mg/mmol and/or a spot urine protein to creatinine ratio over 20 mg/mmol. At 1 year post-donation, there was no significant difference in creatinine, blood pressure and inulin clearance compared Napabucasin mouse with ‘normal’ living kidney donors. Studies to date AZD4547 in healthy donors suggest that there is an increased risk of developing proteinuria following living kidney donation. However, the literature is limited by the lack of appropriate control groups, retrospective nature of most published articles, large loss to follow-up of donors, and small sample sizes. The external validity

of their findings is therefore questionable. There is only one study that examined the outcomes of living kidney donors who had elevated levels of proteinuria pre-donation. This study included a small sample size and had a follow-up of only 1 year. In addition,

PAK6 the controls they used were healthy donors rather than healthy non-donors. The suggestions for clinical care are therefore based on the assumption that a potential donor who has proteinuria prior to donating their kidney is likely to develop an increase in the level of proteinuria at least equal to that seen in healthy donors. We also know that proteinuria is a risk factor for the development of kidney failure in the general population and assume that it represents a similar risk in this patient group. As the degree of pre-donation proteinuria that is a risk factor is unknown, we have limited our recommendations to any abnormal amount of proteinuria but have opted to take the upper limit of normal (i.e. 300 mg/24 hours). INTERNATIONAL GUIDELINES: The Amsterdam Forum on the Care of the Living Kidney Donor (2006): A 24 hour urine protein of >300 mg is a contraindication to donation. Microalbuminuria determination may be a more reliable marker of renal disease, but its value as an international standard of evaluation for kidney donors has not been determined. The Canadian Council for Donation and Transplantation (2006): We recommend . . . to refer to existing guidelines regarding the assessment and eligibility of potential living kidney donors (e.g. Amsterdam Forum). European Renal Association-European Dialysis and Transplant Association (2000): Exclusion criteria of donor proteinuria >300 mg/day.

Dysfunction of very important tissues have been reported during

septic shock, as well as ARDS, ALI and acute kidney injury (AKI), which are characterized by the accumulation of a large number of neutrophils in the lungs [52]. Yildirim et al. showed that sildenafil provided a significant decrease in tissue MDA levels in a sildenafil-treated lung fibrosis group, and they also found that endogenous anti-oxidant glutathione was restored in the sildenafil-treated group [24]; these data support our study. A possible explanation for this finding might be that glutathione was conserved due to a lower level of lipid oxidation. Thus, our results showing the inhibition of tissue lipid peroxidation along with the replenishment of GSH content by sildenafil imply that the compound is beneficial buy Ku-0059436 in maintaining oxidant–anti-oxidant balance. Navitoclax solubility dmso In a clinical study, Starkopf et al. demonstrated

an increase in lipid peroxidation levels and a decrease in serum anti-oxidant capacity induced by sepsis [53]. In septic shock, the levels and activities of SOD and GSH are due to the oppressive production of free radicals [54]. Therefore, taking these established results into account, we decided to offer insight into the possible mechanism that explains the role of oxidative stress in sepsis. The results are shown in our data, and they are in accordance with our hypothesis that sildenafil exerts ameliorating effects by decreasing LPO and MPO activities as markers of lipid peroxidation. Increased concentrations of LPO and MPO are found in rats with sepsis [55–57], and tissue MPO is a marker of lipid peroxidation levels that increase when septic shock is induced by CLP in rats [58]. GSH is an important constituent of intracellular protective mechanisms Alectinib against oxidative stress [59]. Ortoloni et al. showed that plasma GSH was decreased in septic

shock patients [60]. Another study showed that plasma GSH levels were decreased in children with sepsis [61]. Carbonell et al. showed that depletion of liver GSH potentiated the oxidative stress induced by endotoxins in rats, in which plasma lipid peroxide levels were raised [62]. Ritter et al. showed that MDA and plasma superoxide dismutase levels are markers of early mortality in septic rats [63]. Our study showed increased tissue LPO and MPO levels and decreased GSH and SOD after CLP, consistent with the literature [56]. Another important finding of the present study was that sildenafil attenuated the up-regulation of proinflammatory cytokine TNF-α. Increased serum early release of proinflammatory cytokines is important in the pathogenesis of septic shock [64].

In the brains of mBSE-inoculated mice, coarse particulate and coalescing types of immunostaining were recognized in the hippocampus and brainstem habenular nuclei. In the cerebral cortex, characteristic lamellar accumulation of PrPSc was detected. In addition, plaque-like deposits

were frequently present in the thalamus, corpus callosum, periventricular area, and brain stem of mBSE-inoculated mice. Therefore, the pathological features of each strain group (Chandler and 79A, ME7 and Obihiro, mBSE) were easily distinguishable. Mean survival times (days ± SD) of mice inoculated with 10% Chandler and 79A, ME7, Obihiro, and mBSE-infected brain homogenates were 141 ± 4.6 and Sotrastaurin datasheet 138 ± 6.9, 150 ± 4.6, 147 ± 2.7, and 160 ± 3.5 days, respectively. Although no significant differences were observed between Chandler and 79A or between ME7 and Obihiro, significant differences

in survival times (P < 0.001) were found among the three strain groups. mBSE and the four scrapie strains, Chandler, 79A, ME7, and Obihiro, could be easily distinguished by their glycoform ratios (Fig. 4b) because the mBSE PrPSc bands migrated faster than scrapie strains. In both the Chandler and 79A strains, monoglycosylated PrPSc predominated, whereas the ME7 and Obihiro strains showed comparable amounts of di- and monoglycosylated protein. These data suggest that classification of the five strains by biological and biochemical characteristics correlates with that derived from the binding and conversion reactions of each strain. In this study, we demonstrated that the Selleck PF-2341066 addition of reducing agents did not inhibit binding and conversion of MoPrP or cysteine-less mutant PrP, and significantly accelerated conversion driven by mBSE PrPSc. Thus, reducing conditions result in an acceleration of PrPSc-dependent conversion in at least some prion strains, as has previously been shown for Immune system spontaneous conversion (3–7). Hermann and Caughey

reported a contradictory result; they found that addition of DTT decreased conversion by about 90% (9). This may have been due to use of a different recombinant expression system, the origin of the recombinant PrP used as a PrPC source, the prion strains used as PrPSc seed, the preparation method of seed PrPSc, and/or the reaction composition. Acidic conditions and addition of detergents or denaturants efficiently induce spontaneous conversion of α-helix-rich PrPC into PrPSc-like β-sheet-rich PrP (17, 18). Reducing conditions also stimulate conversion of α-helix-rich recombinant PrP into the β-sheet-rich form (3). In our study, denaturing and mildly acidic reducing reaction conditions were used for the binding and cell-free conversion assays. The conditions in the environment within endosomes and lysosomes, thought to be the location of conversion of PrPC into PrPSc (19–22), are believed to be similar.

1 The rate at which this occurs varies among tissues. For example, epithelial cells of the intestine1 and skin2 have a high cell turnover rate and can completely self-renew within days. In contrast, the kidney has a considerably lower cell turnover rate, with proliferative abilities that differ depending on the specialized cell type.3,4 Unlike mammalian kidneys, where the formation of nephrons ceases at birth, cartilaginous fish have the capacity to form new nephrons after birth through de novo nephrogenesis.5 Moreover, Y-27632 following partial nephrectomy, skate fish show proliferation of progenitor cells that results in ongoing kidney

development.6 In contrast, mammalian adult kidneys undergo compensatory hypertrophy following uninephrectomy without the formation of new nephrons. The mammalian kidney, therefore, has a limited capacity to undergo endogenous cellular replacement and tissue remodelling under normal conditions. Nevertheless, in response to acute injury the adult kidney does

have some capacity for repair and remodelling that can ultimately lead to restoration of renal structure and function.7 Acute insults to the kidney such as exposure to toxins, sepsis or ischemia can lead to apoptotic cell death and/or necrosis of the tubular epithelial cells and glomerular podocytes.3,8 The kidney’s repair selleck inhibitor response, consisting of cellular replacement of the injured tubular epithelium, is most likely mediated by surviving epithelial cells that neighbour the sites Aldol condensation of injury.9,10 These epithelial cells dedifferentiate and migrate to injured sites of apoptosis, necrosis and cell detachment, where they subsequently proliferate and redifferentiate into functional tubular epithelial cells.3,11 In a setting of chronic injury, glomerular repair is less impressive. Ongoing damage to glomerular cells results in the progressive loss of nephrons, leading to the

expansion of the interstitium and development of fibrosis. It is currently unclear if the kidney contains resident stem cells,12 although recent reports suggest that progenitor cell population/s originally identified in embryonic kidneys (CD24+CD133+Oct-4+Bmi-1+) exist within the urinary pole of the glomerular parietal epithelium of the Bowman’s capsule.13–15 These cells, expressing CD24, a surface antigen commonly used for the identification of human stem cells,16,17 and CD133, a surface antigen specific for a variety of adult stem cells,18–20 may represent a residual kidney progenitor cell population within the parietal epithelium.9 The CD24+CD133+podocalyxin+ cells localized to the urinary pole of the parietal epithelium may be responsible for podocyte replacement after injury,13,14 a cell type once thought to be post-mitotic and unable to divide. Cellular loss most often leads to the infiltration of bone marrow (BM)-derived inflammatory cells that may contribute to both tissue destruction or repair depending on the extent of injury.

enterica serovar Typhimurium expressing swIL-18 and swIFN-α showed the lowest severity of clinical signs. In particular, learn more the clinical score of piglets co-administered Salmonella vaccine expressing swIL-18 and swIFN-α was lower than that of piglets administered Salmonella vaccine expressing either swIL-18 or swIFN-α, with apparent differences at seven days post-challenge

(Table 1). Cumulative daily weight gain was measured to more precisely quantify the alleviation of clinical signs. Consistently, piglets co-administered S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α displayed a significantly increased weight gain, compared to groups that received S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α (Fig. 4a). However, when changes in body temperature of PrV-infected piglets were monitored, there were no significant differences between the group co-administered with S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α, and the see more group that received S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α (Fig. 4b). Taken together, these results indicate that co-administration

of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α results in the enhanced alleviation of clinical severity caused by PrV infection, compared to individual administration of S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α. To evaluate the effect of orally co-administered S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α on virus shedding from PrV-infected piglets, the amount of PrV in nasal swabs was determined Rucaparib chemical structure daily in all groups by the use of a

conventional plaque assay from 3 to 14 days post-challenge. PrV shedding was detected from 3 days after PrV infection and peaked at 6 days (Fig. 5). Piglets that received S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α had lower peak levels of PrV shedding at 6 days post-inoculation, when compared to piglets that received no treatment and S. enterica serovar Typhimurium harboring pYA3560. Furthermore, piglets orally co-administered with S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α showed significantly reduced PrV shedding at 6 days post-challenge compared to those administered S. enterica serovar Typhimurium expressing either swIL-18 or swIFN-α. In addition, the co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α provided a shortened duration of virus shedding. These results indicate that co-administration of S. enterica serovar Typhimurium expressing swIL-18 and swIFN-α produced enhanced inhibition of virus shedding from PrV-infected piglets. The present study demonstrates that the co-administration of S.

2 and 3), and the difference of secretion of cytokines on T cells (in Figs. 1 and 4). The comparisons were made between different conditions of stimulation. The Wilcoxon paired test was used to compare between EX 527 datasheet different conditions of stimulation on NK cells (in Fig. 1). Differences were considered as statistically significant when p<0.05. We would like to thank Professor Eric Vivier for providing some NK cell reagents, Eloïse Perrot and Florence Orlanducci for their technical help, and also to Dr. Francois Coulier from the Service informatique of the CRCM for the figure artworks. This work was

supported by grants from Institut National de la Santé et de la Recherche Médicale and the Institut National du Cancer (#PL-06026 click here and #INCa/DHOS 2009) (to J. A. Nunès).

N. Messal was supported by fellowships from Bourse Franco-Algérienne and Ligue Nationale contre le Cancer. E. Mamessier was supported by a fellowship from the Association pour la Recherche contre le Cancer. J. Celis Gutierrez was supported by a fellowship from a joined program FUNDAYACUCHO (Bolivarian Republic of Venezuela)/CNOUS (France). M.-L. Thibult was supported by fellowships from the Ministère de l’Enseignement Supérieur et de la Recherche and the Ligue Nationale contre le Cancer. Y. Guillaume was supported by a fellowship from the Institut National du Cancer. Q. Wang was supported by a postdoctoral fellowship from the Fondation Infectiopole Sud. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“Interferon-gamma (IFN-γ) is a pro-inflammatory

cytokine that plays a pivotal role in Interleukin-3 receptor the defense mechanism against Brucella infection. It was hypothesized that the IFN-γ in (+874 A/T in intron 1) TT and +5644 T/A, TT genotypes, which are reportedly associated with high IFN production, are associated with susceptibility to brucellosis in Iranian subjects. Genotyping of these IFN-γ variants by an allele-specific polymerase chain reaction method was performed in 281 subjects, comprising 153 patients with active brucellosis and 128 healthy controls. It was found that the +874 minor allele (A) and homozygote genotype (AA) were significantly more frequently present in brucellosis patients than in controls (OR = 2.588; 95% CI, 1.313–5.104; P = 0.006 for the AA genotype; OR = 1.575; 95% CI, 1.124–2.216; P = 0.010 for the A allele). However, the allelic and genotypic distribution of the IFN-γ polymorphism at position UTR5644 A>T did not differ significantly between patients and controls (P > 0.05).