OD was measured with a microplate reader (detection wavelength: 570 nm; reference wavelength: 630 nm), and the tumouricidal activity was determined. Tumouricidal activity

(%) = [1−(ODexperiment–ODeffector cells)/ODtarget cells] × 100%. Statistical analysis.  Analysis was performed using spss 11.5 statistics software (SPSS inc., Chicago, IL, USA), and data were expressed as mean ± SD. Group comparisons were carried out by t-tests. The significance level was set at the P-value of 0.05. Pearson correlation coefficient was selected for bivariate correlation analysis. Correlations between variables were evaluated using Spearman’s correlation coefficient (rho). Pembrolizumab price Flow cytometry plots of T cells, Th cells, NK cells and B lymphocytes from PBMCs were shown in Fig. 1. There were no marked differences

in the absolute numbers of check details peripheral blood T lymphocytes, NK cells or B lymphocytes among the three groups (P > 0.05 for each). In addition, there were no significant differences in T lymphocyte subsets or CD4+/CD8+ ratios noted among the three groups (Table 1) (P > 0.05 for each). As described in Methods, T lymphocytes were obtained from peripheral blood samples from 10 randomly selected members of each of the three subject groups. MTT assays were used to determine T cell proliferation. The stimulation index (SI) was the highest in group C (5.7 ± 1.9) and the lowest in group A (11.9 ± 2.8), and that in group B was 8.6 ± 2.6. There were significant differences in SI among the three groups (Table 2 and Fig. 2A) (P < 0.05). Bivariate correlation analysis revealed that the decrease in T lymphocyte stimulation index (SI) was age dependent, with a significant decrease in Cytidine deaminase individuals aged above 70 years, compared with the lower-age groups (r = −0.75; P < 0.0001) (Fig. 3A). As also described in Methods, CIK cells were prepared from PBMC samples of 10 randomly selected subjects from each of the three groups. These CIK cells were assessed for their tumouricidal activities. CIK tumouricidal activity was the highest in group C

(67.8 ± 10.1%) and the lowest in group A (43.8 ± 11.7%), and that in group B was 57.4 ± 10.3%. There were significant differences among the three groups (P < 0.05); CIK tumouricidal activity decreased with an increase in subject age (Table 2 and Fig. 2B). Bivariate correlation analysis revealed that the decrease in CIK tumouricidal activity was age dependent, with a significant decrease in individuals aged above 70 years, compared with the lower-age groups (r = −0.59; P < 0.001) (Fig. 3B). Ageing populations will present great challenges in the 21st century, and changes in immune function with increased age are closely related to senescence. In studies of immune-related senescence, various diseases, medical interventions, unhealthy lifestyles and other factors, except for ageing, that can affect immune function should be excluded.

Förster, Hannover, Germany), anti-CD4-APC, anti-CD25-PE (both acquired from Serotec, Oxford, GB), and anti-Foxp3-FITC (eBiosciences, San Diego, USA). DCs were identified by anti-MHC class II-PE, anti CD11c-APC and CD103-FITC (all acquired from BD Biosciences, Heidelberg, Germany). All FACS analyses were performed on a FACSCanto (BD Biosciences). Isotype-matched mAb served as controls. Immunoglobulin (Ig) isotyping was performed using the mouse immunoglobulin isotyping ELISA Kit (BD Biosciences, San Diego, USA). Serum

samples were diluted at a concentration of 1:2000 to achieve optical density Vismodegib in a range of 0.5–1.2. Furthermore, the concentration of OVA-specific Ig in the serum was analyzed in the ELISA. Therefore, the plates were coated with 0.5 μg/mL OVA (Grade VI; Sigma-Aldrich) in PBS overnight at 4°C. After washing, the

plates were blocked and samples were added to a concentration of 1:10 to 1:500 and incubated 120 min at 37°C. After washing, detection Abs (biotinylated anti-IgG1; anti-IgG2a, anti-IgG2b, anti-IgG3, anti-IgA, anti-IgM; BD Biosciences) were added and later detected with horseradish peroxidase (HRP, BD Biosciences), tetramethylbenzidene (TMB, BD Biosciences) and hydrogen peroxide (1:1) as the substrate. The reaction was stopped with 2NH2SO4 (Merck, Darmstadt, Germany). The optical density was analyzed in an ELISA-reader (Bio-TEK Instruments GmbH, Bad Friedrichshall, Germany). Calculations, statistical analysis and graphs were performed on Graphpad Prism 4.0 (Graphpad Software, compound screening assay San Diego, USA). The comments of Astrid Westendorf have been a great help. The authors also wish to thank Melanie Bornemann for excellent technical assistance, Tim Worbs for advice on DTH reaction and Sheila Fryk for correction of the English. The Progesterone work was supported by the Deutsche Forschungsgemeinschaft (SFB621/A10).

The work was supported by the German Research Foundation (SFB621/A10). 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. “
“This unit describes two different protocols for the measurement of tumor cytolysis by macrophages. Traditionally, cytotoxicity assays have relied on the use of radioactive isotopes. In Basic Protocol 1, cytotoxic activity is measured by the release into the culture supernatant of a radioisotope that had been incorporated by the target cell and is released upon cell death. This poses a problem for some cell lines in which spontaneous isotope release occurs in the absence of effector cell cytotoxicity. In Basic Protocol 2, a nonradioactive approach is used to measure cytolysis that relies on the fluorescence staining of tumor cells with cell-death markers.

coli O78. Further experiments are needed to determine the optimal timing and route of inoculation.

Furthermore, it will be necessary to test other serovars and challenge routes to confirm that the protection conferred by AESN1331 is efficacious under field conditions, where various serovars of APEC can infect birds. APEC strains that cause respiratory infection and septicemia have also been implicated in cellulitis; Romidepsin mouse thus, immunization with AESN1331 may reduce condemnation and downgrading of carcasses resulting from APEC. Clearly, an inexpensive and effective vaccine against APEC infection in broilers would have a significant economic impact on the industry. We are grateful to Professor Chihiro Sasakawa, Institute for Medical Science, University of Tokyo, for the gift of E. coli SM10λpir and pCVD442 and for advice regarding suicide vector selection technique; to Dr. Tetsuo Nunoya and Dr. Akira Iwata for reviewing the manuscript;

and to Dr. Kunio Doi for excellent support. We also thank Yuji Kuroyama, Tamotsu Sato, Kouji Toriumi and our staff for technical assistance. None of the authors of this paper has any financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of the paper. BTK inhibitor “
“Antibodies are well known for their role in humoral immunity, and their prominent involvement in the protection afforded by successful vaccines against infections. A less appreciated function

of antibodies is their capacity to dampen the autoimmune responses associated with some inflammatory diseases. Nevertheless, this paradoxical activity of antibodies is used to treat patients with autoimmune disease. Preparations of polyclonal serum IgG, which are obtained from pools of thousands of human blood donors and ifenprodil are called intravenous immunoglobulin (IVIg), are commonly used to treat patients suffering from immunothrombocytopenia. Although of important clinical significance the anti-inflammatory function of polyclonal IgG remains poorly understood. Previous studies have primarily addressed its mode of action in a prophylactic setting. However, IVIg is usually applied therapeutically in the clinic. In a study published in this issue of the European Journal of Immunology, Schwab et al. [Eur. J. Immunol. 2014. 44: 1444–1453] focus specifically on the protective effect of IVIg in a therapeutic setting, in four different mouse models of autoantibody-mediated pathology, in order to better approach the condition in human disease and therapy. This Commentary discusses how their findings have key implications for our understanding, and further deciphering, of the mode of action of this therapy. Antibodies were discovered for their protective roles against microbial infections, and are thought to mediate most of the beneficial effects afforded by licensed vaccines [1].

34,35 In an effort to determine the significance of the species-specific

difference in STAT2, a knock-in mouse was generated in which the C-terminus of murine STAT2 was replaced with the human sequence, resulting in a chimeric mouse/human STAT2 molecule.36 Interferon-α/β treatment of STAT2 knock-in CD4+ T cells led to normal ISGF3 formation and ISG expression. However, IFN-α/β did not promote STAT4 phosphorylation or IFN-γ expression in CD4+ T cells expressing the chimeric STAT2 molecule. Hence, although the C-terminus of human STAT2 was required in human cells to promote efficient STAT4 phosphorylation in response to IFN-α/β, it was not sufficient to restore this pathway in mouse cells. Indeed, recent studies have highlighted the importance of STAT N-terminal domains in coordinating additional contacts with cytokine receptors selleckchem that form the pre-assembled complexes necessary for cytokine-driven STAT activation.6,37,38 Specifically, the STAT4 N-terminus was found to be critical for IFN-α/β-dependent STAT4 activation through specific contacts made with the human,

but not mouse, IFNAR2 subunit.39 These studies have revealed additional levels of complexity of cytokine receptors and their underlying molecular interactions that coordinate STAT activation. Although the biochemical nature of STAT4 tyrosine phosphorylation differed quantitatively between mouse and human, there still remained BTK inhibitor the issue regarding the function of IFN-α/β-dependent STAT4 activation during Th1 commitment. Given the pronounced role of IL-12 signalling through STAT4 to drive Th1 commitment, Branched chain aminotransferase these early studies assumed that any signalling pathway that activated STAT4 would promote Th1 development. Recent studies have challenged this assumption. Virtually all receptors that signal via the JAK/STAT pathway promote STAT tyrosine phosphorylation within minutes following receptor engagement. However, the duration of signalling varies between receptors and among STAT family members. Hilkens and colleagues40

first demonstrated a clear difference in the duration of STAT4 tyrosine phosphorylation between IL-12 and IFN-α/β signalling in human CD4+ T cells, with IL-12 promoting sustained STAT4 activation compared with IFN-α/β signalling. The inability of IFN-α/β to maintain STAT4 activation was correlated with a marked deficit in IFN-α/β-dependent Th1 development. Further kinetic comparisons of IL-12 and IFN-α/β clearly demonstrated that while IL-12 promoted STAT4 phosphorylation up to 24 hr, STAT4 was rapidly dephosphorylated within 6 hr of IFN-α/β stimulation.26 As a result, only cells treated with IL-12 expressed sustained levels of T-bet sufficient for IFN-γ secretion and Th1 commitment.

[13, 14] Similar studies in patients with haematological malignancies and HSCT[15-18] or solid organ transplantation[19, 20] with invasive aspergillosis have demonstrated several prognostic risk factors of mortality, which may assist in the development of treatment intensity algorithms and clinical trials. In our univariate analysis, 12 such variables were found to be significantly different between 4-week survivors and non-survivors; male sex, total bilirubin, thrombocytopenia, LDH, creatinine clearance, acidosis, GvHD, active malignancy,

severe neutropenia, lymphocytopenia, monocytopenia and voriconazole breakthrough infection. Nevertheless, multivariate analysis accounting for severity of underlying disease revealed only baseline severe lymphocytopenia and a high LDH serum level (>655 mg dl−1) buy Lumacaftor as independent predictors of early death. check details Consequently, we identified two different prognostic groups using these variables: patients with a 28-day crude mortality rate of <15% (score ≤22) and

patients with a mortality rate of 75% (score >22). The outcome of mucormycosis depends on several factors, including the site of infection, the immune status of the host and the use of surgery or other adjunctive treatments.[21, 22] Chamilos et al. [7] reported that the initiation of polyene therapy within 5 days after diagnosis of mucormycosis was associated with improvement in survival, compared with initiation of polyene therapy at ≥6 days after diagnosis (83% vs. 49% survival). In the same study,

active malignancy (P = 0.003) and monocytopenia (P = 0.01) at the time of diagnosis of infection were also independently associated with a poor outcome, whereas salvage posaconazole-based therapy (P = 0.01) and neutrophil recovery (P = 0.009) were predictive of a favourable outcome.[7] However, this analysis included patients prior to 2000 when diagnosis and treatment outcomes were considerably worse than the PAK6 current era. Likewise, previous investigators have emphasised the important role of early neutrophil recovery and treatment with high-dose amphotericin B.[23-25] Of interest, a recent prospective study on 20 patients with mucormycosis (with pulmonary and non-pulmonary sites of infection) showed that active malignancy (P = 0.03), neutropenia (P = 0.03) and iron overload (P = 0.03) were significantly associated with 90-day mortality in univariate analysis, whereas no association was found with amphotericin B dose or the use of other antifungal therapy (i.e. echinocandin and posaconazole).[8] Nevertheless, in the current study, only lymphocytopenia and high LDH levels, which probably reflects activity of the underlying malignant disease, were significant risk factors for poor outcome when analysis was adjusted for underlying severity of illness (APACHE II).

Transfer experiments of iNKT cell subsets reveal the pathogenic role of CD4− iNKT cells containing the iNKT17 cell population in the development of diabetes. Reconstitution of immunodeficient

NOD mice with CD4− iNKT cells enhanced the incidence of diabetes after injection of a low dose of BDC2.5 T cells. Similar exacerbation of diabetes incidence was observed this website after reconstitution with the NK1.1− CD4− iNKT cell population, which exhibits a high frequency of iNKT17 cells. However, due to cell number limitations most of our experiments were performed with the whole CD4− iNKT cell population. Treatment with anti-IL-17 antibodies abolished the pathogenic role of CD4− iNKT cells suggesting that iNKT17 cells are the critical players in the exacerbation MLN8237 of diabetes, however, we cannot rule out that other cell types producing IL-17 are also participating.

Unfortunately, we could not directly demonstrate that only iNKT17 cells were involved in the deleterious effect of CD4− iNKT cells since there is presently no specific surface marker to purify this cell population. IFN-γ is also produced by CD4− iNKT cells and this cytokine could also participate in the exacerbation of diabetes; however, no exacerbation was observed after reconstitution with NK1.1+ CD4− iNKT cells producing high amounts of IFN-γ but low levels of IL-17. Of note, CD4− iNKT cells alone do not induce diabetes after transfer into immunodeficient NOD mice (data not shown). Therefore, we can propose that iNKT17 cells enhanced diabetes Calpain incidence through different mechanisms. In vitro data have shown that IL-17 synergizes with other cytokines

such as IFN-γ and IL-1α/β to induce iNOS expression and subsequent NO production in insulinoma cells or in pancreatic islets of NOD mice 42. Similarly in the pancreas, IL-17 produced by iNKT cells could synergize with IFN-γ secreted by BDC2.5 T cells to induce high expression of NO in β-cells resulting in their destruction. A deleterious loop could take place since β-cell death induced by NO would promote self-antigen presentation by DCs to BDC2.5 T cells. This mechanism could explain the higher frequency of BDC2.5 T cells observed in the PLNs and the pancreas of mice transferred with CD4− iNKT cells as compared with mice devoid of iNKT cells. Furthermore, it has been shown that IL-17A and IL-17F can induce CXCL10 chemokine expression in lung epithelial cells 43, 44. Production of CXCL10 by pancreatic β-cells could contribute to the recruitment of auto reactive T cells expressing the CXCR3 chemokine receptor as previously shown in several mouse models of type 1 diabetes (T10) 45, 46. Thus, iNKT17 cells might not be involved in the initiation of the insulitis but rather could participate in the exacerbation of -β-cell death and diabetes onset. Our data reveal a functional dichotomy between CD4+ and CD4− iNKT cell subsets in the control of diabetes development.

Of the seven species that affect the poultry industry, E. maxima is considered as the most immunogenic (56). Early studies therefore concentrated on the E. maxima model and much work was focused on better understanding the basis of immunity and the lifecycle stages that are predominantly involved in immune responses (56–58). In addition, E. maxima was selected as the model species for initial work on development Decitabine clinical trial of a subunit vaccine as its gametocytes are very large in size and relatively easily visualized and purified (59). The induction

of immunity using the E. maxima model was first demonstrated by Rose (56), who showed that a single low dose of E. maxima oocysts could protect chickens against a challenge with high doses of oocysts of the homologous strain, and that one

cycle of infection was enough to stimulate this protective immunity. It was further demonstrated that sera taken 14 days post-infection with E. maxima can give passive protection Nutlin-3 molecular weight to naive chickens against a challenge (57,58). However, it was first thought that the asexual stages of the lifecycle of Eimeria were predominantly responsible for the immune response invoked in chickens. Analysis of convalescent sera taken 14–20 days after an E. maxima infection, which was shown to passively protect naive birds, demonstrated that the early stages of development have a strong immunogenic effect, and the selleck later sexual stages were poorly immunogenic in E. maxima,

E. necatrix and E. tenella (58,60). Kouwenhoven and Kuil (61) also reported that sera taken from chickens infected with E. tenella showed no reaction with sexual stages or first generation schizonts, indicating that gametocytes had poor immunizing capabilities in chickens. Later studies, however, contradicted these earlier findings (62,63). The antigenicity of sexual stages of Eimeria was first demonstrated when a monoclonal antibody to an E. tenella gametocyte antigen was shown to inhibit fertilization in vitro (64). In 1989, Pugatsch et al. (62) developed a method to isolate and purify gametocytes by enzymatic digestion of the infected mucosa with hyaluronidase, followed by size separation. They showed that whole gametocytes were highly antigenic both in the course of an infection and when injected into rabbits/mice. During the same year, convalescent sera from E. maxima immune chickens were found to recognize two immunodominant macrogametocyte antigens of 56 and 82 kDa in size (63). When these two proteins were administered to a variety of hosts in the form of a crude extract, they were found to be highly immunogenic (63). Following this discovery, it was hypothesized that these macrogametocyte antigens may play a role in conferring protective immunity to the host (63).

Regarding Tregs, numerous studies reported decreased levels of Tregs and/or suppressed Treg function in patients with myocarditis or idiopathic cardiomyopathies [25-29]. In the present study, Ferrostatin-1 research buy similar blood levels of Tregs (defined as CD4+CD25+CD127low and expressed as% CD3+ T cells) were observed in patients with iDCM and age-matched patients with stable and chronic ischaemic cardiomyopathy. A novel finding is that iDCM patients with low levels of Tregs (<4%) showed a significant of improvement of systolic LV function after IA therapy, whereas patients with higher levels (≥4%) did not respond to this treatment.

The number of Tregs increased in responders in the observation period and shows

no difference to other groups 6 months after IA. In addition to these results, we found that another subset of helper T cells is influenced by IA + IgG substitution. These Th17 cells play an important role in the induction of autoimmune tissue injury. They are distinct from Th1 or Th2 cells because they do not produce classical Th1 or Th2 cytokines such as IFN-γ or IL-4. There is a functional antagonism between Th17 and Treg cells. Both populations are regulated by variable levels of TGF-ß and IL-6. At a steady-state level or in absence of inflammatory stimuli, TGF-ß Fulvestrant suppresses the generation of T effector cells and induces FoxP3 regulatory T cells and thereby maintain self-tolerance. In state of inflammation, IL-6 suppresses the generation of TGF-ß-induced Treg cells and induces a pro-inflammatory T cell response predominated by Th17 cells [30, 31]. In our study, IA-responding patients had higher levels of Th17 cells compared to non-responders and control patients with ischaemic heart failure. These observations have to be confirmed in larger trials. But this observation may be a first step to characterize a subgroup of patients with iDCM who do best benefit from IA therapy. It is not known Histone demethylase how IA therapy can affect cell-mediated immune responses.

Particularly, it is not known whether non-specific removal of IgG antibodies and/or non-specific ‘immune-modulatory’ effects secondary to plasmapheresis and/or IgG substitution after IA are responsible for this phenomenon. Autoantibody-induced inflammation can be separated into two components, autoantibody production and local inflammatory response. Tregs suppress both components, thereby controlling autoimmune inflammation. Follicular Tregs may suppress follicular T helper cell–mediated antibody production. CD4+CD25+FoxP3+ Tregs have the capacity to control inflammation by suppressing cytokine production in T helper cells. Furthermore Tregs are able to suppress innate cells via IL-10 production. These IL-10 producing cells may also play a pivotal role in regulating Th17 cells [32].

Moreover, lymphocytes upregulate Fas and FasL on their cell surface upon activation, becoming an important source of FasL, and therefore, cell death inducers for nearby cell types expressing Fas, including β cells 13. NOD mice deficient in either

Fas (NOD/lpr) AZD0530 or FasL (NOD/gld) do not develop spontaneous diabetes and NOD/lpr mice are resistant to adoptively transferred diabetes 14, 15. Interestingly, β-cell-specific Fas deficiency impairs spontaneous diabetes onset 16, 17. Moreover, transgenic expression of FasL on β cells exacerbates the diabetic phenotype in NOD mice 14, 18, suggesting that there may be a gradual upregulation of Fas on β cells during the course of islet infiltration prior to diabetes onset, and the early presence of FasL on neighboring β cells might accelerate fratricidal β-cell death. CD4+ T cells are

required to promote insulitis and diabetes in NOD mice 19. All of the above mentioned suggest a scenario in which the reciprocal activation of macrophages and CD4+ T cells, upon receipt of an inflammatory signal in the local pancreatic environment, triggers IL-1β and IFN-γ production by macrophages and Th1 CD4+ T cells respectively. Both cytokines, in turn, upregulate Fas on β cells causing their death as soon as the Fas receptor is engaged by its ligand, FasL. Nonetheless, several reports have questioned the relevance AZD2281 of Fas-induced β-cell death in T1D 20–23. Several of these studies rely on a single CD4+T-cell specificity, which could be masking the overall in vivo scenario, composed of several CD4+T-cell clones and/or effector mechanisms. The overall aim of our study was to understand the role of Fas and CD4+ T lymphocytes in the induction of β-cell death and, hence, autoimmune diabetes.

In the current Clomifene report, we show that the diabetogenic activity of CD4+ T lymphocytes is Fas-dependent, and, moreover, despite the fact that IL-1β can mediate upregulation of Fas on islets, IL-1β is not required to promote diabetes in NOD mice. Fas expression on β cells has been reported to promote β-cell apoptosis and the development of diabetes 14, 16, 17. We aimed to establish the role of Fas and FasL on CD4+ T-cell-mediated β-cell apoptosis in autoimmune diabetes. For that purpose it was necessary to avoid the pleiotropic effects of Fas deficiency in NOD lpr/lpr mice 24, which affects the T- and B-cell repertoire 25. To this end we purified splenic CD4+ T cells from 8–20-wk-old pre-diabetic (not exhibiting glycosuria) female NOD mice (at this age islet-specific CD4+ T cells should be primed since insulitis is already observed in 8-wk-old females 1, 26), and adoptively transferred 15 million of these CD4+ T cells into NOD/SCID female recipients (deficient in both, T and B cells) combining Fas deficiency and FasL deficiency.

, 2000). STs sharing identity at the majority of these loci are grouped into clonal complexes (CCs) encompassing related lineages of MRSA (Enright et al., 2002). Another highly discriminatory approach that can identify genomic rearrangements and insertions/deletions is pulsed-field gel electrophoresis (PFGE) whereby SmaI digested chromosomal DNA is separated

and similarities in banding patterns reflect relatedness among lineages (Bannerman et al., 1995; McDougal et al., 2003). Selleck Y 27632 This allows for the classification of S. aureus strains into the now familiar PFGE types USA100-1200. Employing these epidemiological approaches, researchers appreciated that most MRSA disease worldwide (nearly 70% of reported infections) was caused by five major CCs: CC5, CC8, CC22, CC30, and CC45 (McDougal et al., 2003; Robinson & Enright, 2003) (Fig. 1). CC5 includes clones belonging to the USA100 PFGE type (e.g. SCCmec-II New York/Japan clone), the most common source of US hospital-acquired MRSA as well as USA800 (SCCmec-IV Pediatric clone). CC8 includes the archaic, or original MRSA clones as well as the

related Iberian clone, the SCCmec-III Brazilian/Hungarian clone, and the SCCmec-IV USA500 clones. CC22 includes the EMRSA-15 clones that dominated hospital infections in the UK during the 1990s along with strains from CC30 encompassing EMRSA-16 as well as the USA200 PFGE type. Finally, CC45 consists of clones belonging to USA600 PFGE type (e.g. Berlin Antiinfection Compound Library chemical structure clone) that caused widespread MRSA hospital infections in PtdIns(3,4)P2 northern Europe. In essence, after 30 years of investigation, the scientific community began to understand the population

structure of the MRSA clones responsible for the majority of hospital-acquired disease. The source of high virulence potential inherent to these five CCs was never fully appreciated before everything we knew about MRSA epidemiology changed at the turn of the century. Initially reported in 1993, patients without any contact with healthcare settings contracted invasive MRSA infections in Kimberly Australia, a region in the northern part of Western Australia (Udo et al., 1993). It was later discovered that simultaneously, strains related to these ‘community-acquired’ MRSA (CA-MRSA) clones were causing serious and fatal respiratory infections in Chicago, again in patients without direct contact with hospital environments (Center for Disease Control & Prevention, 1999). Prior to these reports, MRSA infections were exclusively associated with healthcare settings. These new clones belong to CC1 (USA400 PFGE type), a CC unrelated to the five traditional hospital-associated MRSA (HA-MRSA) complexes (Center for Disease Control & Prevention, 1999).