We retrospectively reviewed medical records of 637 Korean patients

with onychomycosis between December 2000 and December 2006. We examined six clinical factors to evaluate the effects on the CR, DC and RR: age, sex, clinical type, treatment pattern, presence of diabetes mellitus (DM) and the extent of nail involvement. On the view of the clinical nail appearance and potassium hydroxide (KOH) preparation, we designated the CR, DC and RR. In addition, Nutlin-3a chemical structure we examined the differences in the CR, DC and RR in terms of the above-mentioned clinical factors. A total of 207 eligible patients were finally analysed. The CR as a whole was 78.3%, the DC was 31.7 ± 18.4 weeks and the RR was 36.0%. There were significant differences in the CR, DC and RR according to the extent of nail involvement. Age

affects the CR and DC, and DM also affects the DC and RR. We found that the extent of nail involvement, age and DM affect the CR, DC and RR of onychomycosis. “
“The following case report describes a patient with acute liver failure who presented in multiple organ failure and required emergency liver Selleck Ibrutinib transplantation. A complicated postoperative course lead to sepsis which did not respond to conventional anti bacterial therapy. Despite antifungal prophylaxis with an azole invasive candidiasis was diagnosed and the patient was successfully treated with anidulafungin. The difficulties in diagnosis and treatment of invasive fungal infections in this population are highlighted. “
“The production of Secretory Aspartyl Proteases (Sap) is an important virulence factor of Candida albicans. Many studies have shown that a challenge with sub-inhibitory concentrations of antifungals lead species of Candida to the secretion of higher concentrations of Sap. Nevertheless, published studies only reported the secretion of such enzymes by cells growing in planktonic phase, with few mention of biofilms. The present study

evaluated the alterations in the secretion of Sap by C. albicans Silibinin grown in biofilms and exposed to sub-inhibitory concentrations of fluconazole. The MICs for fluconazole of seven clinical strains were determined for planktonic cells. Biofilm and planktonic cells were grown in the presence of ½ MIC, ¼ MIC, and no medication (control). The relative metabolic activity, indirectly related to cell loads, were estimated by the absorbance of reduced XTT and the Sap activity was evaluated by bovine albumin test. It was observed that 72 h-old biofilms under the influence of ½ MIC had fewer cells than ¼ MIC and control. The production of Sap was inversely proportional to the cell content, with higher secretion in ½ MIC, followed by ¼ MIC and control. Biofilms of C. albicans challenged by sub-MICs of fluconazole tend to secrete higher quantities of Sap.

[39] It is reported that cystatin from Nippostrongylus brasiliensis inhibited the processing of OVA protein by lysosomal cysteine proteases from spleen cells of mice. We also observed in a related study that BMDC exposed to rHp-CPI showed a reduced rate of OVA antigen processing (unpublished observation). Inhibition of the activity of these cathepsins by CPI from H. polygyrus may result in reduced expression of MHC-II–antigen complex on the surface of antigen-presenting cells that are unable to competently activate CD4+ T cells and induce immune responses. We have demonstrated in this study that in Selleckchem Metformin the DC and CD4+ T-cell co-culture, the BMDC pre-treated with rHp-CPI exhibited a reduced ability

to activate CD4+ T cells and to induce cytokine production. The recipient mice transferred with the BMDC treated with rHp-CPI before OVA antigen loading produced significantly lower levels of OVA-specific total immunoglobulin

and IgG1 antibody compared with the mice receiving the BMDC that were loaded with OVA antigen alone, indicating that the antigen-presenting function of BMDC was impaired. In summary, the results presented in this study demonstrate that the CPI from H. polygyrus exerts its immunomodulatory effects on multiple stages of BMDC development and molecular events that are important for the function of antigen-presenting cells. The observations made in this study may represent one of the important mechanisms by which the nematode parasites induce immunosuppression in the see more hosts. This work was supported

by a Grant to Z.S. from the National Natural Science Foundation of China (No. 30872370). The authors have no financial conflicts of interest. “
“Citation Pizzonia J, Holmberg J, Orton S, Alvero A, Viteri O, Mclaughlin W, Feke G, Mor G. Multimodality animal rotation imaging system (MARS) for in vivo detection of intraperitoneal tumors. Am J Reprod Immunol 2012; 67: 84–90 Problem  Ovarian cancer stem cells (OCSCs) have been postulated as the potential source of recurrence and chemoresistance. Therefore identification of OvCSC and their complete removal is a pivotal stage for the treatment of ovarian cancer. The objective of the following study was to develop a new in vivo imaging model that allows for the detection and monitoring of Amino acid OCSCs. Method of Study  OCSCs were labeled with X-Sight 761 Nanospheres and injected intra-peritoneally (i.p.) and sub-cutaneously (s.c.) to Athymic nude mice. The Carestream In-Vivo Imaging System FX was used to obtain X-ray and, concurrently, near-infrared fluorescence images. Tumor images in the mouse were observed from different angles by automatic rotation of the mouse. Results  X-Sight 761 Nanospheres labeled almost 100% of the cells. No difference on growth rate was observed between labeled and unlabeled cells. Tumors were observed and monitoring revealed strong signaling up to 21 days.

Caspase activities were tested by their ability to cleave specific substrates. In unstimulated monocytes cultured for 24 or 48 h caspase-9 as well as caspase-3 activity is significantly increased by 9- to 10-fold (caspase-9; Fig. 4A) or 14- to 22-fold (caspase-3; Fig. 4B), as compared

with caspase activity in freshly isolated monocytes. In contrast, activation of both, caspase-9 and –3, is blocked in CXCL4-treated cells. Furthermore, CXCL4-mediated protection from caspase activation is partially reversed in the presence of SKI, indicating that activation of SphK results in an inhibition of caspase activity. Since we have shown previously, that CXCL4-mediated activation of Erk is essential for monocyte survival 3, we included the MEK/Erk ABT-263 solubility dmso inhibitor PD098059 in this study. Comparable to SKI, inhibition of MEK/Erk resulted in partial reversion of the CXCL4-mediated inhibition of caspases (Fig. 4A and B). These results provide evidence, that caspase activity in CXCL4-activated cells is controlled by both, SphK and Erk. As mentioned

above, we have described in a recent report that CXCL4 induces delayed activation of Erk and Erk is absolutely required for monocyte survival 3. Since pretreatment of the cells with SKI also reduces monocyte survival, we were interested whether SphK might also regulate Erk phosphorylation. To this end, isolated monocytes CHIR-99021 mouse were preincubated in the presence or absence of 9 μM SKI, 10 μM PD098059, or solvent DMSO, and subsequently stimulated with CXCL4 (4 μM) for up to 48 h. Activation of Erk was tested by western blot analysis using phospho-Erk specific antibodies. As shown in Fig. 5, CXCL4 induced phosphorylation of Erk and pretreatment of the cells with MEK/Erk inhibitor PD098059 resulted in a strong reduction of Erk phosphorylation in CXCL4-treated cells. A comparable inhibition of Erk phosphorylation is observed in CXCL4-activated monocytes when these

cells were pretreated with SKI. From these data, we have to conclude that activation of Erk Idoxuridine is located downstream of SphK (or of its sphingolipid product S1P) in CXCL4-stimulated monocytes. To examine whether SphK activity can be mimicked by its product S1P, in a next set of experiments we analyzed the effect of exogenous S1P on monocyte survival, ROS production, caspase activation, as well as Erk phosphorylation. As shown in Fig. 6A, in the absence of CXCL4, about 53.9±3.9% of the monocytes developed an apoptotic and 22.2±5.7% a necrotic staining pattern, while CXCL4-treated monocytes were efficiently protected (9.6±4.5% apoptotic and 10.1±7.3% necrotic cells). Treatment of the cells with 50 μM S1P also significantly reduced apoptosis/necrosis rates (36.2±11.2% apoptotic and 11.6±4.

9% among 103 women with acute retention in a mid-sized British city.[35] As we discussed above, depression/anxiety is common in the general population, and approximately one-fourth of patients are supposed to have LUTS. However, in light of these studies, PUD patients who visit a clinic and seek further investigation are much less common. Compared with the severe LUTS of PUD patients, the urodynamic findings were dissociated. For example, in a study by Sakakibara et al. urodynamic findings were normal except for the see more following.[28] The major urodynamic abnormality in the PUD patients with OAB was increased

bladder sensation without detrusor (bladder) overactivity (DO) or low-compliance detrusor, which was noted in 50% of all patients (Table 3). The major urodynamic abnormality in PUD patients with difficulty urinating was underactive/acontractile detrusor, which was noted in 31% of patients. None of the patients had detrusor-sphincter dyssynergia (DSD). Most patients had more obvious mental disorders in addition to LUTS. However, in one patient

(case 12), LUTS was the sole initial presentation; it was considered to be a conversion disorder in the bladder (combined with physical stress incontinence). There were three reasons for this decision: her urinary dysfunction appeared just after a traffic accident, her LUTS was dissociated from urodynamic Cilomilast nmr findings, and other potential causes (including urologic/neurologic causes) were carefully excluded. Dissociation between a patient’s complaint and somatic/laboratory findings is a general feature of somatoform/conversion disorder.[29] Increased bladder sensation is clinically relevant Buspirone HCl to the OAB of patients with PUD or interstitial cystitis[36] as well as in a small proportion of neurologic patients, such as those with diabetic neuropathy.[37]

Despite the relative lack of urodynamic literature concerning psychogenic OAB, Macaulay et al.[38] showed higher incidences of anxiety, depression, and phobia in patients with increased bladder sensation than in those with physical stress incontinence. We still do not know to what extent depression/anxiety might cause urodynamic abnormalities. Previously, the concept of “PUD” included non-situational, long-standing retentions in any environment that might require catheterization for bladder emptying. These “psychogenic” reports have shown almost all types of urodynamic abnormalities, e.g. DO[29, 39, 40] and low-compliance detrusor[29, 41] during bladder filling; and poor flow, large post-void residual, vesicoureteral reflux,[29, 40] underactive/acontractile detrusor,[29, 40] intermittent contraction,[30] and pseudo-DSD[29, 40, 42, 43] during voiding. However, as mentioned above, after carefully excluding organic causes, many PUD patients showed increased bladder sensation during bladder filling or underactive/acontractile detrusor during voiding. Otherwise, none of the patients had DO or DSD.

“
“Macrophages are among the most sensitive H 89 mouse immune cells because of their phagocytic activity and are prone to become dysfunctional

or not able to perform properly if nanoparticle load increases. We have previously reported that zinc oxide nanoparticles (ZNPs) induce inflammatory responses in macrophages that contribute to their death. Recognition of ZNPs by pattern recognition receptors such as toll-like receptors (TLRs) might be a factor in the initiation of these responses in macrophages. Therefore, in this study we explored the role played by TLR6 and mitogen-activated protein kinase (MAPKs) pathways in the inflammatory responses of macrophages during ZNPs exposure. ZNPs-activated macrophages showed enhanced expression of activation and maturation markers (CD1d, MHC-II, CD86 and CD71). Among various TLRs screened, TLR6 emerged as the most potent activator for ZNPs-induced inflammatory responses. Downstream signalling proteins myeloid differentiation 88, interleukin-1 receptor associated kinase and tumour necrosis factor receptor-associated factor were also enhanced. On inhibiting MAPKs pathways individually, the inflammatory responses such as interleukin-1β, interleukin-6, tumour necrosis factor-α, cyclooxygenase-2 and

inducible nitric oxide synthase were suppressed. TLR6 silencing significantly mTOR inhibitor inhibited the pro-inflammatory cytokine levels, reactive nitrogen species generation and inducible nitric oxide synthase expression. Also, inhibition of MAPKs in the absence of TLR6 signalling validated the link between TLR6 and MAPKs in CYTH4 ZNPs-induced inflammatory responses. TLR6 was found to be co-localized with autophagosomes. Macrophages lacking TLR6 inhibited the autophagosome marker protein-microtubule-associated

protein1 light chain 3-isoform II formation and phagocytosis. These results demonstrate that inflammatory responses caused by ZNPs-activated macrophages strongly depend on TLR6-mediated MAPK signalling. “
“We studied the evolution of the G gene in the new genotype ON1 of RSV detected from patients with acute respiratory infection in Japan. Phylogenetic analyses and the evolutionary timescale were obtained by the Bayesian MCMC method. We also analyzed p-distance and positive selection sites. A new genotype ON1 emerged around 2001. The evolution rate was rapid (3.57 × 10−3 substitutions/site per year). The p-distance was short and no positive selection site was found in the present strains. These results suggested that a new genotype ON1 of RSV-A emerged approximately10 years ago and spread to some countries with a high evolution rate. “
“Changes in immune function during the course of systemic lupus erythematosus (SLE) are well characterized. Class-switched antinuclear antibodies are the hallmark of SLE, and T/B-cell interactions are thus critical. However, changes in immune function contributing to disease susceptibility are unknown.

While the aetiology of IBD is not known, it is well established that endogenous bacteria, their components and/or antigenic products have a prevailing role in the initiation mTOR inhibitor and perpetuation of the chronic inflammatory response. Indeed, in these genetically susceptible individuals

there is loss of immune tolerance for commensal faecal bacteria and their antigens and a bacteria-specific mucosal and systemic immune response ensues subsequently [4]. In several animal models it has been demonstrated that genetically susceptible animals remain disease-free in a germ-free (axenic) state, but will develop rapid-onset chronic intestinal inflammation when associated with selleck chemicals normal endogenous microflora [5–7]. We have demonstrated previously that the acquisition of commensal faecal bacteria in pre-weaned neonatal wild-type mice caused a transient release of cytokines, which was important subsequently for the establishment of tolerance to the individual endogenous microflora later in life [8]. Nevertheless, the intestinal immune and injury response and the systemic response to faecal bacteria and antigen exposure to a sterile intestinal lumen of a healthy post-weaned animal with a mature immune

system are not understood clearly. Understanding the natural immune and injury response in the normal and immune competent animal can

be key to understanding the disease state. We thus examined the effects of normal faecal bacteria Aprepitant and antigen exposure on the intestinal mucosal and systemic immune system in wild-type axenic mice. Experiments were performed in two different mouse strains. Axenic Swiss Webster mice were purchased initially from Taconic Farm (Germantown, NY, USA) and were bred at the University of Alberta in specific sterile isolator bubbles. Axenic 129/SvEv mice were purchased from the Gnotobiotic Core Facility at North Carolina State University. The mice in this experiment were used at approximately 15 weeks of age. Results from analyses performed in both mouse strains had identical outcomes. Faecal material was collected from 129/SvEv mice housed under conventional conditions. For each preparation, 20 fresh faecal pellets were mashed into 3 ml of sterile distilled water. Axenic mice were removed from the sterile environment and 100 µl of this faecal slurry was given orally to the mice with a blue tip (Fisherbrand® General Purpose Redi-Tip™; Fisher Scientific, Ontario, Canada). Mice were forced to swallow by blocking their nasal airways temporarily, forcing the mice to gulp. An additional 100 µl was spread over their abdominal skin. Mice were held subsequently under conventional housing conditions.

It is a misconception to state that ‘the TCR holds the secret of self- versus nonself discrimination….. [9]’. The TCR interacting with its ligand/epitope has no way of knowing whether the epitope

is on a S- or NS-antigen. It must be told. Self defined by developmental time is a default concept [10, 11]. A somatically generated random recognitive repertoire can only be sorted into anti-S and anti-NS by a somatic historical process dependent on learning what is the self of the host (individual). Given this, it is obvious Pexidartinib mouse that any theory of the S-NS discrimination by the adaptive system that is based on germline-selected recognitive events can be rejected a priori. Examples of such theories are Janeway’s pathogenicity [12, 13], Matzinger’s danger [14–16], MI-503 Zinkernagel’s localization [17], Cunliffe’s morphostasis [18], Dembic’s integrity [19, 20], Cohen’s cognitive Self [21–25], Tauber’s rejection of the metaphor [26], Anderson’s developmental context

[27], Grossman’s tuning [28], etc. Consequently, while these theories do not confront the problem of the S-NS discrimination, it has been clear that they make major contributions when viewed in the context of Module 3 where germline-selected recognition of pathogenicity, danger, localization, integrity, morphostasis, context, tuning, etc. play relevant roles [5]. Unfortunately, the acceptance of a need for PD184352 (CI-1040) a metamorphosis of these theories of a germline-selected S-NS discrimination into a germline-selected regulation of class has yet to surface (e.g. [29, 30]). If and when it does, we will have the starting point for a meaningful interactive discussion. Rather than treating class regulation as a set of singularities, one pathogen–one model, we will try to step back from the details (as long as they pose no contradictions) and define heuristic general principles. The role of regulation of effector class is to optimize

the destruction and ridding of the pathogen under conditions that minimize the innocent bystander debilitation of the host (i.e. immunopathology as distinct from the autoimmunity associated with Module 2 [5]). The term ‘pathogen’ as used here should be viewed in a broad sense to encompass also any harmful or stressful insult to the cell. To discuss class regulation, it is important to appreciate that the paratopes (TCR/BCR) recognize as ligands, epitopes not antigens. Antigens are isolatable molecular entities that are viewed by the immune system as collections of linked epitopes. Module 2, the purging of anti-S from the repertoire, is mediated epitope-by-epitope. By contrast, Module 3, the regulation of class, is mediated antigen-by-antigen. The term, antigen becomes ill-defined in the context of Module 3.

To analyse further the possible differences in gene expression between learn more psoriasis patients and healthy controls, probe sets from psoriasis patients with negative elicitation reactions as well as healthy individuals, also with a negative elicitation reaction, were selected for further analysis using the t-test and subsequent correction for multiple testing with Bonferroni’s adjustment. Sensitization ratios were lower in both the psoriatic and diabetic groups compared to the healthy subjects group. The sensitization ratio was 26% (3:23) for the psoriatic group, 36% (8:22) for the diabetic group and 65% (15:23) for the

healthy control group (Fig. 1). The logistic regression analysis for a psoriasis patient gave an OR of being sensitized EGFR inhibitor to 0·18 (95% CI: 0·039–0·85), P = 0·031, when adjusted for sex and age. The crude OR of being sensitized for a diabetes type I patient was 0·74 (95% CI: 0·548–1·008), P = 0·056. The percentage increase in dermal thickness, as measured by ultrasound, correlated well with the dose-dependent clinical scores of the visual assessment, and a linear

dose-dependent increase in response to DPCP was seen in all positively sensitized individuals. The overall strength of the elicitation responses of positively sensitized individuals is summarized in Table 1. For sensitized individuals there were no statistically significant differences in strength of elicitation between the groups. The challenge doses used did not show any irritant response in unsensitized individuals. In all five biopsies from subjects with a positive elicitation reaction, including healthy controls and psoriasis patients, a typical histological pattern of allergic contact dermatitis was present. Apart from one single outlier, all five biopsies had a grade 4 infiltration of CD4+, CD8+ and FoxP3+ cells, as demonstrated in Fig. 2. CD4+ cells and FoxP3+ were distributed mainly in the dermis, with only scattered cells in the epidermis. CD8+ cells were also found mainly in the dermis, but with a higher degree of infiltration in the

epidermis. The outlier was a healthy subject tuclazepam with a severe clinical reaction; her biopsies were with grade 4 infiltrations of CD8+ cells, but with very few CD4+ or FoxP3+ cells. The six biopsies from subjects with negative elicitation reactions all showed a histological picture of healthy skin; hence, there were no signs of subclinical reactions. All had a grade 1–2 degree of CD4+ cells, but no CD8+ cells and only a limited number of FoxP3+ cells. No distinction between biopsies from healthy controls and psoriasis patients could be made from the infiltration of T cells in patients with either a positive or negative elicitation reaction. The whole data set and subsets thereof were subjected to PCA. Figure 3 depicts a score plot of the first two principal components of the PCA with DPCP-treated skin biopsies only. The first two dimensions retained 22 and 11% of the variation in the data set, respectively.

Then the mir30 backbone containing the mature miRNA and EGFP were amplified using the primers fwd NotI mir30bb: 5´-attgcggccgcCTAGAAGCTTTATTGCGGT AGTTTATC-3´ and rev mir30bb: 5´-TCGCGGCCGCTTTAC-3´. BMS-777607 research buy The

NotI-mir30bb + mir-EGFP-NotI-PCR-fragment was inserted downstream of the tet-responsive CMVmin promoter of the retroviral vector pSR-LP-TRE cloned and provided by C. Bouquet from our laboratory. This vector allows the expression of the miRNA of interest after binding of a cotransduced reverse transactivator (rtTA) in the presence of doxycycline. For the production of retroviral particles the retroviral packaging cell line PhoenixTM, eco was transfected with 2 μg endotoxin free retroviral vector plasmid mixed with 20 μg LipofectamineTM for 5.5 hours. Supernatant media containing virus particles were harvested 48 hours after transfection; 1 × 105 pre-B cells, stably transduced before with the retroviral plasmid pSR-rtTA-IRES-HISRes, were transduced (1150 g, 3.5 hours, 30°C). Twenty-four hours after transduction the cells were selected depending on the vector by addition of histidinol (1.25 mM; Sigma-Aldrich) or puromycin (1.5 μg/mL; Calbiochem). The establishment of inducible Pax5-expressing or miRNA-expressing pre-B-cell lines has been described [20]. Cell lines overexpressing

Epigenetics inhibitor the miRNA of interest were established under limiting dilution conditions, and the resulting cell lines were tested for their GFP expression in vitro after 24 hours. Cell lines that expressed high GFP were tested in vivo for their migration behavior by transplantation into Rag1−/− hosts. Six- to twelve-week-old Rag1−/− (CD45.2) mice were sublethally γ-irradiated (4Gy) 24 hours before transplantation.

Pre-B cells (5 heptaminol × 106 per host), carrying the overexpression vector of interest, were injected intravenously. GFP+ cells from the BM of doxycycline-fed mice transplanted with miR-221 transduced pre-B cells were sorted 4 weeks after transplantation and differentiated in vitro by addition of αCD40, IL-4, and IL-5 together with doxycycline. After 3 and 4 days of cultivation the cells were analyzed by flow cytometry using anti-CD19 (ID3), MHC class II (TIB120), and IgM (M41) Abs. All Abs used for cell surface stainings were purchased from eBioscience, unless otherwise indicated. Fluorescence tagged Abs: phycoerythrin (PE) conjugated-anti-mouse Flt3 (A2F10), IL-7R (A7R34), CD4 (RM4-5), BST-I (BP-3), CXCR4 (2B11), CD45.1 (A20), CD138 (Syndecan-1, 281-2), Syndecan-4 (KY/8.2), and VLA4 (P/S 2.3, a kind gift of the Deutsches Rheumaforschungszentrum, Berlin, Germany); allophycocyanin conjugated-anti-mouse IgM (M41, a kind gift of Dr. Maria Leptin, Cologne University, Cologne, Germany), CD5 (53-7.3), CD8 (53-6.7) and CD45.1 (A20); PeCy7 conjugated-anti-mouse CD19 (1D3), CD25 (PC 61.

The function of NK cells was also improved as shown by an increase in IFN-γ secretion and cytotoxic activity against an HPV+ cell line. This crosstalk between NK cells and DCs needed CD40 interaction and IL-12p70 secretion, whereas NKG2D was not implicated. Our results provide insight into how VLPs interact with innate immune cells and how NK cells and DCs play a role in the immune response induced by this vaccine agent. “
“Citation Sharma D, Singh A, Trivedi SS, Bhattacharjee J. Role of endothelin and inflammatory cytokines in pre-eclampsia – a pilot north Indian study. Am J Reprod Immunol 2011; 65: 428–432 Problem  Pre-eclampsia is new onset hypertension

during pregnancy with proteinuria. The initiating event in pre-eclampsia is postulated to involve reduced Gefitinib cell line placental perfusion, which leads

to widespread dysfunction of the maternal vascular endothelium. Cytokines also appear to contribute to the development of the pathological condition. The aim of this study was to evaluate the role of cytokines in pre-eclampsia and to study the relationship between endothelin-1 and cytokines with the severity of the disease. Method of study  This cross-sectional study included 300 women with pre-eclampsia and 200 healthy pregnant women. Their blood samples were analyzed for endothelin-1 and inflammatory cytokines. Results  Increased endothelin-1 and cytokines [tumor necrosis factor-α, interleukin-2 (IL-2) and γ-interferon (IFN-γ)] levels were found in pre-eclampsia (P < 0.001). Significant positive correlation was seen between endothelin-1 and cytokine level (IL-2 www.selleckchem.com/products/yap-tead-inhibitor-1-peptide-17.html and IFNγ) in the pre-eclamptic group (P = 0.001). Conclusion  We conclude that pre-eclampsia is associated with increased levels of both endothelin-1 and circulating inflammatory cytokines, which points toward the role of endothelial and inflammatory components. “
“Research on infectious diseases next using animal models has been a successful example of translational research. However, because chronic infections are

still one of the main causes of death and disability in the world, it is expected that a great number of mice will continue to be used to address this subject. Although increasing awareness regarding animal welfare has led to novel recommendations for animal housing enrichment, studies evaluating the impact of these modifications on the immune response to infection are lacking. The present study shows that validated and recommended simple environmental enrichment does not interfere with the immune response to chronic infection with Mycobacterium avium for up to 20 weeks, as assessed by the bacterial load in the spleen and lung, by the number and activation status of the main cell populations of the immune system and the serum concentration of interferon-gamma. Therefore, enrichment can be encouraged without concern regarding comparability of results among laboratories studying this type of chronic infections.