Large 5- to 50-µm-wide deposits (focal type) were found in sCJD-MV2 and sCJD-VV2 subtypes, and occasionally in a few cases of the other studied groups. By contrast, the highest scores for 5- to 50-µm-wide deposits observed in sCJD-MV2 subtype were not associated

with higher neuronal loss. FK506 In addition, these scores were inversely correlated with neuronal counts in the sCJD-VV2 subtype. Conclusions: These results support a putative pathogenic role for small PrPSc deposits common to the various sCJD subtypes. Furthermore, the observation of a lower loss of neurones associated with PrPSc type-2 large deposits is consistent with a possible ‘protective’ role of aggregated deposits in both sCJD-MV2 and sCJD-VV2 subtypes. “
“Malignant transformation or recurrence of intracranial mature teratoma is an extremely rare occurrence, compared to the usual ovarian counterpart. Previously, yolk sac tumor elements have been considered to be selective progenitors of enteric-type adenocarcinoma arising from intracranial germ cell tumors. However, the present case demonstrates the occurrence of enteric-type adenocarcinoma in recurrent intracranial mature cystic Depsipeptide teratoma 12 years after gross total removal,

a case of which has not previously been documented in the literature. The 11.5-cm long, dura mater-based tumor on the right fronto-temporal lobe displaced the brain; however, the patient had no neurologic symptoms or discomfort other than pus-like discharge on the scalp. Microscopic examinations revealed a small focus of adenocarcinoma and dysplastic colonic mucosa in the mature cystic teratoma. No immature elements were seen. The cystic wall was almost denuded and showed an exuberant xanthogranulomatous Non-specific serine/threonine protein kinase reaction with foreign-body type giant cells engulfing keratin materials and cholesterol clefts, suggesting that chronic inflammation due to repeated cyst wall

rupture and the previous resection may contribute to malignant transformation. The adenocarcinoma showed strong immunohistochemical expression of CK20 and p53, but CK7 in patches. The molecular profile of the adenocarcinoma showed a mutation in KRAS and wild-type BRAF, which might be associated with malignant transformation of intracranial mature teratomas. In conclusion, the intracranial mature teratomas should require long-term follow-up, and clinicians, radiologists and pathologists should be aware of the potential for malignant progression of recurrent intracranial mature cystic teratoma despite gross total resection and no neurologic symptoms. “
“We describe herein an autopsied case of multiple system atrophy (MSA) with prolonged clinical course of 18 years, and evaluate the extent of neurodegeneration and glial cytoplasmic inclusions (GCIs) in the entire brain of this rare case.

Comparison of the CD11b activation epitope on peripheral and transmigrated neutrophils was analysed by Wilcoxon matched pairs test. Correlations between IL-8, both endogenous and recombinant, and the expression of CD11b were analysed by Spearman’s rank order analysis. Significant correlations with a regression coefficient (R) ≥0.7

were further analysed. A P < 0.05 was considered significant. The median number of transmigrated cells per skin chamber was 2.14 (1.59–3.96) 106 cells with 82.1 (77.6–84.8) % granulocytes, 13.2 (10.3–16.4) % monocytes and 2.82 (2.37–4.37) % lymphocytes. In the peripheral circulation, the number of leucocytes was 4.85 (3.6–6.1)*109 leucocytes/l with 54.1 (50.5–58.9) % granulocytes, 8.51 (7.61–10.5) % monocytes and 33.3 (30.8–37.9) % lymphocytes. From the original skin blister, analysed for CD11b activation after 14 h of incubation, INCB018424 datasheet the median number of see more extravasated leucocytes was 0.11 (0.04–0.14) million cells per skin blister. The expression of CD11b activation epitope on extravasated neutrophils from the original 14-h blister was 73.2 (18.9–83.4) % and corresponding expression on circulating neutrophils was 1.96 (1.29–2.14) %, P = 0.04. The concentration of IL-8 in serum was 8.5 (1.9–11) pg/ml and in the 14-h blister fluid 338 (194–10,627) pg/ml, P = 0.04. The concentration of soluble mediators in serum and

in the skin chamber fluid was assessed by Milliplex multi-analysis and ELISA and

is presented in Fig. 1. Significantly higher concentrations of soluble markers were detected in the skin chamber fluid compared to that in serum for all markers selleck inhibitor except eotaxin (P < 0.01 for IL-4 and IL-10 and P < 0.001 for the remaining markers). TCC was analysed in chamber fluid, and median concentration was 28 (17–40) AU/ml. Figure 2 demonstrates the correlation between the number of in vivo extravasated neutrophils and the concentration of IL-8 in the chamber fluid at P < 0.05 and R = 0.79. In addition, the number of in vivo extravasated neutrophils also correlated with IL-1β, R = 0.83; IL-6, R = 0.73; IL-7 R = 0.71; and TNF-α, R = 0.71, all at P < 0.05. When the total number of extravasated leucocytes were analysed, the corresponding numbers were IL-8, R = 0.83; IL-1β, R = 0.81; IL-6, R = 0.72; IL-7 R = 0.71 and TNF-α, R = 0.70, also at P < 0.05. Following in vitro transmigration, the mean percentage of neutrophils that migrated towards chamber fluid was 34.2 ± 5.4% and towards cell culturing medium was 1.16 ± 0.55%. The percentage of transmigrated neutrophils correlated with the concentration of IL-8 (R = 0.79), IL-1β (R = 0.77) and TNFα (R = 0.79) at P < 0.05. The expression of CD11b activation epitope was measured following in vitro incubation with serum and skin chamber fluid. Figure 3 displays the expression of CD11b activation epitope following incubation with 50% serum, 50% skin camber fluid or IL-8 at 100 ng/ml.

Because B. parapertussis outcompeted B. pertussis and benefited from its presence in mixed infections, we hypothesized Navitoclax mw that a factor produced by B. pertussis may enhance the virulence of B. parapertussis. A good candidate for this virulence factor is PT, because it is not expressed by B. parapertussis and has been shown to play an important role in the virulence of B. pertussis in this mouse model. We demonstrated previously that the bacterial loads of a PT-deficient strain of B. pertussis (ΔPT) were significantly

higher when present in a mixed infection with wild-type B. pertussis and that an intranasal administration of purified PT up to 2 weeks before inoculation with the ΔPT strain resulted in a significant increase in bacterial infection (Carbonetti et al., 2003). To test the hypothesis that PT enhances B. parapertussis

infection, groups of mice (n=4) were inoculated with 5 × 105 CFU B. pertussis and 5 × 105 CFU B. parapertussis (1 : 1 mix) or 5 × 105 CFU B. parapertussis alone, each inoculum containing either 100 ng PT or an equivalent BMN 673 supplier volume of PBS as a control. Mice were euthanized 7 days postinoculation and the bacterial loads of each pathogen in the respiratory tract were determined. When PT was administered with B. parapertussis alone, a fivefold increase of CFU recovered was observed compared with that recovered from control mice (P=0.04) (Fig. 3a). In the mixed infection, PT addition had no significant effect on the CFU of B. parapertussis (or B. pertussis) recovered (Fig. 3b), which is not surprising because B. pertussis already provides a source of PT during infection. These data support

the conclusion that PT enhances B. parapertussis infection and competition with B. pertussis. Because PT appears to enhance B. parapertussis check details infection of the mouse respiratory tract, we hypothesized that B. parapertussis infection would not be enhanced by coinfection with the PT-deficient strain of B. pertussis (ΔPT). Mice (n=4) were infected with mixed inocula of 5 × 105 CFU of B. parapertussis and 5 × 105 CFU of ΔPT. Two control groups (n=4) were inoculated either with 5 × 105 CFU B. parapertussis or 5 × 105 CFU ΔPT only. Mice were euthanized 7 days postinoculation and the bacterial loads of the two organisms were determined. In the mixed infection, B. parapertussis significantly outcompeted ΔPT, with a mean CI of 188 (P=0.002) (Fig. 4). However, unlike the result observed in mixed infections with wild-type B. pertussis, the recovered CFU of B. parapertussis were not increased by mixed infection with ΔPT, because approximately equal CFU were recovered in mixed and single infections (Fig. 4). These data further support the conclusion that PT enhances B. parapertussis infection during coinfection with wild-type B. pertussis. We found previously that the depletion of resident AM, using intranasally administered CL (Van Rooijen & Sanders, 1994), results in the enhancement of B.

Results: We report that patients with FTLD have a significant increase in synaptophysin and depletion in SNAP-25 proteins compared to both control selleckchem subjects and individuals with AD (P < 0.001). The FTLD up-regulation of synaptophysin is disease specific (P < 0.0001), and is not influenced by age (P = 0.787) or cortical atrophy (P = 0.248). The SNAP-25 depletion is influenced by a number of factors, including family history and histological characteristics of FTLD, APOE genotype, MAPT haplotype and gender. Thus, more profound loss of SNAP-25 occurred in tau-negative FTLD, and was associated with female gender and lack

of family history of FTLD. Presence of APOEε4 allele and MAPT H2 haplotype in FTLD had a significant influence on the expression of synaptic proteins, Selleckchem Decitabine specifically invoking a decrease in SNAP-25. Conclusions: Our results suggest that synaptic expression in FTLD is influenced by a number of genetic factors which need to be taken into account in future neuropathological and biochemical studies dealing with altered neuronal mechanisms of the disease. The selective loss of SNAP-25 in FTLD may be closely related to the core clinical non-cognitive features of the disease. “
“MicroRNAs

(miRNAs) are short regulatory RNAs that negatively regulate protein biosynthesis at the post-transcriptional level and participate in the pathogenesis of different types of human cancers, including glioblastoma. In particular, the levels of miRNA-221 are overexpressed in many cancers and miRNA-221 exerts its functions as an oncogene. Nevertheless, the roles of miRNA-221 in carmustine (BCNU)-resistant glioma cells have not been totally elucidated. In the present study, we explored the effects of miRNA-221 on BCNU-resistant glioma cells and the possible molecular mechanisms

by which miRNA-221 mediated the cell proliferation, survival, apoptosis and BCNU resistance were investigated. We found that miR-221 ADAMTS5 was overexpressed in glioma cells, including BCNU-resistant cells. Moreover, we found that miR-221 regulated cell proliferation and BCNU resistance in glioma cells. Overexpression of miR-221 led to cell survival and BCNU resistance and reduced cell apoptosis induced by BCNU, whereas knockdown of miR-221 inhibited cell proliferation and prompted BCNU sensitivity and cell apoptosis. Further investigation revealed that miR-221 down-regulated PTEN and activated Akt, which resulted in cell survival and BCNU resistance. Overexpression of PTEN lacking 3′UTR or PI3-K/Akt specific inhibitor wortmannin attenuated miR-221-mediated BCNU resistance and prompted cell apoptosis. We propose that miR-221 regulated cell proliferation and BCNU resistance in glioma cells by targeting PI3-K/PTEN/Akt signaling axis. Our findings may provide a new potential therapeutic target for treatment of glioblastoma.

0 mmol/L than for PPG < 8.9 mmol/L (P = 0.002–0.021). Kaplan–Meier survival curves grouped by HbA1c levels showed no correlation between HbA1c and survival during the observational period. No significant difference in mortality hazard selleck products ratios was seen for any HbA1c groups evaluated by Cox proportional hazard

model. Conclusion:  Intensive management of diabetic control at a stringent mean on-study PPG < 10.0 mmol/L will improve the life expectancy in diabetic dialysis patients. However, no range of HbA1c values obtained in this study showed any clear difference in clinical outcomes. "
“Gastrointestinal (GI) symptoms are reported to be common among patients with chronic disorders including end-stage renal disease (ESRD). This questionnaire study assessed the prevalence of GI symptoms among patients undergoing hemodialysis (HD) and to correlate with the presence of diabetes mellitus and psychosomatic symptoms in Asian patients with ESRD. A total of 123 patients (male 47.2%) participated in this study. GI symptoms (upper GI: anorexia, nausea, vomiting, odynophagia, dysphagia, early satiety, heartburn, dyspepsia and lower GI: abdominal bloating, non-epigastrium abdominal pain, bowel habit and bleeding per rectum) and psychosomatic symptoms (anxiety, backache, depression, headache and insomnia) in the previous 12 months were enquired and compared

with age and gender matched controls BMN673 (n = 197). The mean age of patients was 51.8 ± 12.9 years with mean duration of HD of 28 ± 38.2 months. Overall, 70.7% of ESRD patients had experienced any GI symptoms; upper GI, 65% and lower GI, 34.1%, significantly more than controls (P < 0.05). ESRD patients had more anorexia, nausea,

vomiting, dyspepsia, irregular bowel habit and bleeding per rectum (all P < 0.05). Overlap of upper and lower GI symptoms was reported by 34.1%, significantly higher than control (14.2%, P < 0.05). ESRD patients also experienced significantly more anxiety, depressive symptoms and insomnia (all P < 0.05). Among the patients with ESRD, the presence of any psychosomatic symptoms correlated significantly with the presence of any upper or lower GI symptoms and overlapping of Selleck Fludarabine GI symptoms. Such correlations were not seen with diabetes mellitus. Gastrointestinal and psychosomatic symptoms are common among our Asian patients with ESRD undergoing regular HD. The presence of underlying psychosomatic symptoms but not diabetes mellitus correlated significantly with the presence of GI symptoms. “
“Intermedin/adrenomedullin 2 (IMD/ADM2) is a newly discovered peptide closely related to adrenomedullin. We recently reported that IMD/ADM2 gene transfer could significantly reduce renal ischaemia/reperfusion injury. In this study, we evaluated the effect of IMD/ADM2 on cell proliferation and regeneration in a cultured rat renal tubular epithelial cell line (NRK-52E) of hypoxia-reoxygenation (H/R) injury.

9,10 Virtually all cells have the inherent capacity to secrete some level of IFN-α/β in response to certain viral infections. However, professional antigen-presenting cells, GS-1101 in vivo particularly plasmacytoid dendritic cells (pDCs), are a key source of IFN-α/β. Plasmacytoid DCs are a specialized subset of

DCs whose maturation is guided by innate cytokines [interleukin-3 (IL-3), Flt2 ligand, granulocyte–macrophage colony-stimulating factor and IL-4] and signalling through pattern recognition receptors during infections.11,12 These signals promote the secretion of a variety of innate cytokines, notably IL-12, IL-18, and importantly, IFN-α/β.11,13,14 Although these cells are not as efficient at activating CD4+ T cells as monocyte-derived DCs because of their

lower expression of MHC-II, pDCs play a significant role in promoting T helper priming through cytokine secretion.15,16 In this review, we will survey recent advances in delineating the direct from the indirect effects of IFN-α/β in regulating the GSK-3 inhibitor development of T-cell effector responses and its novel role in promoting T-cell memory. Since the discovery of CD4+ T-cell subsets, a major quest in T-cell biology has been to understand the signals that control the differentiation of these subpopulations. One of the first signals identified was found to control T helper type 1 (Th1) differentiation, with IL-12 being the key cytokine governing this pathway.17–19 Binding of IL-12 to its receptor (IL-12R) on CD4+ cells triggers the activation of the JAKs Jak2 and Tyk2,20 leading to the phosphorylation and activation of STAT4.21,22 Phosphorylated STAT4 plays a critical role during Th1 commitment by promoting expression of T-bet,23–26 and recent studies have defined unique roles for both STAT4 and T-bet until in regulating IFN-γ gene expression within committed Th1 cells.27 Finally, IFN-γ enhances both T-bet and IL-12Rβ2 expression, reinforcing IL-12-mediated Th1 commitment.28,29 Hence, in both mice and humans, IL-12 signalling through STAT4 and T-bet was established as a key pathway to IFN-γ production and the Th1 phenotype.

In parallel studies, the role of IFN-α/β in Th1 development was examined with seemingly conflicting results. In mouse, STAT4 activation was not detected in response to IFN-α/β compared with IL-12,22 yet studies with human cells reported just the opposite, suggesting a species difference in IFN-α/β-mediated STAT4 phosphorylation.30–32 However, as new and more specific reagents became available, low levels of phosphorylated STAT4 could be detected in mouse cells in response to IFN-α/β.33 The apparent species difference in STAT4 activation was found to involve STAT2.32 Like the IFNAR, STAT2 is also highly divergent across species, and the mouse sequence harbours a unique minisatellite sequence in the C-terminus that is not found in any other species.

This could, at least in part, explain the PZQ sensitivity of adult cestodes. Although PZQ resistance will most probably never be an issue in the treatment of taeniasis patients, it could become a problem in large scale deworming campaigns against E. multilocularis, E. granulosus and Mesocestoides spp. that have been suggested already for parts learn more of Central Europe and China (25,65,66). Particularly for such projects, genetic information on the cellular targets of PZQ, as available through the genome projects, will be highly valuable in assessing treatment efficacy and the emergence of drug resistance. In sharp contrast to its activity on adult cestodes, PZQ has very limited effects

on metacestode stages (67). The underlying

reason could be that the calcium channel β subunits Akt inhibitor (or other potential PZQ targets) are expressed in an adult-specific manner, and in the currently available transcriptome profiles for E. multilocularis metacestode vesicles, the respective genes are indeed expressed at a marginal level (data not shown). Because of the low efficacy of PZQ treatment, the current drugs of choice in chemotherapy against AE, CE and NCC are BZs that have a high affinity for helminth-specific β-tubulin isoforms, thus inhibiting microtubule polymerization that eventually leads to parasite death. Although prolonged BZ treatment of the intermediate host can be effective in eliminating E. granulosus cysts or T. solium cysticerci (68,69), its activity against E. multilocularis is very limited. In AE, BZ treatment is mostly parasitostatic rather than parasitocidal and, as a consequence, has to be given lifelong Tyrosine-protein kinase BLK (68). Furthermore, in all three types of infection, BZ treatment can be associated with severe side effects that are due

to limited bioavailability of the drug at the site of infection and high structural homology of β-tubulin of parasite and host. Three major β-tubulin isoforms that are expressed by E. multilocularis have already been characterized several years ago and were shown to be highly homologous (>90% amino acid identity) to β-tubulin of humans (40; Table 2). In the E. multilocularis genome assembly, we have identified at least nine β-tubulin encoding loci, although transcriptome profiling clearly shows that the three previously identified isoforms (40) are abundantly expressed in all larval stages, whereas the other six loci are mostly silent or may even represent pseudogenes. Studies on mechanisms of BZ resistance and sensitivity in nematodes previously identified two amino acid residues (Phe200 and Phe167 in BZ-sensitive isoforms) that are particularly important for drug binding to β-tubulin. In BZ-resistant strains of Haemonchus contortus, these residues were frequently exchanged by Tyr or His, leading to diminished BZ binding (70).

[85-88] Other analogues of αGalCer that are able to skew conventional CD4+ T-cell responses more towards either a Th1- or a Th2-like profile will be introduced into clinical studies. In the near selleck kinase inhibitor future, it may be possible to differentially activate or inhibit type I and type II NKT cells for the development of novel immunotherapeutic protocols in the treatment

and prevention of autoimmune diseases. Mechanisms by which NKT cell subsets modulate immunity generally follow events and their interactions with other immune cells after activation by their respective lipid antigens, e.g. αGalCer and sulphatide for type I and type II NKT cell subsets, respectively. As DCs play a crucial role not only in the activation of NKT cells but also may be central to their role in the regulation of immune responses, we will first consider NKT–DC interactions and their control of NKT cell-mediated modulation of

autoimmune disease. The advent of intravital imaging now enables the cell dynamics and function of T-cell–DC interactions to be investigated in vivo. Considerable new information provided by the application of 2P microscopy has been reported about the cellular and molecular dynamics of conventional CD4+ and CD8+ T-cell–DC interactions in vivo.[51, 54] While NKT–DC interactions are also central to the regulation of many immune responses MAPK inhibitor and diseases, less is currently known Carnitine palmitoyltransferase II about the dynamics of movement, recirculation and interaction between NKT cells and DCs in vivo.[51, 54] Some recent observations made using in vivo imaging of NKT–DC interactions are presented in Table 6. A key finding is that bidirectional NKT

cell–DC interactions can elicit and amplify innate and adaptive immune responses. Hence, intravital imaging has identified a central role for NKT cells in the context of other immune cells during various immune responses.[51, 54] This further underscores the importance of learning more about different NKT cell subsets and developing more experimental approaches to track these NKT cell subsets by in vivo imaging. In such studies, it is essential to monitor before and after antigen stimulation: (i) the tracking patterns of type I and type II NKT cells from blood into peripheral tissues (e.g. lymph nodes, spleen, liver), (ii) the differences in the number, time and stability of encounters of these NKT subsets with DCs, (iii) the time and sites of migration of these subsets after DC interaction, and (iv) these various parameters in environments of health (e.g. normal disease-free mouse strains) or disease (e.g. mouse strains that develop different autoimmune diseases, as described below).

Some studies have reported that PI3K inhibition reduces Th2 cytokine production, pulmonary eosinophilia, airway inflammation, and bronchial hyperresponsiveness in a mouse asthma model 48, 49. In addition, PI3K is shown to be involved in HIF-1α activation induced by oxygen-dependent or oxygen-independent pathways 50, 51. Recently, p110δ and p110γ isoforms have sparked a great deal of interest, as there is increasing evidence that click here these isoforms play key roles in immunity 52. We have also demonstrated that OVA-induced HIF-1α

activation is significantly reduced by administration of a PI3K-δ inhibitor and suggested that inhibition of the p110δ signaling pathway has therapeutic potential for allergic airway inflammation 33. Consistent with these observations, in the present study, levels of p-Akt protein and PI3K activity in lung tissues were increased after OVA inhalation. The increased levels of p-Akt and PI3K buy PLX3397 activity were significantly reduced after administration of IC87114, a PI3K-δ inhibitor. Moreover, the increased levels of HIF-1α after OVA inhalation were significantly reduced by IC87114 in primary tracheal epithelial cells isolated from OVA-treated mice. These findings suggest

that PI3K-δ regulates HIF-1α activation therewith inducing VEGF expression in a murine model of allergic airway disease. In summary, we have examined the roles of HIF-1α in allergen-induced airway inflammation and bronchial hyperresponsiveness using an HIF-1α inhibitor,

2ME2, and siRNA targeting HIF-1α and evaluated the role of PI3K-δ signaling in HIF-1α activation in allergic airway disease. The administration of 2ME2 was effective in reversing all pathophysiological symptoms examined. Our data have also revealed that HIF-1α inhibition substantially reduces the increase in VEGF expression as well as the activity of VEGF in lungs, especially in bronchial epithelial cells, of our murine model of allergic selleck products airway disease. In addition, administration of IC87114 reduced the increase in HIF-1α activity in OVA-treated airway epithelial cells. Therefore, one likely mechanism for the roles of HIF-1α in pathobiology of allergen-induced airway inflammation and hyperresponsiveness is induction of vascular leakage via up-regulation of VEGF expression in lungs as well as bronchial epithelium. Thus, these findings provide a crucial molecular mechanism for the potential of HIF-1α inhibition in preventing and/or treating asthma and other airway inflammatory disorders. Female C57BL/6 mice, aged 8–10 wk and free of murine specific pathogens, were obtained from the Orientbio (Seoungnam, Korea) were housed throughout the experiments in a laminar flow cabinet and were maintained on standard laboratory chow ad libitum.

, 2008; Qualls et al., 2010; Murray & Wynn, 2011). Expression

of Arg1 by M2 ABC294640 manufacturer macrophages is required for the suppression of T cell proliferation (Pesce et al., 2009), although the corresponding studies in humans have yet to be performed. Moreover, experiments to test T-cell proliferation regulation by Arg1 in Mtb infection need further investigation. In M1 macrophages that are involved in Mtb infection, Arg1 expression and activity is an important mechanism by which Mtb regulates macrophage function by suppressing NO production (El Kasmi et al., 2008; Qualls et al., 2010). Additional studies are necessary to determine whether Arg1 expression by macrophages in human lungs of patients with TB facilitates or not pathogen survival. In humans, it has been reported that Arg1 is released by polymorphonuclear granulocytes and accumulate extracellularly inducing suppression of T-cell proliferation, cytokine synthesis, and also leads to CD3-chain down-regulation without altering T-cell viability (Munder et al., 2006). Besides regulating NO production, these Arg1-dependent events may also play a role in human Mtb infection. In addition, our results demonstrated that, iNOS is also expressed within macrophages associated with granulomas in human TB

lung samples. Interestingly, the number of Arg1-positive cells was higher than the iNOS-positive cells (Fig. 1h). Coexpression of Arg1 and iNOS in mycobacteria-infected cells has been documented, and indeed, competition Oxymatrine between iNOS and arginase for arginine this website has been suggested to contribute to the outcome of infection, because coexpression of Arg1 and iNOS alters the arginine balance such that NO production cannot be maximal (Modolell et al., 1995; Chang et al., 1998; Mills, 2001). Studies have demonstrated

that the expression of host Arg2 may also be up-regulated in macrophages infected by several intracellular pathogens such as Trypanosoma cruzi, Trypanosoma brucei, and Helicobacter pylori (Das et al., 2010). We have found that Arg2 expression is rarely observed in TB lungs, suggesting that Arg2 is not up-regulated in the Mtb-infected human lungs. Whether Arg2 is up-regulated in other tissues (e.g. lymph nodes and spleen) during TB infection remains to be investigated. Type II pneumocytes are specialized cells responsible for the secretion of surfactants such as SP-A, a lipoprotein complex that reduces the surface tension at the air–liquid interface of the lung, which in turn enables any fluid to be converted into droplets that can be rapidly removed. Type II pneumocytes also possess some phagocytic properties (Bermudez & Goodman, 1996; Sato et al., 2002). Mtb multiplies within human type II cell line in vitro, leading to pro-inflammatory citokyne production, which directly influences macrophage function (Sato et al., 2002).