2a). Previous reports on DS have suggested that limited thymic output would lead to decreased function and immunosenescence in peripheral immune cells.[14] To assess lymphocyte functional capacity in Ts65Dn mice, whole splenocytes were stimulated with immobilized anti-CD3 antibody (at 0.5 or 5 μg/ml) for 48 and 72 hr in vitro. Proliferation of CFSE-labelled splenocytes was measured in TCR+ T cells by flow cytometry (representative flow data shown in Fig. 2b,c) as described in the ‘Materials and methods’. There was a significant decrease in the percentage of TCR+ cells that had undergone

at least one division in cells from Ts65Dn mice compared with euploid Bortezomib cell line controls after 48 hr (Fig. 2d) and 72 hr (Fig. 2e). There was also a significant decrease in the percentage of TCR+ cells that had undergone more than three divisions after 72 hr (Fig. 2f) in cells from Ts65Dn mice. Changes in proliferation were not the result of cell death because the percentage of viable cells was not different between euploid and Ts65Dn cells at both time-points (not shown). Hence, although the proportions

of peripheral immune cells in Ts65Dn mice are relatively unchanged, there are significant defects in the function of peripheral T cells that suggest a senescent phenotype in this mouse model of DS. As a possible mechanism for thymic alterations in Ts65Dn mice, IL-7Rα was assessed because it plays a non-redundant role in thymic development,

promoting proliferation and survival of immature, DN thymocytes.[18] Consistent with our previous observations Opaganib in bone marrow lymphoid progenitors,[6] the percentage of specific thymocyte subsets that were IL-7Rα+ was decreased in the lineage-negative (total DN thymocytes), DN2 and DN3 populations (Fig. 3a). The absolute number Dichloromethane dehalogenase of cells expressing the IL-7Rα chain was significantly decreased in the Lin− and all the DN thymocyte populations (Fig. 3b). Interleukin-7Rα is normally down-regulated in DP thymocytes and re-expressed in positively selected CD4 and CD8 SP thymocytes.[15] In contrast to the data in DN thymocytes, when mature DP and SP thymocytes were analysed neither the percentage of IL-7Rα+ cells (Fig. S1c) nor the number of positive cells (not shown) was decreased. To measure whether changes in IL-7Rα were associated with altered cell proliferation in the thymus, mice were injected with BrdU for 2 days and incorporation was assessed ex vivo. Consistent with those populations having decreased IL-7Rα expression, lower percentages of BrdU+ cells were found in the DN2 and DN3 populations (Fig. 3c), and significantly fewer BrdU+ cells were detected in the DN2, DN3 and DN4 populations of Ts65Dn mice in comparison to euploid mice (Fig. 3d), indicating defects in thymocyte proliferation.

Heat-killed E. faecalis (5×107 CFU/mL) were prepared by heating bacteria at 65°C for 30 min. No viability of the bacteria was confirmed by plating an aliquot of the heat-killed bacteria on TSB agar plates. Murine rCCL2 was purchased from BD Biosciences (San Jose, CA, USA), and mAb

directed against CCL2 was obtained from BioLegend (San Diego, CA, USA). rCCL5, rCCL17 and mAbs directed against these chemokines were purchased from R&D Systems selleck chemicals llc (Minneapolis, MN, USA). Biotin-conjugated anti-CD3, anti-F4/80 and anti-CD19 mAbs were obtained from eBioscience (San Jose, CA, USA). Phosphorothioated CCL2 antisense ODNs (5′-AAGCGTGACAGAGACCTGCATAGTGGTGG-3′) and scrambled ODNs (5′-CCACCACTATGCAGGTCTCTGTCACGCTT-3′) were purchased from Sigma-Genosys (The Woodlands, TX, USA). RPMI-1640 medium supplemented with 10% heat-inactivated FBS, 2 mM L-glutamine, 100 U/mL penicillin and 100 μg/mL streptomycin was utilized for the cultivation of various Mϕ preparations. Thermally injured mice were created according to our previously reported protocol 23–25. This procedure consistently produced a third degree burn on approximately 25% of total body surface area (TBSA) for a 26-g

mouse. Immediately after thermal injury, physiologic saline (1 mL per mouse, i.p.) was administered for fluid resuscitation. Deaths within 5 days of 25% TBSA flame burn were not demonstrated Ensartinib mw after our burn procedure. As controls, mice were anesthetized and shaved but were not exposed to the gas flame. They also received physiologic saline (1 mL per mouse, i.p.). Buprenorphine (2 mg/kg) was given s.c. every 12 h during the postburn period. Sham burn animals also received identical regimens of analgesics (buprenorphine) throughout the study period. Mϕs (F4/80+ cells) were prepared from MLNs of various groups of mice, as previously described 24, 25. F4/80+ cells with

94% or more purity were consistently obtained using this technique. Severely burned mice were subjected to CCL2 antisense ODN gene therapy. Thus, burned mice were treated twice with CCL2 antisense ODNs at 2 and 12 h after burn injury. Based on our Amobarbital preliminary studies, CCL2 antisense ODNs were administered s.c. to burned mice at doses ranging from 0.01 to 100 μg/mouse. Weight loss, reduced appetite and abnormal body temperature were not demonstrated in normal mice treated with 100 μg/mouse of CCL2 antisense ODNs twice a day for 7 days. The effect of the gene therapy was confirmed by measuring CCL2 levels in the sera of these mice 24 h after burn injury, because the maximum level of CCL2 in sera of these mice was reached within 24 h of severe burn injury. CCL2 in serum specimens was assayed by ELISA. To determined the efficacy of CCL2 antisense ODNs on the generation of M2Mϕs, MLN-Mϕs were isolated from severely burned mice treated twice with 10 μg/mouse of CCL2 antisense ODNs (2 and 12 h after burn injury) 1–8 days after burn injury.

However, NK cells also produce several cytokines and their role as mediators in regulating innate and adaptive immune response is a main topic of current research 1–6. Human NK cells find more are defined as CD3−CD56+, whereas murine NK cells, which lack CD56, are discriminated as CD3−NK1.1+. Recently, NKp46 (CD335) has been identified as a common marker for NK cells in both species, simplifying the future definition of NK cells 7. In contrast to other lymphocytes, it is mainly the balance of activating and inhibitory signals, mediated by respective receptors, that regulates NK-cell function 8. Human NK cells express two structurally unrelated MHC class I-specific receptor families, the killer

cell immunoglobulin-like receptors (KIR) and the killer cell lectin-like receptors (KLR). Mouse NK cells lack KIR, but they possess functional homologues with a lectin-like structure (Ly49 receptors). Research over the last two decades has revealed that NK cells do not represent a homogeneous

lymphocyte fraction but can be subdivided into functionally distinct populations 9–13. In humans, the two common NK-cell subsets are defined according to the density of the surface marker CD56. As reviewed in Wilk et al.14, CD56dim NK cells represent the classical cytotoxic NK-cell subset, whereas CD56bright NK cells exert only marginal cytotoxic capacity and produce higher amounts of cytokines such as IFN-γ and TNF-α 14, 15. The predominant function of CD56bright NK cells as cytokine producers indicates a primary role of these Antiinfection Compound Library cells in immune regulation. Recently, a new approach to categorize NK cells by differentiating between “target cell responsive” and “cytokine responsive” has been proposed 16. The proportions of the NK-cell subsets vary between the different compartments of the body. For instance, the ratio of CD56dim and CD56bright NK cells in peripheral blood is inverted in LN (ca. 10:1 in blood versus ca. 1:10 in LN) 12, 17, 18. The particular phenotype of decidual NK cells (CD56superbrightKIR+) Carnitine palmitoyltransferase II also hints to a specialized “equipment” of NK cells in certain locations

18–20. The lack of identical or comparable surface molecules is a major obstacle when transferring information from mouse models to human biology. Several attempts have been made to find markers defining mouse NK-cell subsets equivalent to those in humans. Murine IFN-γ-producing killer DC with a B220+CD11c+NK1.1+ phenotype are suggested to belong to the NK-cell lineage and overlap with human CD56bright NK cells in cytokine production and lymphoid tissue distribution. However, lysis of YAC-1 target cells did not differ from CD11c− NK cells 21. Recent data indicate CD127 as a potential marker for murine thymic NK cells that correspond to the human CD56bright NK-cell subset 22. Currently, CD27 is discussed as a potential NK-cell subset marker for murine as well as for human NK-cell subsets since CD27 is almost exclusively expressed on CD56bright NK cells.

C57BL/6 mice were bred in a pathogen-free environment at the Institute for Animal Experimentation, Tohoku University Graduate School

of Medicine. All mice were used for experiments at 6–8 weeks of age. All experimental protocols described in the present study were approved by the Ethics selleck chemicals llc Review Committee for Animal Experimentation of our university. A serotype 3, clinical strain of S. pneumoniae, designated as URF918, was established from a patient with pneumococcal pneumonia (Kawakami et al., 2003). The bacteria were cultured in Todd–Hewitt broth (Difco, Detroit, MI) at 37 °C in a 5% CO2 incubator, harvested at 6 h, at the midlog phase of growth, and then washed twice in phosphate-buffered Tamoxifen cell line saline (PBS). The inoculum was prepared at 4–6 × 107 CFU mL−1. To induce pulmonary infection, mice were anesthetized by an intraperitoneal injection of 70 mg kg−1 of pentobarbital (Abbott Lab., North Chicago, IL) and restrained on a small board. Live S.

pneumoniae were inoculated at 50 μL per mouse by insertion of a 24-G blunt needle into and parallel to the trachea. In every experiment, a quantification culture was performed to confirm the inoculation dose. Mice were sacrificed before or at various time intervals after infection and samples of BALFs were collected as described below. Briefly, after bleeding under anesthesia with ether, the chest was opened and the trachea was cannulated with the outer sheath of a 22 G intravenous catheter/needle unit (Terumo, Tokyo, Japan), followed by lavage of the lung three times with 1 mL of chilled PBS. The obtained BALFs were centrifuged at 450 g for 5 min. The cell pellets were analyzed for the fractions of leukocytes and the expression of surface antigens and intracellular TNF-α, and the supernatants were kept at −80 °C until measurement of cytokines. Axenfeld syndrome Approximately 1 × 105 BALF cells were centrifuged onto a glass slide at 110 g for 3 min using an Auto Smear CF-12D (Sakura Co., Tokyo), stained by May–Giemsa or Diff-Quick (Sysmex,

Kobe, Japan) and observed under a microscope. The number of leukocyte fractions was estimated by multiplying the total leukocyte number by the proportion of each fraction in 500–1000 cells. The BALF cells were preincubated with anti-FcγRII and III mAb, prepared by a protein G column kit (Kirkegaard & Perry Laboratories, Gaithersburg, MD) from the culture supernatants of hybridoma cells (clone 2.4G2), on ice for 15 min in PBS containing 1% fetal calf serum (FCS) (Cansera, Rexdale, ON, Canada) and 0.1% sodium azide, and stained with phycoerythrin (PE)-conjugated anti-F4/80 or Gr-1 mAb (clone BM8 or RB6-8C5; BD Biosciences, San Jose, CA, or e-Bioscience, San Diego, CA, respectively).

The work of Zhao et al. has suggested that foetal AVB is far more complex than previously appreciated with complex changing rhythms, variable atrioventricular conduction in second-degree AVB,

abnormal QRS waveforms, co-existence of junctional and ventricular ectopy, and atrial and ventricular rate responsivity in complete AVB [29]. They observed the presence of junctional ectopic tachycardia or ventricular tachycardia in nearly one-third of foetuses with complete AVB they had examined, all requiring pacing at birth. Disease progression before birth was reflected in the escape rhythm, which deteriorated to a non-reactive pattern, particularly at rates of <56 beats per minute, often in association with intermittent QRS broadening and/or

tachycardia. selleck Junctional ectopic tachycardia and frequent ventricular ectopy were early predictors of more severe disease. On the basis of their observations, Zhao and colleagues https://www.selleckchem.com/screening/kinase-inhibitor-library.html speculated that ventricular tachycardia, junctional ectopic tachycardia and frequent ectopy may be characteristic of an acute stage of complete AVB and that their prevalence may relate to the severity of the disease during the acute phase. Through the use of magnetocardiography, their findings offer an insight into the dynamic disease process of foetal AVB that may no longer exist later in the disease. Several abnormalities of cardiac

conduction and rhythm have also been observed in the neonate. Prolongation of the QTc occurs in the presence of AVB in 15–22% of patients after birth and this may warrant both pacemaker and beta-blockade therapy [47, 48]. Sodium butyrate Whether prolonged QT interval in AVB represents the extent of myocardial damage analogous to the prolongation seen after myocardial infarction or is a functional phenomenon as suggested by Van Hare et al. [49] remains unclear. In the absence of AVB, transient QT prolongation has been reported in small cohorts of neonates with autoantibody-positive mothers, all resolving within the first year of life and without associated complications typical of other causes of prolonged QTc [50]. This has not been consistently demonstrated by others [51]. Sinus bradycardia has also been observed in neonates both in the presence and in the absence of AVB. Brucato and colleagues observed sinus bradycardia in 4 of 24 neonates within the first 3 days of life, all four of whom had spontaneous resolution by 2 weeks [52]. As is true for long QTc, this has not been confirmed in a larger investigation of Costedoat-Chalumeau et al. [51]. Finally, in the presence of AVB, junctional ectopic tachycardia has been reported in isolated cases and small series of affected neonates. Villain et al.

6). Interestingly, high levels of IL-22 were also detected

in the BGJ398 concentration serum samples of individuals with latent (P = 0·002) and active TB infection (P = 0·003) compared to healthy controls (Fig. 6). IL-1β concentrations in serum of individuals with latent TB infection were increased significantly compared to healthy individuals (P = 0·02). The levels of IL-1β were also higher in individuals with active TB infection but were not statistically significant. Significantly elevated levels of IL-8 were detected in the serum of individuals with latent TB infection only. Mean IL-8 concentrations were significantly higher in latent TB group compared to healthy controls (P < 0·0001). However, the levels of IL-8 were higher but not statistically significant in individuals with active TB infection when compared to healthy individuals (Fig. 6); there was

no difference in the circulating levels of IL-17, IFN-γ (Fig. 6), IL-12p70, IL-2 and TNF-β (data not shown) in serum samples of healthy, latent and active TB subjects. The mean levels of IL-4 in serum of individuals with latent and active TB infection were significantly higher (P = 0·02) than the levels found in healthy subjects (Fig. 6). Levels of IL-5 and IL-10 cytokines were below the detection limit in both antigen-stimulated PBMC culture supernatants as well as in serum samples in all three groups of individuals (data not shown). The present study demonstrates small molecule library screening differential induction of IFN-γ-, IL-17- and IL-22-expressing CD4+ T cells in learn more circulation and following specific stimulation with mycobacterial antigens in TST-negative healthy controls, TST-positive latent and active TB subjects. While the expression of IFN-γ and other cytokines has been analysed in human plasma and PBMC supernatants ex vivo[32,33], the levels of IL-17- and IL-22-expressing CD4+ T cells

and granulocytes in the whole blood of TB patients is not well reported. Herein, we show that the percentage of individuals with active TB expressing IL-17-, IL-22- and IFN-γ-producing CD4+ T cells were decreased significantly compared to the individuals with latent TB infection and healthy controls (Fig. 1). However, such differences were not found in CD8+ T cells (data not shown). The reasons for the decreased IFN-γ-, IL-17- and IL-22-expressing CD4+ T cells in the circulation remain unclear. The differential expression of cytokines in circulation and in affected tissues such as lungs, spleen and lymph nodes have been described in tuberculosis [23,34]. It is possible that antigen-specific IFN-γ-, IL-17- and IL-22-producing CD4+ T cells are recruited to the affected tissues by chemokines released by infected resident macrophages and dendritic cells.

However, this may not indicate the outcomes of AKI in Japan are worse than other counties such as US and AU/NZ. We need to clarify the lowest dose that will not reduce the effects of RRT for AKI. TERADA YOSHIO, OODE KAZU, MATSUMOTO TATSUKI, TANIGUCHI YOSHINORI, HORINO TARO Department of Endocrinology,

Metabolism and Nephrology, Kochi Medical School, Kochi Univesity, Japan Acute kidney injury (AKI) is common in hospitalized patients and is associated with significant morbidity and mortality especially in critically ill condition. Unfortunately, prevention trials of AKI are especially difficult to conduct. Attention Gemcitabine should be given to assessment of volume status and fluid administration because volume depletion is a common and modifiable risk factor for AKI. Prevention or prompt management of complications like fluid overload, hyperkalemia and metabolic acidosis improves outcomes. Immediate initiation of renal replacement therapy is indicated in the presence of life threatening changes in fluid, electrolyte and acid-base balance. Other measures like treating the underlying

cause of AKI, adapting dosage of drugs to renal function, treatment of infections and providing adequate nutrition is important. In the recent Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guideline (2012), the use of diuretics, low-dose dopamine, ANP is not suggested for the treatments of AKI. Diuretics are frequently used in patients selleck at risk of AKI and in the management of these who develop Cisplatin mw AKI. Since fluid overload in one of the major

symptoms of AKI. However, diuretics can also be harmful, by reducing the circulating volume excessively and adding a prerenal insult, worsening established AKI. Therefore, it is essential to evaluate usefulness of diuretics to improve outcome of AKI, not just fluid management. Dopamine was once commonly used for renal protection in the critically ill. However, because of the multiple negative studies, its use has been abandoned by most. Doppler ultrasound study found that dopamine significantly increased renal vascular resistance in AKI patients. The KDIGO guideline recommended not using low-dose dopamine to prevent or treat AKI. Several natriuretic pepetide are in clinical use or in development for treatment of congestive heart failure or renal dysfunction, and could potentially be useful to prevent or treat AKI. However, there have been several negative studies of prophylactic ANP therapy, ANP failed to prevent primary renal transplant dysfunction and ANP prophylaxis also failed prevent contrast-induced AKI. As mentioned above, besides renal replacement therapy, no other supportive measures are available for patients with AKI.

In the reports by Gallina et al., graft overgrowth was observed in all transplanted patients and as early as 4 months after surgery. The latter tissue growth had virtually ceased 9–10 months after transplantation. BMN 673 chemical structure However, the grafts had enlarged aberrantly and were not confined to the surgical target sites. In fact, they encompassed regions of the white matter within the overlying cortex and ventral striatum. Hypermetabolic activity was demonstrated by FDG-PET 6–9 months after surgery but had decreased by 12 months after transplantation. Changes in D1 receptor binding varied between patients,

which correlated with limited improvement, if any [21,52]. One additional MRI report showed large cysts and well-delimited masses in one patient 10 years after transplantation [45]. The very first post-mortem study of a transplanted HD-affected brain was conducted in a patient who died 18 months after transplantation of causes unrelated to the procedure.

This study provided the initial proof of concept that solid foetal striatal grafts could survive in a human HD brain [42,53] (Table 3). In this find more patient, most grafts survived (six out of 10), with three localized in the right putamen, two in the left putamen as well as one in the anterior limb of the internal capsule. The majority of transplants could be identified macroscopically. Using immunohistochemical staining, the grafts exhibited a compartmentalized organization with the formation of striatal patchy areas known as p-zones, as well as areas lacking a striatal phenotype (non p-zones) [54]. Large and medium-sized neurones were predominantly seen in the p-zones of the grafts using typical striatal

markers such as dopamine receptor-related phosphoprotein 32 kDa (DARPP-32), calretinin, acetylcholinesterase (AChE), calbindin, enkephalin and substance P. Interneurones positively stained for choline acetyltransferase (ChAT), NADPH-diaphorase (NADPH-d) and parvalbumin were also detected within p-zones. Non p-zones were largely devoid of these markers but were richer in glial fibrillary acidic protein (GFAP)-positive astrocytes. Human leucocyte antigen-DR (HLA-DR), a marker for PAK6 macrophages and microglia, was rarely found in the transplant but was abundantly expressed in the host brain. There was no perivascular cuffing or T-cell infiltration, as visualized with CD4 and CD8. mHtt inclusions within the grafted tissue were not detected [42]. One additional case from the Freiburg University cohort provided a description of graft status at early time interval following transplantation [22] (Table 3). In that report, the authors confirmed the presence of three putaminal and two caudate grafts per hemisphere. DARPP-32-positive neurones, as visualized by immunohistochemistry, were found within the grafted tissue and were interspersed with calretinin- and somatostatin-positive interneurones.

6). As shown, Listerianeg CD8α+ DCs up- (or down-) regulated the distinct maturation markers with a 1.5- to a 2.5-fold difference between mice that received a protective and a non-protective dose of secA2−Lm. In agreement with our hypothesis, Listeriapos CD8α+ DCs purified from protected animals also exhibited a stronger modulation of their maturation markers (∼two-fold)

than those from non-protected mice. In correlation with this result, cell-surface expression levels of CD86, CD80 and CD40 costimulatory molecules on infected GFP+ CD8α+ cDC KU-57788 manufacturer only but not on the non-infected cDC (CD8α+ or CD8α−) was 2–3 times stronger (Supporting Information Fig. 6). Therefore, in addition to receiving signals from bacteria replicating inside their cytosol, CD8α+ DCs from protected mice integrated additional buy R428 signals – likely from the stronger inflammatory environment – which accounted for

the observed difference of maturation with non-protected mice. We have investigated the ability of the two splenic cDC subsets to induce antibacterial memory CD8+ T cells that can protect against a recall infection. We found that CD8α+ cDCs from primary immunized hosts are the most efficient cDC subtype for transferring long-term, anti-Lm memory CD8+ T-cell-mediated protection to naïve recipient animals. Since both DCs subsets were loaded with saturating amounts of the same antigenic peptide and expressed equivalent cell-surface levels of MHC class I molecules, such features are independent of their capacity to process MHC class AZD9291 datasheet I-associated antigens. Interestingly, CD8α+ cDCs become endowed with these functional features as early as 5 h following the primary immunization and this requires cytosolic signals that are potentiated by extracellular inflammatory signals delivered by bacterial infection of the host. Several

seminal studies established that cDCs are key players to prime naïve antigen-specific CD8+ T cells in vivo 3, 4. While these reports support a critical function for splenic CD8α cDCs in initiating primary CD8+ T-cell responses in vivo 3, 4, 9, 11, 12, 14, 27–30, none of them had addressed the question of their ability to set memory development, i.e. whether – and to which extent – they exhibit the functional capacity to induce antibacterial protective CD8 memory. By showing that splenic CD8α cDCs become rapidly conditioned to induce anti-Lm protective memory CD8+ T cells and are best to provide such effect in vivo, we highlight a novel feature of these cells. In addition, we uncouple this functional property of CD8α+ cDCs from their ability to process the antigens from the bacteria.

burgdorferi genospecies. Therefore, we performed an analysis of the total lipid extracts of a wide spectrum of genospecies of B. burgdorferi sensu lato using thin-layer chromatography as well as Western blot and dot-blot assays. We show that ACGal is present in substantial quantities in all B. burgdorferi genospecies tested. Therefore, this molecule might improve the serological

selleck inhibitor detection of rarely pathogenic genospecies, and may be used as a protective vaccine regardless of the prevailing genospecies. Lyme disease (LD) is a multisystemic, often chronic infectious disease prevalent in Europe, North America, and Asia. In endemic areas, LD reaches an incidence of up to 160 cases per 100 000 (Berglund et al., 1995; Strle, 1999). The clinical manifestations are divided into early and late manifestations: early localized check details disease is characterized by erythema migrans. Disseminated early

disease primarily encompasses neuroborreliosis, lymphocytoma, or myocarditis. Late manifestations predominantly comprise Lyme arthritis, acrodermatitis chronica atrophicans, and rarely late neuroborreliosis (Huppertz et al., 1999). LD diagnosis is based on the clinical signs and serodiagnosis using ELISA and confirmative immunoblots (Wilske et al., 2007). A number of Borrelia burgdorferi sensu lato genospecies are etiologic agents of LD causing early localized as well as early and late stages of disseminated disease: B. burgdorferi sensu stricto,

Borrelia afzelii, and Borrelia garinii. Furthermore, the OspA serotype Unoprostone 4 of B. garinii, which has been associated with LD affecting the skin and CNS (Wilske et al., 1993), was recently delineated as a novel genospecies, Borrelia bavariensis (Margos et al., 2009). To the contrary, Borrelia spielmanii causes the localized stage while disseminated disease caused by this agent has not been reported as yet (Fingerle et al., 2008). Three further genospecies are rarely found in skin biopsies and only in single cases in CSF or cardiac tissue. The pathogenic potential of these genospecies, namely Borrelia bissettii (Fingerle et al., 2008; Rudenko et al., 2008), Borrelia valaisiana (Diza et al., 2004), and Borrelia lusitaniae (Collares-Pereira et al., 2004), remains unclear. Furthermore, eight genospecies of the group have been found only in ticks or in animals, for example Borrelia japonica (Kawabata et al., 1993), and are considered nonpathogenic for humans. We and others have identified 6-O-acylated cholesteryl β-d-galactopyranosides (ACGal) as the major glycolipids in B. burgdorferi sensu stricto, B. afzelii, and B. garinii (Ben-Menachem et al., 2003; Schröder et al., 2003; Stübs et al., 2009). On the other hand, Borrelia hermsii – the causative agent of relapsing fever – contains 6-O-acylated cholesteryl β-d-glucopyranosides (ACGlc) (Stübs et al., 2009).