Patients with

selleck HCV infection with and without fibrosis were similar apart from the level of HCV-RNA (Table 1). The group of co-infected patients varied in gender distribution and age compared with HCV-infected patients and healthy controls (P < 0.05) (Table 1). The CD4+ count was as expected significantly lower in patients with HIV co-infection (P < 0.05). The distribution of HCV genotypes was comparable in the three hepatitis groups, and significant associations between genotype, ALT, HCV-RNA and fibrosis were not found (data not shown). According to our definition of fibrosis and cirrhosis, 12 of the 25 HCV-infected patients with a liver stiffness above 8 kPa had a fibroscan defined as cirrhosis. However, no difference in any aspects was found between HCV-infected HCS assay patients with fibrosis and cirrhosis (data not shown). To evaluate chronic immune activation, the frequency of activated T cells (CD38+ HLA-DR+) within the CD4+ as well as the CD8+ compartment were determined. The median frequency of both CD4+- and CD8+-activated T cells were elevated in HIV/HCV co-infected patients (2.2%; 1.4–2.6 and 7.0%; 4.1–9.2, respectively), compared with HCV-infected patients

without fibrosis (1.5%; 1.1–1.9, P = 0.03 and 3.4%; 2.1–8.7, P = 0.03), and healthy controls (1.3%; 1.1–1.7, P = 0.01 and 3.5%; 2.5–4.1, P < 0.001) (Fig. 2). There were no differences in activated CD4+ and CD8+ T cells between the two groups of mono-infected

patients and the healthy controls (Fig. 2). CD4+ Tregs, CD8+ Tregs and Th17 cells were determined to evaluate the composition of pro- and anti-inflammatory GPX6 lymphocyte subsets. Patients with HCV infection with fibrosis (5.0%; 4.5–5.6) as well as without fibrosis (5.6%; 4.2–6.4) had significantly higher frequencies of CD4+ Tregs compared to healthy controls (4.4%; 3.4–4.7, P = 0.03 and P < 0.001, respectively) (Fig. 3A). Furthermore, the HIV/HCV co-infected patients appeared with even higher frequencies of CD4+ Tregs (6.5%; 6.0–7.0) compared with HCV-infected patients without fibrosis (P = 0.01) and to healthy controls (P < 0.001). To further describe the composition of CD4+ Tregs, three CD4+ Tregs subpopulations were determined based on co-expression of CD45RA and Foxp3 (Fig. 1). HCV-infected patients with fibrosis and HCV infected without fibrosis as well as HIV/HCV co-infected patients had significantly lower frequencies of resting Tregs compared with healthy controls (P < 0.001, P = 0.001 and P = 0.005, respectively) (Fig. 4A). No difference was observed between the three groups of patients. In contrast, the frequency of activated Tregs was higher in both HCV-infected patients and HIV/HCV co-infected patients compared with healthy controls, although, significant difference was only observed when comparing HCV-infected patients without fibrosis and healthy controls (P = 0.022) (Fig. 4B).

8). This assay revealed a 2.5- to 4-fold reduction of the amounts of detectable mature miR-221 in specific antagomir-treated cells,

compared with that of cells treated with unspecific scrambled antagomir. In two separate experiments, transplanted mice were analyzed 1 week after transplantation for the presence of donor-derived CD45.1+ cells that had migrated to BM. Antagomir-221 pretreated cells migrated half to one-third as efficiently to the BM as cells treated with scrambled antagomir (Fig. 5). These experiments indicate that miR-221 overexpression, and not the overexpression of another genetic locus near the retroviral insertion site, controls migration of early B lineage cells to, and residence CH5424802 of early B lineage cells in BM. In order to search for possible targets of miR-221 regulation involved in the observed change of migration and residence of pre-B-I cells we subjected total RNA of miR-221-transduced pre-B-I cells

to microarray analyses before, and 8 and 24 hours after miR-221 induction by doxycycline in vitro. At 8 and 24 hours, mRNA of 425 and 360 genes, respectively, were found down-regulated at least 1.15-fold (Fig. 6A). Of these genes, 62 were found BVD-523 research buy downregulated at both times after miR-221-induction. By a target scan with miRecords, including all target prediction databases, 25 genes were found to be miR-221 targets (Supporting Information Table 1). The validated miR-221 targets c-kit, PTEN, Trail, ICAM-1, estrogen receptor, and p27Kip1, were found not to be downregulated at the RNA-expression level in pre-B-I cells. The mean signals for syndecan-4 and Gpbp1 for each timepoint (0, 8, 24 hours) are shown as examples of the downregulation on mRNA levels (Fig. 6B). The target analyses were extended for a limited number of surface-bound proteins known to be upregulated at the transition from Pax5−/− multipotent CLP-like pro-/pre-B cells MycoClean Mycoplasma Removal Kit to Pax5+/+ pre-B-I cells, for which

specific monoclonal Abs were available for flow cytometry analyses. Pax5+/+ miR-221 transgenic or empty vector control cells were cultured for 3 days in the presence or absence of doxycycline. Surface expression of syndecan-1, CD44, CD49d (integrin α4), VLA-4 (integrin α4β1), BILL-cadherin, CXCR4, and BST-1 were unchanged. Only syndecan-4 surface expression was downregulated by 25% after 72 hours of incubation (data not shown). In conclusion, our microarray and FACS analyses have not detected a direct target for miR-221 regulation of expression on RNA and protein levels, with syndecan-4 as the only possible, potential target. Our miRNA expression analyses have detected miR-221 and miR-222 upregulated in the earliest, infrequent pHSCs and multipotent CLP-like pro-/pre-B hematopoietic progenitors, that could have been missed in an earlier analysis done by another laboratory [7].

Results:  We observed that S1P stimulates migration of HDMECs concomitant with upregulation of CTGF/CCN2 expression. Furthermore, the blockade of endogenous CTGF/CCN2 via siRNA abrogated S1P-induced HDMEC migration and capillary-like tube formation. Full-length CTGF induced cell migration and capillary-like tube formation with a potency similar to that of S1P, while C-terminal

domain of CTGF was slightly less effective. However, N-terminal domain had only a residual activity in inducing capillary-like tube formation. Conclusions:  This study revealed that CTGF/CCN2 is required for the S1P-induced endothelial cell migration, which suggests that CTGF/CCN2 may be an important mediator of S1P-induced physiological and pathological angiogenesis. Moreover, this study shows that the pro-migratory activity of CTGF/CCN2 is located in the C-terminal domain. “
“Please cite this paper as: Ritter, check details Davidson, Henry, Davis-Gorman, Morrison, Frye, Cohen, Chandler, McDonagh and Funk (2011). Exaggerated Neutrophil-Mediated Reperfusion Injury after Ischemic Stroke in a Rodent Model of Type 2 Diabetes. Microcirculation 18(7), learn more 552–561. Objective:  We tested the hypothesis that both chronic and acute inflammatory

processes contribute to worse reperfusion injury and stroke outcome in an experimental model of T2DM. Materials and Methods:  Twelve- to thirteen-week-old male Zucker Diabetic Fatty (ZDF) rats vs. Zucker Lean Controls (ZLC) rats were tested at baseline and after middle cerebral artery occlusion PAK6 (ischemia) and reperfusion

(I–R). Neutrophil adhesion to the cerebral microcirculation, neutrophil expression of CD11b, infarction size, edema, neurologic function, sICAM, and cerebral expression of neutrophil–endothelial inflammatory genes were measured. Results:  At baseline, CD11b and sICAM were significantly increased in ZDF vs. ZLC animals (p < 0.05). After I–R, significantly more neutrophil adhesion and cell aggregates were observed in ZDF vs. ZLC (p < 0.05); infarction size, edema, and neurologic function were significantly worse in ZDF vs. ZLC (p < 0.05). CD11b and sICAM-1 remained significantly increased in ZDFs (p < 0.05), and cerebral expression of IL-1β, GRO/KC, E-selectin, and sICAM were significantly induced in ZDF, but not ZLC groups (p < 0.05) after 2.5 hours of reperfusion. Conclusion:  Both sides of the neutrophil–endothelial interface appear to be primed prior to I–R, and remain significantly more activated during I–R in an experimental model of T2DM. Consequently, reperfusion injury appears to play a significant role in poor stroke outcome in T2DM. "
“Please cite this paper as: Shi VY, Bao L, Chan LS. Inflammation-driven dermal lymphangiogenesis in atopic dermatitis is associated with CD11b+ macrophage recruitment and VEGF-C up-regulation in the IL-4-transgenic mouse model. Microcirculation 19: 567–579, 2012.

[1] In a study from our centre, 9% of all mucormycosis cases were found to be nosocomial in origin. These patients acquired infection either at the site of the ECG leads or the adhesive tapes, or from contaminated intramuscular injections, signaling pathway or from air in the hospital environment.[4] The risk factors for mucormycosis differ significantly amongst the developed and developing world.[1, 7] While haematological

malignancies and transplants are designated as the key risk factors for mucormycosis in developed nations, the disease is majorly associated with uncontrolled diabetes with or without ketoacidosis in developing countries including India.[1, 7] Nearly 24–64% of the mucormycosis cases reported from India are in patients with uncontrolled diabetes, with or without ketoacidosis.[4-6, 21] Although other risk factors have also been implicated, Temsirolimus the overwhelming number of mucormycosis cases with uncontrolled diabetes overshadows their role.[1, 7] This is possibly linked to a large diabetic population in such countries, as discussed previously.[1] Unless complication develops, these patients avoid seeking medical attention.[3] In India, a considerable number (16–23%) of diabetics remain undiagnosed of their underlying disease before presentation of mucormycosis; mucormycosis, in fact, acted as diabetes-defining illness in those

cases.[4, 5] The mean informed duration of diabetes was found to be 6.7 ± 4.6 years before acquiring mucormycosis.[16] Amongst the diabetic patients, poorly controlled type II diabetes is the most common risk factor for mucormycosis, being involved in nearly 44–88% of the cases mainly from north to south India, with nearly

half of them exhibiting ketoacidosis.[4-6, 10, 21] Type I diabetes (10–15%) and secondary diabetes have also been detected in some patients.[5, 28, 29] In contrast, diabetes was the risk factor in only 36% of Erastin nmr the global series of 929 cases,[24] 17% of the Trans-European series,[25] 16% of France series,[30] 6% of Belgium series[31] and 18% of Italy series.[23] It should be noted, however, that as confounding factors, renal failure and alcoholism related chronic liver disease have also been detected in patients along with diabetes in India.[4] Several factors relate the unique predisposition of diabetic patients to mucormycosis. Firstly, diabetes and ketoacidosis render the phagocytic cells dysfunctional. Both neutrophils and macrophages exhibit an impaired chemotaxis and defective killing by both oxidative and non-oxidative pathways under such conditions, although the precise mechanisms mediating these remain to be elucidated.[32-34] Secondly, patients with diabetic ketoacidosis have an acidic serum pH with elevated levels of free iron, which is a major nutrient element governing susceptibility to Mucorales.

First, we established a correlation between LPS treatment and Foxp3+ cell numbers. Next we showed that CD25+CD4+ T cells are enriched in CD103-expressing cells, a marker associated with enhanced regulatory function [52, 53] and preferential homing to inflammatory sites including the pancreas [57]. Moreover, we revealed that Foxp3+ BVD-523 purchase cells within the CD25+CD4+ T cell subset display enhanced levels of Foxp3 expression, a phenotype also associated with enhanced suppressor function [58–60]. We also ascertained

that the frequency of CD25+ cells among the CD4− cell subset remained unchanged by LPS treatment (Fig. S8). Finally, other publications support our claim that LPS treatment protects from disease through the action of Treg. Hence, LPS administration prevents experimental autoimmune encephomyelitis by enhancing

Treg effector function [61]. More importantly for the scope of this study, CD28−/− NOD mice that present a severe Treg defect [19] are refractory to the protective effect of LPS treatment [39]. This latter finding strongly supports Pritelivir concentration our conclusions that Treg are involved in the mechanism of protection afforded by LPS. Several studies have placed Treg in the aetiology of diabetes in NOD mice. Impaired Treg function is detectable in aged animals [4–7], and adoptive transfer of Treg isolated from young animals protects adults from diabetes [2, 19]. Moreover, both Foxp3+CD4+ (-)-p-Bromotetramisole Oxalate and CD103+CD4+CD25+ cells were shown to be significantly decreased and to correlate with autoimmune disease predisposition in NOD as well as in other autoimmune-prone strains of mice [3]. Hence, therapeutic strategies aiming at expanding Treg and/or enhancing their regulatory activity or, on the other hand, at preventing the decay of their effector activity, are expected

to protect NOD mice from diabetes. We previously reported that mouse Treg express a number of TLR, notably TLR-4, -2 and -5 [41], all of which bind to bacterial compounds, namely LPS, peptidoglycans and flagelin, respectively. These ligands have been shown by us and others to enhance Treg survival and function [40–43]. Moreover, LPS through its adjuvanticity induces APC maturation and activated DC support Treg expansion [62]. In addition, end products of innate and adaptive immune responses, such as IL-2, also enhance Treg survival, expansion and activation ([13, 44, 45] and I. Caramalho, T. Lopes-Carvalho, J. Carneiro and J. Demengeot, unpublished results). Whether LPS treatment induces immune tolerance to pancreatic islet in NOD mice through direct or indirect effects on Treg, or more likely through both pathways, remains to be assessed. The systematic comparison between LPS-treated animals with the few untreated NOD mice that do not develop diabetes also revealed the robustness of the induced tolerance.

To identify Syk interactors in activated B cells, the approach was repeated with differentially labeled cells

that were subjected to BCR stimulation for either 1, 2, 5, 10 or 20 min. Relative quantification of MS peptide spectra from all approaches was performed using MaxQuant software 32 and is shown in Supporting Information Table 2. In resting B cells, Syk associates with only a few proteins (Table 2). However and in agreement with the original identification of Syk as a BCR-associated kinase in resting B cells 11, membrane-bound IgM as well as Igα and Igβ appeared as prominate Syk interactors in untreated DT40 selleck chemicals llc cells. Following BCR activation, the number of Syk interactors increased dramatically (Table 2). In addition to known binding partners such as the phosphorylated BCR 12, 33, the guanine nucleotide exchange factor VAV3 34, p85-β regulatory subunit of PI3 kinase 35 and the proximal Syk substrate SLP65 16, 17 we found more than 15 novel ligands belonging to different functional categories (Table 2). For example, binding of Syk to Sek1, a MAP kinase kinase, suggests a direct link to the regulation of JNK and p38 36. The GTPase-deficient RhoH ligand has

been implicated in the communication between the Syk paralog ZAP70 and its effector proteins in T cells 37 and hence may provide an adaptor for the phosphorylation selleck compound of Syk substrates. Cytoskeleton interactors included actin-α2, coronin-1C and dynein, indicating a role of Syk for activation-induced cytoskeleton dynamics. This conclusion is further supported by the Syk ligand TOM1L1 (target of Myb1-like ADAMTS5 protein) implicated in ubiquitinylation-controlled intracellular trafficking processes including growth receptor endocytosis 38. An inducible interaction was also observed for several isoforms of the 14-3-3 family of adaptor proteins involved in a plethora of cellular responses 39. Of note, we did not detect the E3 ubiquitin ligase Cbl whose phosphotyrosine domain has been reported to bind phosphorylated tyrosine

323 of Syk in B cells 9. The same phosphotyrosine residue is however also recognized by the SH2 domain of p85β with even higher affinity 35 suggesting a biased competition between the two Syk ligands. As to the reported binding between Syk and the γ1 isoform of phospholipase C (PLC) 40, which is not expressed in DT40 cells, it should be noted that we did not detect the second PLC-γ isoform, i.e. PLC-γ2. Similarly, Src family kinases, protein phosphatases and the adaptor proteins CrkL and Gab have been described to associate with Syk in other signaling systems but were not confirmed as Syk ligands in B cells. Collectively, our data established a B-lymphoid Syk interaction network, which appears to affect a diverse array of cellular functions.

He visited our hospital due to fever lasting for 7 days with cloudy dialysate. He was on no immunosuppressive therapy, was known to be human immunodeficiency virus (HIV) negative, and had no previous episodes of peritonitis. Physical examination found no signs other than pyrexia (37.3°C). The white blood cell count of the CAPD fluid was 3,500/μL, and serum C-reactive protein (CRP) levels were elevated. We performed Gram staining

using centrifuged sediment of the peritoneal effluent, and identified yeast cells with large Gram-positive budding by microscopy. Based on these findings, we started administration of intravenous micafungin and oral fluconazole. The peritoneal catheter was removed on day 7 after admission. Cryptococcus sp. was isolated on day 10 of hospitalization, PF-02341066 datasheet and the antibiotic regimen was altered. Based on the results of antifungal susceptibility testing, voriconazole was administered. A search for disseminated disease was also performed, including microbiological studies of blood and sputum; however, both were negative. CRP levels improved and the patient was discharged on day 18. He has been

in good condition for 1 year after completing 3 months of antibiotic therapy. Later, genetic HDAC inhibitors in clinical trials testing revealed the pathogen as Cryptococcus laurentii (C. laurentii). Discussion: Fungal peritonitis is serious and leads to death in approximately 25% or more of episodes. Cryptococcus peritonitis is an unusual form of PD-related peritonitis. To the best of our knowledge, only 2 cases of peritonitis caused by C. laurentii have been reported in PD patients. Both were adolescent females, and were not on immunosuppressive therapy. It is reported that the presence during of an invasive device is a significant risk factor for C. laurentii infection. In the present patient, as well as in the two previous cases in the literature, we could not determine any risk factors other than a PD catheter with end-stage renal disease (ESRD). The PD catheter was removed in all cases, and all patients survived. Conclusion: C. laurentii infection can occur in

young people who have no risk factors other than PD catheter with ESRD. Prompt catheter removal and anti-fungal therapy effectively treat the infection. JUNG HEE-YEON, KWON EUGENE, KIM HYUN-JI, KWON OWEN, CHOI JI-YOUNG, CHO JANG-HEE, PARK SUN-HEE, KIM CHAN-DUCK, KIM YONG-LIM Division of Nephrology, Department of Internal Medicine, Kyungpook National University Hospital Introduction: Previous studies have suggested the association between thyroid hormones and mortality in dialysis patients. However, little is known regarding the association of free thyroxine and mortality in peritoneal dialysis (PD) patients. This study assesses the association between basal and annual variation of free thyroxine and mortality in PD patients.

“
“The aim of our studies was to investigate the expression of Toll-like receptor (TLR)-2 and TLR-4 (and in some studies TLR-5) in myofibroblasts and small and large intestinal crypt epithelial cells from control patients and those affected by Crohn’s disease and ulcerative colitis. Isolated and disaggregated crypt epithelial cells and monolayers Pembrolizumab manufacturer of myofibroblasts were used for studies by reverse transcription–polymerase chain reaction (RT–PCR), real-time RT–PCR, flow cytometry,

immunocytochemistry and Western blot analysis. Compared to control cells, crypt epithelial cells isolated from active ulcerative colitis and Crohn’s disease colonic mucosal samples showed significantly higher expression of TLR-2 and TLR-4 transcripts and protein (on the cell surface). There was also enhanced expression of TLR-4 in crypt cells from ileal Crohn’s disease. Expression of TLR-2 and TLR-4 transcripts in crypt epithelial cells isolated from inflamed mucosa of distal ulcerative colitis did not differ

significantly from such cells obtained from the normal proximal colon. Crypt epithelial cells with side population characteristics (putative stem cells) also expressed transcripts and protein for TLR-2, TLR-4 and TLR-5. Colonic myofibroblast buy Quizartinib expression of these TLRs was much weaker than in crypt epithelial cells. In conclusion, enhanced TLR-2 and TLR-4 expression by crypt epithelial cells in active inflammatory bowel disease likely reflects greater ability to respond to microbial products. Cytidine deaminase Results from our studies using mucosal samples from patients with distal ulcerative colitis suggest that the enhanced expression of these TLRs could be constitutive. TLR-2, TLR-4 and

TLR-5 expression by stem cells imply ability to respond to distinct bacterial products. “
“Clinical progression of cancer patients is often observed despite the presence of tumor-reactive T cells. Co-inhibitory ligands of the B7 superfamily have been postulated to play a part in this tumor-immune escape. One of these molecules, PD-L1 (B7-H1, CD274), is widely expressed on tumor cells and has been shown to mediate T-cell inhibition. However, attempts to correlate PD-L1 tumor expression with negative prognosis have been conflicting. To better understand when PD-1/PD-L1-mediated inhibition contributes to the functional impairment of tumor-specific CD8+ T cells, we varied the levels of antigen density and/or PD-L1 expression at the surface of tumor cells and exposed them to CD8+ T cells at different levels of functional exhaustion. We found that the gradual reduction of cognate antigen expression by PD-L1-expressing tumor cells increased the susceptibility of partially exhausted T cells to PD-1/PD-L1-mediated inhibition in vitro as well as in vivo.

7:1) were studied. Mean age was selleck chemical 63.8 ± 2.9 years. The most common clinical syndrome observed in our study was nephrotic syndrome (46%), followed by acute nephritic syndrome (28%), acute kidney

injury (18%) and RPGN (13%). Sixty three % patients had secondary cause identified predominantly among them were due to post infectious glomerular nephritis (PIGN) and vasculitis, (23% & 17%) respectively. 37% patients had primary glomerular diseases (TABLE 1), which consisted of membranous nephropathy, focal segmental glomerulosclerosis, minimal change disease, IgA nephropathy, membranoproliferative glomerulonephritis. In PIGN, 65% had complete recovery, 25% had persistent renal dysfunction and 10% developed ESRD. On univariate analysis, peak serum creatinine of more than 4 mg/dl at presentation, need for dialytic support and the presence of crescents in biopsy were found to have statistical

significance for poor outcomes. In multivariate analysis, only peak serum creatinine at presentation had statistical significance- p value 0.012 (95% confidence interval 0.044 to 0.03352). In patients with Vasculitis, the outcome was poor.15% died on initial admission, 30% became dialysis dependent, 30% had persistent renal dysfunction and only 5% made complete recovery. Conclusion: Sixty four percent of glomerular diseases were due to secondary causes, primary renal disease contributed to about 36%. The Palbociclib in vitro most common cause of glomerulonephritis was post infectious glomerulonephritis (23%). Vasculitis was the second most common cause glomerulonephritis in our elderly population, comprising 17% patients. Membranous nephropathy was the most common cause of nephrotic syndrome in our study accounting for 46% of patients with nephrotic

syndrome. NOTO RIO1, KAMIURA NOZOMU1, ONO YUICHIRO2, TABATA SUMIE2, HARA SHIGEO3, YOKOI HIDEKI4, YOSHIMOTO AKIHIRO1, YANAGITA MOTOKO4 1Department of Clinical Nephrology, Kobe City Medical Center General Hospital, Hyogo, Japan; 2Department of Clinical ADAMTS5 Hematology, Kobe City Medical Center General Hospital, Hyogo, Japan; 3Department of Diagnostic Pathology, Kobe University Hospital, Hyogo, Japan; 4Department of Nephrology, Kyoto University Hospital, Kyoto, Japan Introduction: Proliferative glomerulonephritis with monoclonal IgG deposits (PGN-MID) is a form of renal involvement by monoclonal gammopathy that mimics immune-complex glomerulonephritis. PGN-MID associated with a hematological or lymphoproliferative malignancy is rare. Now we present the first case of a patient with PGN-MID leading to the diagnosis of multiple myeloma and subsequent successful treatment by dexamethasone and bortezomib (BD). Case: A 75-year-old male with a history of hypertension presented for evaluation of progressive leg edema and fatigue. His laboratory data involved nephrotic-level proteinuria, urine occult blood, low serum albumin, and moderate renal impairment.

Low numbers of circulating endothelial progenitor cells appear to be associated with an enhanced likelihood of disease relapse, but are not predictive of progression of renal disease, number of organs involved or death from any cause [35]. In summary, advances in understanding the pathogenesis of ANCA vasculitis on all fronts has progressed apace in the past 2 years. Translating this knowledge into better therapies for patients will be the next challenge. The author is currently employed by GlaxoSmithKline. “
“Helicobacter heilmannii induces gastric lymphoid follicles in mice. However, the pathogenic mechanisms behind the

induction of gastric lymphoid follicles by H. heilmannii infection have not been elucidated. The aim of this study was to investigate the roles of Peyer’s patches (PP) in H. heilmannii-induced immune responses CTLA-4 antibody and the development of gastric lymphoid follicles. C57BL/6J and PP deficient mice were infected with H. heilmannii, and in addition to

histological and immunohistological examinations, the expression levels of cytokines and chemokines in gastric mucosa were investigated. Gastric lymphoid follicle formation and the infiltration of dendritic cells, B cells, and helper T cells were milder in the PP-deficient mice 1 month after infection, but they were similar in both types of mice after 3 months. The mRNA expression levels of tumor necrosis factor α and CC chemokine ligand 2 were significantly high in the H. heilmannii-infected groups, and CXC chemokine ligand check details 13 expression was significantly increased in the infected C57BL/6J wild-type mice 1 month after infection. These results suggest that PP are not

essential for the formation and development of gastric lymphoid follicles induced by H. heilmannii infection, although they are involved in the speed of gastric lymphoid follicle formation. Helicobacter heilmannii, a Gram-negative rod bacterium that belongs to the Helicobacter family, which includes Helicobacter pylori, is characterized by a relatively large size (5–9 μm) and a corkscrew ID-8 appearance. Helicobacter heilmannii is located in the stomachs of primates, cats, pigs, and humans (Singhal & Sepulveda, 2005), and causes gastritis, peptic ulcer, acute gastric mucosal lesion, gastric carcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma in humans (Okiyama et al., 2005). Previously, rRNA and urease gene sequence analysis revealed that ‘H. heilmannii’ is not a single species, but includes H. heilmannii type-1 and H. heilmannii type-2 strains (O’Rourke et al., 2004). The former strain can be especially classified as Helicobacter suis, which is found in pigs and humans. The latter strain was found in humans and a variety of feline species. Although there are no reliable diagnostic measures of H. heilmannii infection, it was reported that the infection rate of H. heilmannii is 0.1% in Japanese (mean age: 60.8 years) (Okiyama et al., 2005).