The scavenging of oxygen radical provides a theoretical basis for the treatment of ITP patients. Primary immune thrombocytopenia, previously referred to as idiopathic thrombocytopenic purpura (ITP) is an immune-mediated acquired disorder characterized by isolated thrombocytopenia, defined as a peripheral platelet count less than 100 × 109/l in the absence of any specific cause of the thrombocytopenia [1]. It is further classified according to its duration

since diagnosis: newly diagnosed (<3 months), persistent (3–12 months) and chronic (>12 months) [2]. Oxidative stress is often defined as an imbalance of pro-oxidants and antioxidants, which can be quantified in humans with the redox state of serum GSH/GSSG. Serum GSH redox in humans becomes Navitoclax in vitro oxidized with age, in response to oxidative stress (chemotherapy, smoking) and in common diseases (diabetes mellitus type 2, cardiovascular diseases) [3, 4]. see more Oxidative stress is caused by an imbalance between the production of reactive oxygen and a biological system’s inability to readily detoxify the reactive intermediates or easily repair the resulting damage. All forms of life maintain

a reducing environment within their cells. This reducing environment is preserved by enzymes that maintain the reduced state through a constant input of metabolic energy [5]. Disturbances in this normal redox state can cause toxic effects through the production of peroxides and

free radicals that damage all components of the cell, including proteins, lipids and DNA [6]. In humans, oxidative stress is involved in many diseases, such as atherosclerosis, Parkinson’s disease, heart failure, myocardial infarction, Alzheimer’s disease, fragile X syndrome Cyclin-dependent kinase 3 and chronic fatigue syndrome (CFS), but short-term oxidative stress may also be important in prevention of ageing by induction of a process called mitohormesis [7]. ITP in adults is associated with infection of hepatitis C virus, HIV and other viruses, and Helicobacter pylori [8, 9], although the mechanism is not clear. It is still unknown how platelets are targeted by the host’s immune system. Infection-related oxidative stress may induce disturbed immune response, and ongoing oxygen stress may be a significant factor in patients with chronic ITP in adult. In this study, serum SOD, MDA, TAC, TOS and other oxidant/antioxidant stress parameters were studied in patients with chronic ITP. Our purpose is to determine oxidant and antioxidant status in patients with chronic ITP in comparing their presence in healthy subjects and to detect the relationship between these parameters and platelet count. This study, conducted from October 2011 to October 2012, was approved by the Ethics Committee of the Attached Hospital of Jining Medical College, and informed consent was obtained from each subject prior to the start of our study.

6A, white arrows). The percentage of T cells that were IFN-γ+ in each patient sample varied from 33 to 90% (Fig. 6B and Table 1). Selleckchem Stem Cell Compound Library Taken together, the presence of pro-inflammatory

TAMs and type-1 T cells, and the correlation of numbers of TAMs and T cells in the primary tissue sections support our in vitro findings (Figs. 3 and 4). We aimed to elucidate the mechanisms underlying the tumour-suppressive effects of TAMs in colorectal cancer, an important but under-studied property of TAMs. We found that TAMs in the colorectal cancer model were pro-inflammatory (Fig. 3B). Pro-inflammatory TAMs have been associated with anti-tumour properties, such as production of cytotoxic products such as reactive oxygen intermediates, serine proteases and lytic factors, and enhanced the ability to process and present tumour antigens to T cells 2, 6, 16. Notably, IFN-γ was amongst the pro-inflammatory cytokines secreted by the colorectal TAMs, in the co-cultures as well as in vivo (Fig. 5A). This is an important observation as the production of IFN-γ has been mainly associated with type-1 T cells or NK cells 17. Protease Inhibitor Library concentration Activated macrophages can secrete IFN-γ, but at lower levels 18. IFN-γ is a potent anti-tumour cytokine; its production has been highly correlated with tumour

regression in immunotherapy 17. Recently, IFN-γ has been shown to switch tumour-promoting, anti-inflammatory (M2-like) TAMs to the tumour-suppressive, pro-inflammatory (M1-like) phenotype 19, 20, supporting the hypothesis that T-cell responses orchestrate TAM polarisation early on during cancer development 8. Here, our data suggest an alternative: TAMs can produce IFN-γ and other pro-inflammatory cytokines to create a pro-inflammatory microenvironment which activates type-1 T cells, which in turn produce more IFN-γ (Figs. 4–6). IFN-γ can elicit other Amisulpride downstream anti-tumour immune responses, such as sensitising tumour

cells to apoptosis 17, potentiating monocyte cytotoxicity against tumour cells 21 and anti-angiogenic activities in vivo 22. Notably, the production of the tumour-promoting angiogenic factor, VEGF, by the tumour cells was suppressed by the colorectal TAMs in co-cultures (Fig. 3B). Besides promoting angiogenesis, VEGF has been associated with increased risk of relapse in colorectal cancer patients 23. VEGF also exerts other undesirable tumour-promoting effects, such as decreasing production of cytotoxic mediators like granzyme B and perforin by T cells, and decreasing TNF-α and IFN-γ secretion by NK cells 24. Additionally, VEGF promotes the infiltration of immune-suppressive cells such as myeloid-derived suppressor cells and regulatory T cells into tumours 25, which facilitate tumour growth. In fact, clinical studies have shown VEGF to be a valid therapeutic target for colorectal cancer 12.

The patient had undetectable levels of IgG, IgA and IgM and normal numbers of circulating lymphocytes (10 686 cells per µl) with remarkable eosinophilia (4030 cells per µl). The rest of his initial immune work-up is summarized

in Table 1. Genetic work-up revealed a compound heterozygous RAG2 defect (G95V+E480X). The patient was commenced on CsA treatment; however, his cutaneous symptoms did not improve despite maintaining a high CsA trough level (100–150 ng/ml). Therefore, methylprednisone (2 mg/kg/day) was added and slow resolution of his cutaneous symptoms was observed. The patient was kept on both CsA and methylprednisone treatments until a successful HLA-matched cord blood transplantation was performed AZD5363 order at the age of 6 months. In both patients, transplantations were successful and they have been currently followed for 2 years (patient 1) and 1 year (patient 2), with complete recovery of their symptoms and full reconstitution of their immune system. TCR repertoire.  Examination of TCR-Vβ at presentation

revealed peripheral expansion of oligoclonal T cells with dominant specific receptors. In patient 1, the dominant clone was TCR-Vβ 20, while in patient 2, TCR-Vβ 17 and TCR-Vβ 7·2 were dominant (Fig. 1a,b). Clonal patterns were also seen in the examined TCR-Vγ repertoire in both patients (Fig. 2a,b). These results suggest abnormal thymocyte selection and peripheral Ponatinib expansion, as expected in

Omenn patients. Patient 1 showed a significant clinical improvement during CsA therapy; therefore, a follow-up analysis of his TCR repertoire this website was not indicated. However, in order to show that the patient did not have any expanded peripheral T cells, prior to the HSCT procedure, analysis of his TCR-Vγ repertoire was performed. The analysis revealed complete lymphopenia and no TCR expansion (Fig. 2c). In contrast, patient 2 did not respond completely to the initial treatment with CsA and remained symptomatic, therefore a follow-up analysis of his TCR repertoire was performed (Fig. 1c–e). Surprisingly, while the expression of the dominant TCR-Vβ 17 clone was reduced, the TCR-Vβ 7·2 clone did not respond to CsA therapy. Moreover, a few other TCRs, such as TCR-Vβ 14 and TCR-Vβ 5·1, started to appear (Fig. 1c). Only the addition of methylprednisone treatment resulted in suppression of these clones (Fig. 1d). However, even before the transplant, the patient still suffered mild skin symptoms, which were probably attributed to the presence of the TCR-Vβ 14 clone (Fig. 1e). Changes in the relevant TCRs during the treatment are presented in Fig. 3. During that time the patient was clinically stable apart from his skin symptoms and had no overt infection or other reason to explain clonal expansion. Trec quantification.

Peyer’s patches may also support some IgA production through a TI mechanism [[78]]. In addition to IgA-inducing FDCs, Peyer’s patches include TipDCs, a TNF-inducible nitric oxide synthase (iNOS)-producing DC subset that usually occupies the intestinal lamina propria [[79]]. These TipDCs elicit IgA production learn more by increasing the expression of the TGF-β receptor on B cells via nitric oxide, thereby rendering B cells more responsive to IgA-inducing signals provided by TGF-β [[79]]. Of note, recent findings

show that IgA-secreting plasma cells acquire TipDC-like phenotypic features in the intestinal microenvironment, including expression of the antimicrobial mediators, TNF and iNOS [[80]]. Thus, some of the functions previously ascribed to intestinal TipDCs also involve IgA-secreting plasma cells. Follicular B cells from Peyer’s patches and mesenteric lymph nodes further undergo IgA CSR and production in response to TI signals from plasmacytoid X-396 ic50 DCs (pDCs), which release large amounts of BAFF and APRIL upon being “primed” by type I interferon from intestinal stromal cells [[81]]. Together with Peyer’s patches and mesenteric lymph nodes, isolated lymphoid follicles represent another intestinal site for IgA induction. Isolated lymphoid follicles contain lymphoid tissue-inducer cells that

release the TNF family member lymphotoxin-β upon exposure to TLR signals from commensals [[42]]. The interaction of lymphotoxin-β with its cognate receptor stimulates local stromal cells to release TNF and DC-attracting chemokines

such as CCL19 and CCL21 [[42]]. By inducing DC production of matrix metalloproteases 9 and 13, TNF stimulates DCs to process active TGF-β from a latent precursor protein [[42]]. In the presence of TLR signals, DCs further release BAFF and APRIL, which activate Tau-protein kinase a TI pathway for IgA production by cooperating with TGF-β [[42]]. In addition to isolated lymphoid follicles, the intestinal lamina propria contains a diffuse lymphoid tissue comprised of scattered B cells that can undergo IgA class switching and production, although less efficiently and at a lower frequency than follicular B cells (reviewed in [[82, 83]]). This IgA production is supported by multiple subsets of lamina propria DCs that can activate B cells in a TI manner. When exposed to microbial TLR signals, lamina propria TipDCs release nitric oxide, which in turn enhances the production of BAFF and APRIL [[79]]. Another lamina propria DC subset with IgA-licensing function is represented by DCs constitutively expressing the flagellin receptor TLR5 [[84]]. These DCs express little or no TLR4 and induce TI IgA class switching and production by releasing retinoic acid and IL-6 upon sensing flagellin from commensal bacteria [[84]]. Also, epithelial cells deliver IgA-inducing signals to lamina propria B cells by releasing BAFF and APRIL after recognizing bacteria via multiple TLRs [[38, 85]].

In this study, we determined that the

excretory–secretory (ES) protein from the parasite Anisakis simplex could elicit neutrophil recruitment and IL-17 production. Interleukin-8 and CXCL1 are known LBH589 to be typical neutrophil attractants in lung inflammation (15,25). In this study, we also determined that the expression of the CXCL1 gene was increased as a result of ES protein treatment. Interleukin-17 is generated and released as a free protein from T-lymphocytes of the memory (CD45RO+) subset (27). Linden suggested that IL-17 can recruit and activate neutrophils in the airways; this recruitment is mediated by the neutrophil chemoattractant IL-8, CXCL1 and macrophage inflammatory protein-2 (27). In this study, the level of IL-17 in the BALF of ES protein and OVA-treated mice was significantly higher than those in the OVA-only treatment group (Figure 1c). In addition, IL-17 producing cells were recruited to the lung and lung draining lymph node as the consequence of intranasal ES protein treatment (Figure 1d,e). The ES proteins were also determined to induce IL-6

that enhances the activation of Th17 cells, and gene expression in lung epithelial cells (Figure 2a). Therefore, Anisakis ES proteins may activate IL-17 producing this website cells and neutrophil recruitment in the airway via an induction of IL-6 cytokine production in lung epithelial cells. These findings reveal that IL-17 plays a critical role in the Anisakis-associated allergic reaction. Shainheit et al. previously reported that schistosome egg-stimulated dendritic cells plus naive CD4

T cells from next CBA mice resulted in increased levels of pre-inflammatory cytokines, as well as IL-17 and the chemokines CXCL1, CXCL2 and CCL2. They demonstrated that after neutralization of IL-23 and IL-1, but not of IL-6 or IL-21, egg-induced IL-17 production was profoundly inhibited. They also emphasized that parasite recognition followed by a genetically determined innate pro-inflammatory response induces the development of Th17 cells, and thus controls the outcome of immunopathology in schistosomiasis (28). Specific recognition of conserved molecular motifs associated with different classes of pathogens – particularly viruses, bacteria, fungi and protozoa – by antigen presenting cells (APCs) can be mediated by pattern recognition receptors (PRRs) including the TLR, C-type lectin and Nod-like receptors (26). Toll-like receptors are important initiators of innate immune responses, owing to their ability to recognize a variety of microbial products harbouring pathogen-associated molecular patterns (PAMPs) (29). However, there are no apparent uniformly expressed PAMPs for helminth parasites, although a number of helminth-derived products have been shown to interact with innate immune cells and to modulate their functions.

In vitro, kinetic analysis of CD1 expression shows that proteins are

detectable over a fairly narrow time range between 2 and 4 days, rather than a highly durable effect (Fig. 3A). Conclusions relating to CD1 expression in the dermis of infected skin can be formally stated for CD1b and CD1c. We also noted an upward trend in CD1a expression, but it did not reach statistical significance (Fig. 1). However, HM781-36B solubility dmso large numbers of CD1a expressing LCs in the nearby epidermal compartment provide a higher baseline of staining that complicates interpretation of CD1a expressing cells in the dermis. Collectively, the results show that CD1b and CD1c proteins are rare or absent on cells in the dermis under normal conditions, but are locally upregulated on DCs in the dermis

after coming into the proximity with the infecting borrelial pathogen. Although CD1a selleck products induction is linked to CD1b and CD1c in myeloid cells, only CD1a is constitutively expressed at high levels on epidermal LCs. Previous ex vivo studies showed that human dermal DCs and epidermal LCs play distinct roles in response to borrelia infection, with dermal DCs having more efficient mechanisms of internalization and processing of B. burgdorferi25, so it is of interest that the new CD1 appears on the same type of cell that may be most directly exposed to foreign lipid antigens. Triacyl-CSK4 and natural triacylated lipoproteins present in mycobacteria and borrelia bind to hydrophobic pockets in the TLR1-2 heterodimer and signal through Myd88 and NF-κB to stimulate secretion of diverse cytokines 49. The cellular signaling pathway

leading to increased CD1 gene translation might result from cell autonomous signals within TLR-2-expressing cells. However, direct connections between NF-κB signaling and CD1 promoters are not known, and our data show that secreted factors are sufficient to transfer CD1-inducing activity from cell to cell under conditions in which TLR-2 is not activated. These results suggest that the pathogen sets up a local field whereby cytokines stimulate CD1 expression in many cells near the site of infection, even if individual CD1 expressing cells themselves are not infected or in direct Oxymatrine contact with the pathogen. Although the effects of GM-CSF were known 12, 17, 50, the identification of IL-1β as a regulator of CD1 protein expression provides a new downstream function of this innate cytokine 51. IL-1β has been implicated as an in vitro factor for inducing CD1a expression on LC precursors 52, but identification of mature IL-1β as a group 1 CD1 inducing factor on myeloid cells is a new finding with several implications. First, IL-1β can be used therapeutically as an adjuvant to stimulate CD1 antigen processing function in human monocytes.

[34] The misclassification of ectopy may also explain the discrepancy of findings across studies due to the lack of standardized criteria in

addition to variations in age and parity of participants. One of the most important methodological limitations Epigenetics Compound Library research buy of cross-sectional data is the imprecision of the timing of cervical ectopy in relation to HIV acquisition, which can introduce bias. Hence, studies have often been unable to assess the appearance of the cervix at the time of HIV acquisition.[12, 26] If cervical ectopy facilitates HIV acquisition and transmission, then it is important to identify other factors that influence the development of ectopy. Prior studies have noted an association between hormonal forms of contraception, primarily oral contraceptive pills, and the injectable depot medroxyprogesterone acetate, with increased ectopy[12]; this effect is likely mediated by the influence of estrogen on columnar epithelium.[5, 9, 35] Additionally, C. trachomatis has been shown to preferentially infect columnar cells, and hence, ectopy may increase exposure of susceptible cells to infection.[4]

C. trachomatis increases the susceptibility to acquiring HIV infection in women.[36] The interrelationships between cervical ectopy, hormonal contraception, C. trachomatis, and HIV are important Autophagy Compound Library cell line to discern in young women, given that cervical ectopy, hormonal contraception use, and C. trachomatis are highly prevalent in this population. Additional mechanisms by which the cervical mucosa can be disrupted include Papanicolaou smears, trauma during sexual intercourse, as well as certain intravaginal practices by women in certain social settings. Because human studies cannot ethically

be designed to demonstrate HIV acquisition with or without Cobimetinib supplier cervical ectopy, animal studies or ex vivo studies (i.e., explants, tissues samples) may provide the data to arrive at this causal association. Future studies would need to be mindful of additional confounding factors that could affect HIV acquisition, including STIs, ulcerative lesions, phase of menstrual cycle, inflammation, bacterial vaginosis, exudate, and alcohol use (see Table 2). It is difficult to reconcile the divergent results of observational studies assessing the impact of cervical ectopy on the increased risk of HIV acquisition. Ectopy is difficult to measure, and even when present, it is difficult to interpret. A recent review study did not find any evidence for the routine treatment of cervical ectopy.[37] Given that cervical ectopy is a common feature of the immature cervix, this may contribute to the disproportionate risk of HIV infection faced among young sexually active women in resource-limited settings, particularly in the hyperendemic regions of sub-Saharan Africa.

IRF-8 was originally identified as a repressor of IFN-stimulated response elements and through its ability to inhibit the transcriptional activation buy MK-1775 of other IRFs [50, 51]. Yet, studies of human monocytes and murine cDCs found that IRF-8 promoted type I IFN production [35, 52]. Current findings show that IRF-8 is a strong negative regulator of CpG-driven IFN-β and IL-6 production by human pDCs (Fig. 4B). This is an important observation, as pDCs constitutively express high levels of IRF-8 [13] and IRF-8 KO mice

fail to generate pDCs [36]. Taken together, current findings demonstrate that IRF-8 expression plays a role in negatively regulating pro-inflammatory and IFN responses following TLR9 stimulation of pDCs. We are in the process of examining whether the elevated levels of IRF-8 in the nucleus of unstimulated pDCs (Fig. 2) reflect a constitutive role for IRF-8 in the regulation of gene activation and whether IRF-8 interacts with IRF-5. Several findings support the technical reliability of results from the knockdown experiments upon which these conclusions are largely based. First, no off-target (i.e. nonspecific) CH5424802 nmr activity was detected

with any of the siRNAs tested (Fig. 3A and C and 4A, and Supporting Information Fig. 2A–C). Second, cells transfected with siRNA were not stimulated unless CpG ODN was added (in contrast to the report by Hornung et al. [34]) (Supporting Information Fig. 2D and E). Third, siRNA administration significantly reduced the level of expression of both mRNA and protein of the targeted gene (Fig. 3A and C and 4A, Supporting Information Fig. 2A–C). Finally, siRNA knockdown of MyD88 and TRAF6 blocked the induction of IFN-β and IL-6 mRNA by CpG-stimulated

pDCs, consistent with earlier reports (Fig. 3B; [15, 31, 32]). K” ODN triggered the rapid translocation of NF-κB p50 and p65 (RelA) from the cytoplasm to the nucleus in CAL-1 cells and human pDCs (Fig. 2D, 6, and 7). Interestingly, the knockdown of p105/p50 but not p65 significantly reduced IFN-β production (Fig. 3D), whereas both p105/p50 and p65 contributed to the induction of IL-6. Accumulating evidence indicates that IκBξ (also known as MAIL, a nuclear ankyrin repeat protein) is required for TLR-dependent upregulation of IL-6 [53, 54]. As IκBξ associates with both p50 and Evodiamine p65 [55], current findings suggest that eliminating either impairs IκBξ-dependent induction of IL-6. K” ODN induced the rapid nuclear translocation of both IRF-5 and NF-κB p50 (Fig. 2, 6, and 7). PLA, a technique used to identify protein–protein interactions under physiologic conditions, was employed to examine whether these transcriptional factors associated upon stimulation [40]. Only proteins in close proximity (<40 nM) are visualized by PLA, yielding results comparable to resonance energy transfer techniques (such as fluorescence resonance energy transfer analysis).

1A). NF1 site is located between positions -3992/–3982 from the ATG (A corresponding to position +1 of isoform 1). This site has been previously described and characterized in human airway epithelial cells [16]. NF2 site is located between positions

–369/–359 of Selleck Vorinostat the human TSLP promoter. Two additional putative NF-κB sites, named NF3 and NF4 are located, respectively, at positions –1528 and –3421 of TSLP promoter. A search of the relevant vertebrate databases revealed that the region of human TSLP promoter containing the NF2 site, is conserved in numerous mammals namely Pongo abelii, Pan troglodytes, Mus musculus, Rattus norvegicus, Equus caballus, and Bos taurus (Fig. 1B). Within these species, no sequence corresponding to human NF1 was found in M. musculus and R. norvegicus. A sequence similar but not identical to human NF1 was found in E. caballus and B. taurus. As expected, both NF1 and NF2 sites, as well as NF3 and NF4 sites, were

conserved in primates. The latters were also found in E. caballus MK-2206 datasheet and M. musculus but not in B. Taurus or R. norvegicus. Three putative AP-1 binding sites (AP1–1, AP1–2, and AP1–3), are located at positions –3942, –1255, and –263, respectively (Fig. 1). Like NF1 binding site, AP1–1 site has been described in human airway epithelial cells [16]. Moreover, AP1–2 and AP1–3 are conserved between human and mice but not AP1–1. Since NF-κB and AP-1 are key transcription factors involved in various inflammatory pathologies in both humans and mice and several reports suggest TSLP to be regulated by NF-κB [16, 19] we focused our work on a number of inflammatory SB-3CT agonists including IL-1, TNF-α, and PMA as well as TLRs ligands to evaluate, at the transcriptional level, TSLP regulation

in human IECs. For this purpose, we used a luciferase reporter assay where the luciferase gene was cloned under the control of a 4-kb-long fragment of TSLP promoter. Among the TLRs ligands used Flagellin and FSL1 were able to stimulate the reporter gene activity in HT-29 and Caco-2 cells, respectively (Supporting Information Fig. 1). When Caco-2 cells were stimulated with IL-1, a 12-fold increase in luciferase activity was measured at 24-h poststimulation, whereas a weaker activation was observed in cells stimulated with TNF (twofold) (Fig. 2A). PMA, a diacyglycerol analog that activates PKC and butyric acid, is an end-product of bacterial fermentation, that strongly regulates gene expression in IECs [20-22]. We found that PMA also strongly induced TSLP-dependent luciferase activity (ninefold). Moreover, when Caco-2 cells were co-incubated with PMA and butyric acid a dramatic stimulation (100-fold) of luciferase activity was noted (Fig. 2A). Similar results were obtained with HT-29 cells, however as expected, HT-29 cells were less sensitive to PMA and much more to TNF (data not shown).

In many cases, PTLD occurs within the first post-transplant year.[4] One-year protocol biopsy is a prerequisite for diagnosing early PTLD, which allows for early intervention and leads to better outcomes.[7] The patient

should continue to be followed up to determine the long-term prognosis. “
“Some ALK inhibitor drugs Chinese herbs have been known for their kidney toxicity. Andrographolide, the primary component of a traditional medicinal herb, Andrographis paniculata, is widely used in China for the treatment of upper and lower respiratory tract infection, and dysentery etc. The aim of the study was to identify and summarize any case of kidney injury attributed to its use in the Chinese literature. A systemic analysis of the Chinese literature from January 1978 to August 2013 was conducted of case reports of andrographolide induced acute kidney injury (AKI). We identified 26 cases of andrographolide induced AKI (22 males and four females), with an average age of 31.3 years (range: 21 months to 47 years). 100–750 mg (58% 500 mg) of andrographolide CYC202 clinical trial was administered in 100–500 mL 5% glucose solution or normal saline by intravenous drip once a day. The adverse event appeared after one to six doses (19 [73.1%] patients got only one dose; cumulative dose 690 ± 670 mg) of andrographolide was given, or 0–96 h (median 1 h) after

andrographolide was given. The symptoms included flank pain in 23 cases (88.5%), decreased urine volume in five cases (19.2%), and nausea or vomiting in six cases (23.1%). Laboratory tests showed maximum creatinine 352.8 ± 184.1 (158–889) μmol/L and blood urea nitrogen 12.1 ± 7.6 (4.0–40.6) mmol/L. Urine analysis showed proteinuria in 10 (38.5%) cases and occult blood in eight (30.8%) cases. Kidney biopsy was carried out in two MycoClean Mycoplasma Removal Kit cases and both revealed acute tubular necrosis. Management of this adverse event included withdrawal of the culprit drug, conservative therapy, and renal replacement therapy (six cases,

23.1%). All the patients recovered and were discharged with a normal or close to normal serum creatinine. Their average length of hospital stay was 12.1 ± 4.8 days. Acute kidney injury may occur shortly after intravenous infusion of andrographolide, with symptoms including flank pain, decreased urine output, and nausea or vomiting. The pathological change might be acute tubular necrosis. Renal replacement therapy may be needed in some patients and with a good recovery rate. The mechanisms of andrographolide induced AKI need to be further studied. Traditional Chinese medicine (TCM) has spread beyond China and Asia over the past several decades and has become increasingly popular in Europe and the USA.[1] There are roughly 13 000 medicinals used in TCM in China, in which the most common elements are plant elements and extracts.