The highest rates of chronic and end-stage kidney diseases occur within remote, regional and indigenous communities in Australia. Advance care planning is not common practice for most ATSI people. Family/kinship rules may mean that certain family members of an indigenous person, who in mainstream society would be regarded as distant relatives, may have RGFP966 concentration strong cultural responsibilities to that person. It is imperative therefore to identify early in the planning stages who is the culturally appropriate person, or persons to be involved in the decision-making process so that they can give consent for treatment and discuss goals of care. There are

many barriers to providing effective supportive care to ATSI people. One barrier is that failure to take culture seriously may mean that we elevate our own values and fail to understand the value systems held by people of different backgrounds. Choice of place of death, or being able to ‘finish up’ in the place of their choice, is very important to many indigenous Australians, with strong connections to traditional lands playing an important cultural role. Family meetings, preferably in the presence of a cultural broker to explain treatment pathways and care FK506 chemical structure issues will lead to informed choices being made in an environment where all are able to participate

freely. Each indigenous person is different and should not be stereotyped. For Māori, as within any culture, there will be variation in the preferences of any individual influenced by iwi (tribal) variation, degree of urbanization of the individual and his/her whānau (extended family), ethnic diversity and personal experience among other factors. When providing end-of-life care to Māori it may be helpful to use the holistic Māori concept of ‘hauora’ or wellbeing. Many Māori will prefer to die at home and whānau often prefer to take their terminally ill relative home, although, as with other groups in society, the

pressures of urbanization and geographical next spread of modern whānau mean that this should not be assumed. Care of the tūpāpaku (deceased) can be a particularly sensitive area as it is generally highly ritualized in Māori culture. Whānau may have specific cultural and spiritual practices they wish to observe around handling of the body, including washing and dressing and staying with the tūpāpaku as they progress from the ward, to the mortuary and to the funeral director then marae. Patients in rural areas are both economically and medically disadvantaged Access to specialist services in rural areas is limited. More care is likely to be outsourced to local physicians, GPs and palliative care nurses who will need ‘on the ground’ outreach support from renal/palliative care services Patients want to be treated close to where they reside to avoid the cost of travel and dislocation involved in visiting metropolitan-based clinics.

We were unable to find circulating pro-apoptotic factors in PAH patients that would support the EC apoptosis hypothesis of PAH. It is important to mention that we used HUVECs in our study and that, ideally, PS-341 in vivo patients’ own pulmonary ECs should be used to study pro-apoptotic activities of circulating IgG. Nevertheless, our study demonstrates that

circulating IgG from AECA-positive patients differ bioactively between diseases and cannot, therefore, be incorporated in a general cause–consequence relationship solely on the basis of their shared feature of binding to EC. Special thanks go to Drs B. Broers (cardiologist) from the Orbis Medisch Centrum in Sittard-Geleen, the Netherlands, for recruitment of PAH patients. The authors also thank N. Deckers from the Cardiovascular Research Institute Maastricht Selleck Silmitasertib (CARIM), the Netherlands, for his excellent technical assistance and advice with regard to the RT–CES™ assays. This research was supported by financially Actelion Pharmaceuticals Nederland BV (Woerden, the Netherlands). The authors declare that they have no conflict of interests. “
“Rapidly induced, specific Ab generated in extrafollicular foci are important components of early immune protection to influenza virus.

The signal(s) that prompt B cells to participate in extrafollicular rather than germinal center responses are incompletely understood. To study the regulation of early B-cell differentiation events following influenza infection, we exploited earlier findings of a strong contribution of C12 idiotype-expressing B cells to the primary HA-specific response against influenza A/PR/8/34. Using an idiotype-specific mAb to C12 and labeled HA, in conjunction with multicolor flow cytometry, we followed the fate of C12Id-expressing influenza HA-specific B cells in WT BALB/c mice, requiring neither genetic manipulation Carnitine palmitoyltransferase II nor adoptive cell transfer. Our studies demonstrate that HA-specific C12Id+ B cells are phenotypically indistinguishable from follicular B cells. While they induced both extrafollicular and germinal

center responses, extrafollicular responses were strongly predominant. Provision of increased HA-specific T-cell help increased the magnitude of the extrafollicular response, but did not shift the C12Id+ response toward germinal center formation. Collectively the data are consistent with the hypothesis that B-cell fate determination following activation is a stochastic process in which infection-induced innate signals might drive the preferential expansion of the early extrafollicular response. Influenza virus infection-induced anti-viral Ab can contribute to survival from primary and secondary infection 1–7. Rapid B-cell responses in the local respiratory tract draining mediastinal LN (MedLN) are induced as early as 48–72 h after infection 8.

2) of 6–10 weeks of age were used as the source of BM for in vitro cultures.

GMKO mice [43], GM-CSF receptor βcKO mice [44] on C56BL/6 background, and GM-CSF transgenic mice on SJL × C57BL/6 mixed background [45] were generated, and maintained in the selleckchem animal facility of The Walter & Eliza Hall Institute (WEHI) Animal Facility. All mouse procedures were approved by the WEHI animal ethics committee. Cultures were setup as previously described [4, 12, 46]. Briefly, BM cells were extracted, and erythrocytes were removed by exposure to 0.168 M NH4Cl. Cells were cultured at a density of 1.5 × 106–3.0 × 106 cells per mL in RPMI 1640 medium with 10% (v/v) fetal bovine serum containing either recombinant mouse Flt3L (made in-house), recombinant GM-CSF (R&D systems), or both at 37°C in 10% CO2. DCs induced by Flt3L, GM-CSF, or both are termed FL-DCs, GM-DCs,

or GMFL-DCs, respectively. OT-I T cells (H-2Kb-restricted anti-OVA257–264) and OT-II T cells (I-Ab-restricted anti-OVA323–339) were purified from pooled lymph nodes (inguinal, axillary, brachial, cervical, and mesenteric) by Ab depletion of non-T cells (non-CD8 T cells for purification of OT-I T cells and non-CD4 T cells for purification of OT-II T cells). T cells were then dye labeled by incubating them for 10 min at 37°C in FCS free PBS containing 0.1% BSA and 2.5 mM CFSE. The T-cell preparations were routinely >80% pure, as determined by flow cytometry. The capacity of the FL-DCs, GM-DCs, or GMFL-DCs to generate buy C59 an antigen-specific T-cell Bcl-2 inhibitor stimulatory response was evaluated using isolated OT-1 and OT-II T cells. FL-DCs, GM-DCs, or GMFL-DCs were plated at 104 cells per well in U-bottom 96-well plates and pulsed for 45 min at 37°C at the indicated concentration of OVA. Cells were washed and resuspended with 5 × 104 CFSE-labeled OT-I/OT-II cells. Proliferation of the T cells was determined after 60 h of culture as described

above. To quantify proliferation, the T cells were stained with anti-CD4 or -CD8 (for OT-II and OT-I, respectively) and anti-TCRVα2 antibodies, and resuspended in 100 μL of balanced-salt solution and 2% FCS-containing 2.5 × 104 blank calibration particles (BD Biosciences Pharmingen). Samples were analyzed by flow cytometry on a FACScallibur (Beckton Dickinson) and the total number of live dividing lymphocytes (propidium iodide-negative, CFSElo) was calculated from the number of dividing cells per 5 × 103 beads. Each determination was done in duplicate. Samples were then analyzed using Flowjo Software (Tree Star Inc). As previously described [22], BM cells were suspended in nycodenz medium (1.086 g/cm3) and cells of lighter density were isolated by centrifugation. The cells of lighter density were then coated with biotinylated monoclonal antibodies to the following lineage markers: CD3 (KT3–1.1), CD19 (ID3), CD45R (B220, RA36B2), CD11b (M1/70), CD11c (N418), Ly6G (IA8), Ly6C.2 (5075–3.6), NK1.1 (PK136), CD127 (IL-7R; A7R34–2.2), and Ter119.

5). Furthermore, all of the anti-Gr1 Ab-injected mice died within 3 days of inoculation (Fig. 4). However, 83% of mice injected with the anti-M-CSFR Ab survived (Fig. 4). These results indicate that host innate immune defenses in the respiratory tract of normal mice are mediated by neutrophils rather than

by macrophages, which suppress bacterial growth and prevent the development of severe disease. The number of infiltrating NK cells in the lungs of both anti-Gr1 Ab-injected and control mice also increased from Day 1 post-inoculation (Fig. 6C); therefore, we next examined the effect of NK1.1+ cells on the elimination of A. baumannii. Although NK cells play a key role in the immune response to tumors, viruses, and intracellular bacteria (33–36), little is known about their role this website in the response to extracellular bacterial infection (37). There are no published reports assessing the contribution of NK cells to the response against A. baumannii pneumonia. The functional role of the NK1.1+ cells was examined by injecting mice with an anti-NK1.1 Ab. As observed for the Lapatinib in vivo anti-Gr1 Ab-injected mice, mice injected with anti-NK1.1 Ab showed a reduced ability to eliminate the bacteria, and the overall survival rates

were less than those in control mice (Figs 4, 5B). These results indicate that NK1.1+ cells play a crucial role in host defense against respiratory infection by A. baumannii. In anti-NK1.1 Ab-injected mice, the number of infiltrating neutrophils decreased compared with those in control mice up until Day 3 post-inoculation, and the viable bacterial count in the lungs was 100-fold higher than that in control mice by Day

3 (Figs 5B, 7A). Moreover, as shown in Fig. 8, the expression levels of KC in anti-NK1.1 Ab-injected mice were significantly lower than those in control mice. These results suggest that NK1.1+ cells induce the recruitment of neutrophils by increasing the expression of KC during the early phase of Acinetobacter infection. NK1.1 is expressed on NK cells and NKT HSP90 cells, so anti-NK1.1 Ab treatment depleted NK cells and NKT cells. In this experiment, these results may be caused by NK cells and/or NKT cells. However, it is likely that NK cells rather than NKT cells play an important role in the recruitment of neutrophils during A. baumannii infection, because the numbers of NKT cells were not significantly increased in the lung during infection. NK cells, along with CD8+ T cells, function as key effector cells during Th1-type immune responses, and secrete inflammatory cytokines such as IFN-γ and TNF-α. A recent study shows that A/J mice are much more sensitive to Acinetobacter baumannii infection than C57BL/6 mice, due to delayed neutrophil recruitment during the early phase of infection (38).

Apoptosis on the other hand may inactivate IL-33. It is likely that both inactivation and release of IL-33 take place linking between apoptosis and cell damage in many chronic inflammatory diseases in which GSK-3 inhibitor IL-33 has been detected. The crucial role of IL-33 in asthma has been assumed due to several pieces of evidence. Administration of IL-33 results in lymphocyte-independent airway hyperreactivity, goblet

cell hyperplasia and eosinophilic and monocytic infiltration. Hypertrophy and enhanced mucous secretion in the bronchi and bronchioles occurs after repeated applications in mice 5. In addition, IL-13-dependent differentiation of alveolar macrophages towards alternatively activated macrophages with increased airway inflammation has been reported in a murine model 19. Furthermore,

CD34pos progenitor cells express the receptor for IL-33, ST2, and secrete large amounts of Th2-type cytokines and chemokines in the presence of IL-33. IL-13- and IL-5-expressing CD34pos cells have been found in the sputum of asthmatic individuals and were up-regulated upon allergen-challenge 12. Moreover, IL-33 contributes to the recruitment and activation of eosinophils to the same degree as IL-5. The in vivo relevance of IL-33 in human asthma is further supported by its higher expression in epithelial cells and smooth muscle cells in moderate to severe asthmatics, but not mild asthmatics. This has been confirmed Dabrafenib ic50 at the protein level in broncheoalveolar lavage fluid 20. Finally, a genome-wide association study has reported the association between single nucleotide polymorphisms in the IL-33 gene and in the ST2 gene and an increased risk to develop asthma 21. In conclusion, IL-33 is evolving as a candidate molecule that acts on DCs and bridges innate and adaptive immune responses in the lung. IL-33 thereby affects both the development of allergic sensitization and the aggravation of lung inflammation. The study by Besnard et al. 13 demonstrates this in an elegant way, defining DCs as effector cells in vivo and confirming ST2-specific GNA12 DC activation. However, further work is required to fully delineate the role of IL-33 in allergic disease. Conflict of

interest: The authors declare no financial or commercial conflict of interest. See accompanying article: http://dx.doi.org/10.1002/eji.201041033 “
“In this study, we investigated the characteristics of the infection and subsequent immunity induced by Strongyloides venezuelensis in Lewis rats. Animals were infected with 4000 L3 of S. venezuelensis and number of eggs per gram of faeces indicated an acute phase around day 8 and a recovery phase around day 32 after infection. A strong Th2 polarization during recovery phase was ascertained by a significant increase in IgG1 and IgE compared with that in the acute period. A shift in the cytokine profile confirmed these findings. A predominant production of IFN-γ during the acute phase was followed by IL-10 production during recovery.

Recently, long-lived TRM cells have been identified in peripheral tissues, especially the skin (reviewed in [32]). TRM cells do not recirculate as compared to TEM and TCM cells. While the characterization of TRM cells is still in its infancy in humans, mouse studies have recently

X-396 cost shed more light on this novel T-cell population, which is best characterized in the CD8+ T-cell compartment. This is due to the preferential use of viral infection models such as models for herpes simplex and human immunodeficiency virus infections and the fact that tissue-resident memory T cells are located in the epidermal skin layer, which in mice is exclusively populated by CD8+ but not CD4+ T cells (reviewed in [33]). In humans, however, CD4+ T cells can reside in the epidermis. Therefore, it can be anticipated that insights gained in mouse models will only reflect the situation

in humans with some limitations. Nevertheless, mouse models have so far been crucial for providing evidence of fundamental principles, such as the concept INCB024360 of tissue residency versus tissue recirculation, due to the fact that it is possible to easily perturb the immune system by infections and parabiosis, as well as by virtual unrestricted tissue accessibility for further analysis. A prerequisite for defining the specific role(s) for Th-cell subsets in tissue is to define how they reach their target organ. In line with a specific chemokine repertoire, distinct Th-cell subsets show characteristic homing abilities. Important chemokine receptors for skin homing are CLA, CCR4, CCR6, and CCR10 (reviewed in [34]). The chemokine receptor CCR10 has been shown to be

abundantly present on Th22 cells [5] and reflects PJ34 HCl a characteristic feature of these cells, namely migration to higher layers of the epithelium according to a CCL27 gradient [35]. In line with this observation, Th22 cells are present in inflammatory skin diseases and predominantly found in the epidermal compartment [4]. This holds also true for other immune cells. For example, Th17 cells induce keratinocytes to secrete CXCL8, which in turn recruits neutrophilic granulocytes into the epidermis and drives the development of neutrophil microabscesses, a hallmark of psoriasis [36]. Thus, not only the differential expression of chemokine receptors but also the chemokine repertoire that distinct Th cells induce in the tissue are critical for their functional abilities. This can have a critical impact on the pathogenesis of tissue-restricted diseases. Once Th cells reach their target organ, a T-cell activation cascade is necessary to fully activate them. This may happen in different ways.

Furthermore, IgG3 binds with high affinity to Fc receptors on macrophages, and thus may be important in antibody-mediated find more phagocytosis [2]. These factors may explain why patients with isolated IgG3 deficiency present with recurrent upper respiratory tract infections. However, the propensity for infections in these patients may not be attributed solely to IgG3 deficiency. There have been reports of patients with complete absence of IgG3 due to gene deletion in the heavy chain constant

regions, but these patients have had no infectious complications [3]. Therefore, other immune dysfunctions might exist in those patients with isolated IgG3 deficiency and recurrent infections. A more detailed analysis of immune function in IgG3-deficient patients is needed. The majority of reported studies for IgG subclass deficiency have been in children [4–6], and very few studies have reported detailed clinical and immunological features of adult patients with IgG3 deficiency [7–8]. In some of these reports, IgG3 subclass deficiency was associated with either IgA deficiency or another subclass deficiency, and therefore may not be considered selective IgG3 deficiency. R788 cell line Moreover, none of these studies reported immunological data. Finally, there is a lack of information about the use of intravenous

immunoglobulin for treatment of IgG3 subclass deficiency. In this study, we present detailed information regarding immune functions of patients with recurrent infections and isolated IgG3 deficiency, and their response to intravenous Ig therapy (IVIG). We reviewed the charts of patients with recurrent infections referred to one of us (S. G.) at Immunology Clinic, University of California, Irvine (UCI) from 1998 to 2007. We identified 17 adult patients with a diagnosis of selective IgG3 deficiency. The diagnosis was made according to published guidelines [9]. Patients

were 16 years of age or older at the time of diagnosis, suffered from recurrent Cell press infections, had an IgG3 level that was greater than 2 standard deviations below the mean on at least two separate occasions and had normal levels of IgA, IgM, IgG, IgG1, IgG2 and IgG4. The charts of these 17 patients were reviewed for immunological data, the type and frequency of infections and response to IVIG treatment. This study was approved by the UCI Institutional Review Board, and the patients signed informed consent. Fluorescein isothiocyanate (FITC)- and phycoerythrin (PE)-conjugated monoclonal antibodies to CD3, CD4, CD8, CD19, CD16, CD56, CD14, Toll-like receptor-4 (TLR-4) and isotype controls were obtained from Becton Dickinson (San Jose, CA, USA). Tritiated thymidine [3H] for lymphocyte transformation assays was obtained from New England Nuclear (Boston, MA, USA).

OVA, complete, and incomplete Freund’s adjuvant (CFA and IFA, respectively) were purchased from Sigma-Aldrich. Tissue culture media Dulbecco’s-Modified Eagle’s Medium (DMEM) was supplemented with 10% heat-inactivated fetal bovine serum (FBS), 2 mM L-glutamine, 100 U/mL penicillin, and 100 μg/mL streptomycin (all

from Gibco). Mice were immunized s.c. under ether anesthesia at two sites (base of the tail and along the back) with 100 μg of OVA in 100 μL of 1:1 PBS:CFA. Three weeks later, they were boosted s.c. with 50 μg of OVA in IFA. Arthritis was induced 2 wk after the boost, by intra-articular (i.a.) injection of 100 μg OVA in 25 μL PBS in one paw (day 1). The paw thickness was measured every day during the course of the AIA using a caliper calibrated with 0.01-mm graduations. Adoptive transfer experiments for AIA development

were performed as follows: LNCs from OVA-immunized GDC 973 WT mice were isolated and stimulated in vitro in the presence of OVA (20 μg/mL). To overexpress miR-21, cells were transfected with 150 nM pre-miR21 miRNA precursor (cat no. PM10206, Ambion, Austin, TX, USA) using siPORT NeoFX transfection agent (cat no. AM4511, Ambion) for the entire period of antigenic stimulation. As a negative control, OVA-stimulated cells were treated with the transfection reagent alone. After 72 h of stimulation, cells were washed and adoptively transferred (day 0) into syngeneic naïve recipients (5×106 cells/mouse). Subsequently, NVP-LDE225 in vitro mice were immunized s.c., with OVA in incomplete Freund’s adjuvant (day 1) and 6 days later (day 7) were intra-articularly injected with OVA/PBS. The development of AIA was monitored on a daily basis as mentioned above. Mice were immunized s.c. with OVA (100 μg) in CFA as described above, and 9–10 days later, draining LNs were collected. A single-cell suspension was prepared and cells were adjusted at 4×106 cells/mL. LNs were then cultured in the presence or absence of Ag in flat-bottomed 96-well plates for 72 h at 37°C in a 10% CO2 90% air-humidified incubator. Eighteen hours before harvesting, 1 μCi of [3H]-thymidine (Amersham Biosciences) was added to each well. The cells were harvested and incorporated

radioactivity was measured using Astemizole a Beckman β counter. Stimulation index (S.I.) is defined as (cpm in the presence of Ag/cpm in the absence of Ag). LN cells from WT and PD1−/− mice were isolated at days 9 and 10 after OVA immunization and restimulated in vitro with OVA (50 μg/mL). After 72 h, cells were collected and analyzed for the expression of CD4 (RM4-5), CD44 (Pgp-1, Ly24), and CD3e (145-2C11) (all from BD Pharmingen) by flow cytometry. Antibody staining was performed for 20 min at 4°C in PBS/5% FCS. Cells were acquired on a FACSCalibur (BD Biosciences) and the analysis was performed with the FlowJo software (Tree Star). Cytokine production was determined in culture supernatants harvested following 48 h stimulation of Ag-primed LNCs with OVA (20 μg/mL).

“
“Tumors of the Peripheral Nervous System’ is the 19th Fascicle in the 4th series of Armed Forces Institute of Pathology (AFIP) Atlases of Tumor Pathology.

The book is divided into a total of 15 chapters. The first chapter is an overview of peripheral nerve tumours, including a historical background, a brief account of early investigators (such as Theodor Schwann, Rudolf Virchow and Santiago Ramon y Cajal), and a section describing specimen presentation, handling and assessment. The second provides an overview of the development, gross anatomy, Small molecule library supplier histology and ultrastructure of the peripheral nervous system. Chapters 3 through 6 (a total of almost 100 pages) cover a variety of non-neoplastic lesions which would be included in the differential diagnosis of peripheral nervous system tumours. These are subdivided into selleck reactive lesions; inflammatory and infectious lesions; hyperplastic lesions; and lipomatosis and neuromuscular choristoma of nerve. The remainder of the book is broken down into chapters dedicated to neoplastic entities including schwannoma, neurofibroma, perineurial cell tumours, miscellaneous benign neurogenic tumours, benign and malignant non-neurogenic tumours, malignant tumours of the peripheral nerves, tumours of the neural transmitting mesenchymal cell component of the peripheral nervous system, and secondary neoplasms. The final chapter is dedicated to neurofibromatosis

(types 1 and 2) and schwannomatosis. Each diagnostic entity is broken down into various subsections (the number of which vary depending on the type of lesion), but which typically include a definition, general features, clinical features, gross findings, microscopic findings, immunohistochemical findings, ultrastructural findings, differential diagnosis, and treatment and prognosis. Each chapter ends with an extensive selection of references for readers wishing to refer to the original papers. Within the chapter dedicated to neurofibroma additional subsections include ‘diagnostically confusing PtdIns(3,4)P2 microscopic features’ (including a review of features such as hypercellularity with and without epithelioid

cell change, densely aggregated small nuclei, melanin containing cells, and a variety of other histological appearances), ‘histological atypia and malignant change’ and ‘tumors of proposed neurofibromatous nature but unconfirmed’. As with all AFIP fascicles the book is lavishly illustrated throughout with well-annotated clinical pictures, radiology, macroscopic, microscopic and ultrastructural findings. The great strength of this book is its practical approach to diagnosis. This is the sort of book pathologists will keep by their microscope to refer to when reporting day-to-day work, as well as more challenging cases. The histological features are clearly illustrated and the differential diagnoses are particularly useful, providing a concise yet clear approach to dealing with problematic cases.

Electrophysiological evidence from ECs in isolation is compared

with those in intact arteries and arterioles and the possible physiological relevance of EC Ca2+ entry driven by hyperpolarization discussed. “
“The effects of RT on muscle mass, strength, and insulin sensitivity are well established, but the underlying mechanisms are only partially understood. The main aim of this study was to investigate whether RT induces changes in endothelial enzymes of the muscle microvasculature, which would increase NO bioavailability selleck compound and could contribute to improved insulin sensitivity. Eight previously sedentary males (age 20 ± 0.4 years, BMI 24.5 ± 0.9 kg/m2) completed six weeks of RT 3x/week. Muscle biopsies

were taken from the m. vastus lateralis and microvascular density; and endothelial-specific eNOS content, eNOS Ser1177 phosphorylation, and NOX2 content were assessed pre- and post-RT using quantitative immunofluorescence microscopy. Whole-body insulin sensitivity (measured as Matsuda Index), microvascular Kf (functional measure of the total available endothelial surface area), and arterial stiffness (AIx, central, and pPWV) were also measured. Measures of microvascular density, microvascular Kf, microvascular eNOS content, basal eNOS phosphorylation, and endothelial NOX2 content did not change from pre-RT to post-RT. RT increased insulin sensitivity (p < 0.05) and reduced resting selleck chemicals blood pressure and AIx (p < 0.05), but did not change central or pPWV. RT did not change any measure of muscle microvascular structure or function. "
“School of Nursing, McMaster University To characterize the effect of systemically

administered AGP on early leukocyte recruitment in the livers of endotoxemic or septic mice and to determine whether this is influenced by LPS sequestration. Endotoxemia was induced in C57Bl/6 mice via intraperitoneal injection of LPS. Sepsis was induced in mice by cecal ligation and perforation. AGP (165 mg/kg) or saline (20 mL/kg) or HAS (200 mg/kg) was administered immediately after surgery or LPS injection and the hepatic microcirculation was examined by intravital microscopy at four hour. Leukocyte adhesion in the Casein kinase 1 PSV was reduced by treatment with AGP in mice subjected to either LPS or CLP protocols compared to either saline or HAS treatment. AGP-treated mice also had significantly higher sinusoidal flow in both models. Pre-incubation of LPS with AGP reduced the ability of LPS to recruit leukocytes to the liver microcirculation. AGP was more effective in limiting hepatic inflammation and maintaining perfusion than saline or HAS, in both endotoxemic and septic mice. AGP sequestration of LPS may contribute to its anti-inflammatory effects.