[99] Both hypertension and proteinuria are well-recognized major traditional risk factors for the progression

of CKD.[9] In addition to hypertension and proteinuria there is evidence that ADMA could be directly involved in the progression of CKD. Indeed, in rats with a unilateral nephrectomy ADMA administration for 8 weeks in one group and its comparison with the other group that did not receive any ADMA, provided the following results: (i) Increased ADMA levels in serum are related to increased renal oxidative stress, since elevated renal levels of superoxide anion (O2−) were also found.[78] (ii) ADMA administration had as a result the induction R788 of glomerular fibrosis (increase of synthesis of the intravascular substance), as well as vascular fibrosis, apparent by the increased collagen type I and II and fibronectin deposition.[78] (iii) PD0325901 chemical structure In rats receiving ADMA, a decrease of the peritubular capillary network was noted.[78] (iv) The mRNA expression of collagen type I and the renal concentration of TGF-β1 (transforming growth factor-β1) were

higher in rats receiving ADMA.[78] (v) Elevated levels of TGF-β1 were correlated with the higher levels of angiotensin II as well as the increased expression of HIF-1a (hypoxia inducible factor-1a) and endothelin 1 (approximately thrice the normal levels).[78] There is evidence suggesting that chronic renal hypoxia may have an important role in the progression of tubulointersttial fibrosis in CKD,[100] and also the role of tubulointerstitial fibrosis is more important than glomerulosclerosis in terms of renal prognosis.[100, 101] The administration of a recombinant adenovirus vector, encoding DDAH-1 and resulting

in the increased expression of DDAH in rats with subtotal nephrectomy (5/6), the model that is currently considered as the most representative of kidney Atazanavir disease in human,[92, 102] has led to the decrease of ADMA concentrations and has slowed the progression of kidney damage, since the tubulointerstitial fibrosis was contained. This occurred to a larger extent compared with the rats with nephrectomy that received hydralazine aimed at the restoration of their blood pressure, suggesting that there is a mechanism for the progression of kidney damage totally independent to arterial hypertension.[92] It is therefore suggested that the amelioration of ADMA levels has decreased the peritubularischaemia and lead to the decrease of TGF-β1 expression. Also in normal rats the chronic NOs inhabitation causes arterial hypertension and FSGS.[103] Two studies have determined that there is a faster deterioration of renal function in CKD patients presenting with high ADMA serum concentrations, suggesting that it may act as an independent prognostic marker for the progression of renal disease.

cruzi metacyclic trypomastigotes, released in the faeces and urine of reduviid bugs taking a blood meal, invade keratinocytes and other cell types in the skin and mucosa [1–3]. Inside the host cells, trypomastigotes differentiate into amastigotes and undergo several cycles of replication by binary fission before redifferentiation into the non-dividing trypomastigotes. Upon exiting infected cells, trypomastigotes migrate through the extracellular matrix

to invade neighbouring cells or, through the circulation, distant cells in the heart, gastrointestinal tract, central nervous system and other organs. Repeated cellular cycles of T. cruzi SCH727965 invasion through the body are a characteristic feature of acute Chagas’ disease, which lasts only a few months. Acute disease ends when parasitemia becomes undetectable by optical microscopy, setting the stage for the onset of the

chronic phase of infection. This can be sub-divided in two clinical forms: 1) indeterminate, when patients are asymptomatic and https://www.selleckchem.com/products/AZD2281(Olaparib).html exhibit normal heart and digestive tract functions evaluated by electrocardiogram and radiography. And 2) symptomatic, when patients, for reasons that remain unknown, present pathological alterations that lead to electrical disturbances and enlargement of the heart (cardiomegaly), oesophagus (megaoesophagus) and/or colon (megacolon), accompanied by strong inflammation, fibrosis and destruction of the peripheral nervous system [4, 5]. Chronic Chagas’ infection, including those individuals in the indeterminate form, may last many years or decades. Innate and adaptive immunity play a critical role

in reducing parasite growth in the acute/chronic phase transition of Chagas’ disease and in maintaining low parasite burden that characterizes chronically infected individuals [6]. However, the relevant antigens, specific antigenic determinants and corresponding immune response governing these mechanisms remain incompletely understood. Recently, we discovered that sera of ∼80% patients with chronic Chagas’ disease contain find more autoantibodies (ATA) to TrkA, TrkB and TrkC, the tyrosine kinase receptors of the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), respectively [7], that underlie development and repair of the nervous system [8, 9]. As T. cruzi uses TrkA and TrkC to enter and activate neurons and glial cells [10–12], binding of ATA to TrkA and TrkC blocks invasion of neuronal, glial and non-neural cells in culture by the parasite [13]. Furthermore, when passively administered to mice, ATA potently blocked parasitemia, pathology and mortality [13]. Thus, ATA may represent a mechanism responsible for the low tissue parasitism that distinguishes chronic Chagas’ disease. If ATA reduces cellular invasion, underlying low tissue parasitism, then Trk autoimmunity should emerge in the acute phase of Chagas’ disease, as it ends with a drastic decline in parasitemia and tissue parasite load.

1a). Using these boundaries and the level of CD127 expression by CD4+ lymphocytes, CD4+ CD25inter CD127low/− and CD4+ CD25high CD127low/− Treg cells and CD4+ CD25− CD127−/+ and CD4+ CD25+ CD127+ effector T cells were identified and isolated (Fig. 1b), with the prevalence of Treg cells expressed as a percentage of the total CD4+ population (mean ± SEM). Foxp3 expression on the two Treg cell populations (CD4+ CD25inter CD127low/− and CD4+ CD25high CD127low/−) was assessed following fixation and permeabilization of

the cells, as directed (Human Foxp3 Buffer Set; BD Biosciences), before incubation with a mouse anti-human Foxp3-Alexa Fluor 488 antibody (clone 259D/C7; BD CH5424802 concentration Biosciences) or its corresponding isotype control (BD Biosciences) for 30 min protected from light. The labelled cells were washed, re-suspended and the same gating strategy as detailed above was applied during the acquisition of the samples. The suppressive activity of isolated Treg cells on the proliferation of autologous effector T cells was determined by a co-culture carboxyfluorescein diacetate succinimidyl ester (CFSE) assay. Effector T-cell populations (CD4+ CD25− CD127−/+ or CD4+ CD25+ CD127+) were incubated with 5 μm of CFSE (Sigma, Poole, UK) for 10 min EMD 1214063 solubility dmso at 37°C. The labelling

was quenched by the addition of 2·5 ml of ice cold culture medium [X-VIVO 20 medium (Lonza, Slough, UK) supplemented with 5% volume/volume heat-inactivated AB serum (Invitrogen) and penicillin/streptomycin (final concentration:

0·1 U/ml and 0·1 mg/ml, respectively; PAA)] before the cell suspension was incubated on ice for 5 min. Following three washes with pre-warmed medium the labelled effector T cells were co-cultured with Treg cells (CD4+ CD25inter CD127low/− and CD4+ CD25high CD127low/−) in 200 μl of culture medium at various ratios (Treg : effector; 0 : 1, 1 : 1, 1 : 2, 1 : 5 and 1 : 10). Depending on the number of Treg cells available; the 1 : 1 ratio was always prepared. Where possible http://www.selleck.co.jp/products/Adrucil(Fluorouracil).html the CFSE assay was run with 5 × 104 effector cells cultured in each well of a 96-well round-bottomed plate, however, when insufficient cells were isolated the number of effector cells plated was successfully scaled down to 1 × 104/well. Lymphocyte stimulation was provided by Human T-Activator CD3/CD28 Dynabeads (Invitrogen) at a cell : bead ratio of 1 : 3 and 100 U/ml recombinant human IL-2 (AbD Serotec, Kidlington, UK). Following 4 days of co-culture, the cells were harvested and the proliferation of the CFSE-labelled effector T cells was determined using flow cytometry.

, 2003; Glansdorp et al., 2004; Rasmussen et al., 2005). Recently, several crystal structures of the quorum-sensing regulatory proteins with their cognate AIs have been reported

(Vannini et al., 2002; Bottomley et al., 2007; De Silva et al., 2007; Kim et al., 2010), and in line C59 wnt with that computational modelling approaches have been employed to design potential QSIs. Yang et al. (2009a b) applied molecular docking and virtual screening and identified three recognized drugs, salicylic acid, nifuroxazide, and chlorzoxazone, as QSIs of P. aeruginosa (Yang et al., 2009a b). AI structurally unrelated QSIs were discovered by Soulere et al. (2010) through docking-based screening on a 2344 chemical compounds library (Soulere et al., 2010). Besides docking, structure-activity relationship methods

are also applied to design and identify novel QSIs (Steenackers et al., 2010; Brackman et al., 2011). Over the past few years, researchers have identified quorum-quenching enzymes from many prokaryotic and eukaryotic organisms, which degrade quorum-sensing signal molecules (Dong et al., 2007). Bacillus spp. produces a N-acyl-homoserine lactone lactonase that hydrolyses this major group quorum sensing AI in Gram-negative Carfilzomib mouse bacteria (Augustine et al., 2010). Mammalian cells was shown to produce paraoxonases (PON1, PON2, and PON3) that hydrolytically inactivate quorum sensing signal N-(3-oxododecanoyl)-l-homoserine lactone from P. aeruginosa (Teiber et al., 2008). Recently, metagenomic approaches are widely applied to identify novel enzymes from nature. Bijtenhoorn et al. (2011) isolated and biochemically characterized SPTLC1 a novel N-acyl-homoserine lactone hydrolase, BpiB05, from the soil metagenome (Bijtenhoorn et al., 2011). BpiB05 is not distantly related to any of the currently

known N-acyl-homoserine lactone hydrolases and strongly reduces motility, pyocyanin synthesis and biofilm formation by P. aeruginosa (Bijtenhoorn et al., 2011). Quorum-quenching enzymes have been immobilized on surfaces and applied as anti-biofilm agents (Kim et al., 2011; Ng et al., 2011). Secondary metabolites may serve as intercellular pathogenic signals, which regulate numerous phenomena including biofilm formation (Dufour & Rao, 2011). Thus, metabolic intervention can be used to affect development and differentiation of biofilms. The green tea epigallocatechin gallate was shown to reduce both quorum sensing and biofilm development of P. aeruginosa through inhibiting the enoyl-acyl carrier protein reductase from the type II fatty acid synthesis pathway (Yang et al., 2010). A cyclopropane-containing fatty acid, lyngbyoic acid, from the marine cyanobacterium was shown to directly inhibit LasB enzymatic activity and reduce the production of pyocyanin and elastase in P. aeruginosa (Kwan et al., 2011).

However, it is not 100% specific or sensitive due to the presence of skip lesions. A positive biopsy is associated with a history of jaw claudication and diplopia, and temporal artery beading, prominence and tenderness on examination [18]. The European Vasculitis Study Group recommends the use of structured clinical assessment and that patients with ANCA-associated systemic vasculitis (AASV) are categorized according to disease severity to guide treatment decisions [19]. A number of clinical tools are available

to provide a detailed description of the HDAC inhibitor patient’s clinical status to aid diagnosis, treatment decisions and assist in measuring response to therapy including the BVAS, VDI DEI and the Five Factor Score (FFS). The BVAS is the current standard assessment tool to score disease activity in systemic vasculitis [20–23]. It includes 66 clinical features divided into nine organ systems. Each item has a numerical value according to its clinical relevance. Items are scored only if attributable to active vasculitis. This is based on clinical judgement and difficulties arise when distinguishing between ongoing active vasculitis and symptoms due to scars Selleck DAPT without active disease. Training in scoring is recommended to reduce interobserver variation by overscoring for infection or established disease features due to scars [24]. A simplified checklist of BVAS items is

shown in Table 1. While most patients are unlikely to have all the abnormalities listed, the spectrum covered by BVAS accounts for most of the features present in individual patients with different forms of vasculitis. The DEI is validated against the BVAS in Wegener’s granulomatosis [25] and scores the number of organ systems affected by medium vessel vasculitis. It can be calculated as a subset of BVAS items, and complements the BVAS score. The FFS evaluates disease activity at the time of diagnosis

and was developed to evaluate the initial severity of vasculitis [26]. It provides a prognostic indication and guide to the Reverse transcriptase intensity of treatment for patients with polyarteritis nodosa and Churg–Strauss syndrome [26,27]. It has also been applied to microscopic polyangiitis [28]. It scores the presence of serum creatinine above 1·58 mg/dl, proteinuria above 1 g/day, severe gastrointestinal tract involvement, cardiomyopathy and central nervous system involvement. It is not appropriate for follow-up, and is complementary to the BVAS. It is not entirely satisfactory, as the 5-year mortality is 12% with none of the risk factors. It is up to 46% with two or more risk factors and 45·95% when three or more of the five factors are present [26]. The VDI is a cumulative score describing long-term outcomes for vasculitis patients [29]. It contains 64 items in 11 organ-based systems and defines damage as an irreversible scar present longer than 3 months.

, 2005). Whilst reductions in bacterial

susceptibility have been observed following repeated exposure (Perron et al., 2003), HDPs are reportedly less likely to induce bacterial resistance, in comparison with conventional antibiotics (Steinberg et al., 1993; Ge et al., 1999; Mosca et al., 2000). Human salivary HDPs comprise various short-chain peptides that are commonly associated with mucosal surfaces and which exhibit broad-spectrum antimicrobial activity. They have been classified into three subcategories: defensins, histatins and cathelicidin LL37 (Boman, 2000); defensins and cathelicidins constitute < 1% of total salivary proteins, whilst histatins constitute c. 5% (van Nieuw Amerongen et al., 2009). AZD1208 order Oral HDPs are derived from various sources (Fig. 1) including neutrophils, which produce human neutrophil proteins (HNPs) (Selsted et al., 2009, 1992); gingival epithelia, which produce β defensins (Krisanaprakornkit et al., 1998); and salivary glands that secrete Tanespimycin research buy histatins (Imamura et al., 2009) (Fig. 1). HDP production levels may vary in a stimulus-dependent manner (reviewed by Dale & Fredericks, 2005; Gorr & Abdolhosseini, 2011) and their

biological functions include chemotaxis, where HNPs 1 and 2 for example attract monocytes (Territo et al., 2000); stimulation of epithelial cell turnover during wound healing; neutralization of bacterial lipopolysaccharides; antiviral activity, and direct antibacterial effects (Dimond et al., 2009). Antibacterial activity occurs by interaction with the cell envelope, causing progressive leakage of cell contents (Zasloff, 2002).

Previous investigations into the antimicrobial activity of human oral HDPs suggest that they exhibit varying potency against oral bacteria when pure cultures are exposed in endpoint susceptibility tests (Hancock & Devine, 2004; Dimond et al., 2009). The role of HDPs in influencing the microbiological composition 17-DMAG (Alvespimycin) HCl of the oral microbiota has been suggested by investigations of human subjects. For example, a single nucleotide polymorphism in Type I diabetics which reduces the efficacy of β defensin 1 has been associated with increased carriage of the pathogenic yeasts Candida glabrata and Candida tropicalis (Jurevic et al., 2003), whilst salivary proteomics of diabetic children has revealed a lack of histatins, which has been correlated with an increased periodontitis incidence (Cabras et al., 2010). In Chediak–Higashi syndrome, where individuals lack neutrophil azurophilic granules (a major source of HDPs), elevated susceptibility to bacterial and fungal infections has been reported (Ganz et al., 1988). Finally, levels of LL37 increase in response to the progression of periodontitis, and this HDP may therefore act as an inducible protective factor (Turkoglu et al., 1989).

Based on infant behavior in a structured laboratory situation, Q-sort techniques were used to rate three attachment markers: infant secure base behavior, interaction quality, and negative emotionality with mother. At 12 months, infant weight was positively related to interaction quality. At 18 months, infant iron FDA-approved Drug Library high throughput status was positively related to secure base behavior. This pattern of findings remained even after

statistically controlling for family socioeconomic status and maternal education. Our findings indicate that infant nutritional status is associated with markers of infant attachment and these associations are not restricted just to severely malnourished infants. “
“Infants and toddlers are often spoken to in the presence of background sounds, including speech from other talkers. Prior work has suggested that infants 1 year of age and younger can only recognize speech when it is louder than any distracters in the environment. The present study tests 24-month-olds’ ability to understand speech in a multitalker environment. Children were presented with a preferential-looking task in which a target voice told them to find one of two objects. At the same time, multitalker babble was presented as a distracter, at one of four signal-to-noise

ratios. Children showed some ability to understand speech and look at the appropriate referent at signal-to-noise ratios as low as −5 dB. Selleck Sirolimus These findings suggest that 24-month-olds are better able to selectively attend to an interesting voice in the context of competing distracter voices than are younger infants. There were significant correlations between individual children’s performance and their vocabulary size, but only at one of the four noise levels; thus, it does not appear that vocabulary size is the driving factor in children’s listening

improvement, although it may be a contributing factor to performance in noisy environments. “
“This study investigated two aspects of mother–child relationships—mothers’ mind-mindedness and infant attachment security—in relation to two early aspects of children’s theory of mind development (ToM). Sixty-one mother–child dyads (36 girls) participated in testing phases at 12 (T1), 15 (T2), and 26 months of age (T3), allowing for assessment of maternal mind-mindedness (T1), infant attachment (T2), and child ToM MYO10 understanding (T3). Results indicated that children’s understanding of discrepant desires and visual perspectives was positively related to their mothers’ earlier use of appropriate mind-related comments in certain contexts. Furthermore, more securely attached boys, but not girls, performed better on a task requiring comprehension of their mothers’ visual perspective. Hence, the links previously found between competent parenting and older children’s ToM performance appear to extend, to a certain degree, to toddlers’ first manifestations of ToM understanding. “
“Means-end actions are an early-emerging form of problem solving.

We used antisense transfection, over-expression, or knock-down of IL-32 to assess the effects of the HPV-16 E7 oncogene on IL-32 expression in

cervical cancer cells. Cyclo-oxygenase 2 (COX-2) inhibitor treatment PS-341 molecular weight was conducted, and the expression levels, as well as the promoter activities, of IL-32 and COX-2 were evaluated in human HPV-positive cervical cancer cell lines. E7 antisense treatment reduced the expression levels and promoter activities of COX-2, which is constitutively expressed in HPV-infected cells. Constitutively expressed IL-32 was also inhibited by E7 antisense treatment. Moreover, IL-32 expression was blocked by the application of the selective COX-2 inhibitor, NS398, whereas COX-2 over-expression resulted in increased IL-32 levels. These results show that the high-risk variant of HPV induces IL-32 expression via E7-mediated COX-2 stimulation. However, E7 and COX-2 were down-regulated in the IL-32γ over-expressing cells and recovered by IL-32 small interfering RNA, indicating that E7 and COX-2 were feedback-inhibited by IL-32γ Silmitasertib cell line in cervical cancer cells. Cervical cancer is the second most frequent cause of cancer death in women worldwide, and molecular epidemiological studies

have demonstrated clearly that human papillomavirus (HPV) is a prerequisite for the development of cervical carcinoma.1,2 Approximately 200 different HPV types have been characterized, Carnitine palmitoyltransferase II and the two most frequent high-risk HPV genotypes, HPV-16 and HPV-18, account for at least 50% of cervical cancers worldwide.3,4 Several HPV-16 type oncoproteins expressed during the early stage of infection have been associated with oncogenicity; specifically, E5, E6 and E7 have been demonstrated to contribute to the maintenance

of malignant cervical cancer phenotypes.5 The function of the E5 oncoprotein-activating epidermal growth factor receptor remains to be clearly elucidated, and E6 promotes the degradation of p53 via its interaction with E6AP.6 The E7 oncoprotein binds to the pRb retinoblastoma protein, and disrupts its formation of a complex with the E2F transcription factor in the G1 phase of the cell cycle. E7 also binds to and activates cyclin complexes such as cyclin-dependent kinase cdk2 and cyclin A, which control cell cycle progression.7 The viral genes E6 and E7 found in a specific subset of HPVs are invariably expressed in HPV-positive cervical cancer cells.8 It has also been previously reported that the E7 gene of HPV-16 triggers a cellular immunosuppression and profoundly enhances the release of angiogenic cytokines by macrophages or dendritic cells.9 The E6 and E7 oncogenes also inhibit the IL-18-mediated immune response, which carries out crucial functions in host defence mechanisms against infection and cancer.

Our study was undertaken to establish the kinetics of sCD14 concentrations in BALF in patients with allergic asthma following segmental allergen challenge at different time points (10 min, 18, 42 and 162 h). Moreover, the study attempted to establish stimuli involved in sC14 production and/or shedding, respectively, such as LPS,

which has been shown to increase sCD14 levels in vitro [21] and in vivo [22] and leukotriene D4 (LTD4), which has been implicated in allergic inflammation and the pathogenesis of airway hyperresponsiveness [34]. Furthermore, LTD4 has been shown to induce TNF-α release from macrophages [35] that was inhibited by the leukotriene-receptor antagonist (LTRA) Verlukast [35]. IL-17 has been associated with an Ivacaftor order increase in IL-8 and GM-CSF production from bronchial epithelial cells [36], the regulation of ICAM-1 expression [37] and the selective recruitment of neutrophils [38]. Moreover, it plays a role in the LPS-induced chemotaxis of neutrophils into the airways after LPS inhalation [39] and increases after organic dust inhalation in healthy subjects [40]. We therefore investigated whether IL-17 might influence sCD14 production in cell cultures. Eighteen patients with allergic asthma (nine men and nine women), mean age 26.3 ± 5.4 years with a duration of asthma for more than 2 years (mean duration 11.7 ± 5.2 years), were studied. Bronchial asthma had previously GDC-0941 cell line been diagnosed

by an independent physician. Each patient had a positive skin prick test to either birch pollen (n = 8), rye pollen (n = 3), or house dust mite allergen (n = 7) extracts (Allergopharma, Reinbek, Germany), and all had either elevated total IgE levels (293.6 ± 233.1 kU/l) and / or elevated specific IgE levels (32.2 ± 49.1 kU/l) (Kabi Pharmacia CAP System, Uppsala, Sweden) to their respective allergen as well as a history of reversible bronchoconstriction after inhalation of these particular allergens. C59 There was no history or clinical evidence in any of the patients, suggesting a respiratory tract infection prior to or at the time of segmental

allergen challenge. All patients were non-smokers. Baseline FEV1 (forced expiratory volume in 1 s) was 3.8 ± 0.96 l (94.9 ± 13.1% of predicted, normal values [41]). All patients received inhaled ß2-agonist therapy on an as needed basis except for three patients who did not require any medication. In addition, five patients had inhaled corticosteroids and three had inhaled cromoglycate. Both were withheld at least 10 days prior to entry into the study. All patients gave their written informed consent. The study protocol was approved by the local Ethics Committee. Prior to the segmental allergen provocation, patients underwent an inhaled allergen challenge as previously described [29, 42] to establish dual bronchial reactions to the inhaled allergen and to determine the individual PD20FEV1 for the respective allergen.

62 Evidence for active regional regulation against an autoimmune response to these antigens has been obtained in the study of mice that have undergone thymectomy within 3 days of birth.63 In certain strains, neonatal thymectomy leads to the development of orchitis. Regulatory T lymphocytes have been identified within the interstitium of the testes in these animals,64 and autoimmune orchitis can be prevented by infusion of normal T cells. T cells

are also present within seminal fluid and gain entry of the female reproductive tract at coitus.42 It has been speculated that these cells could play roles in altering the female reproductive tract response to spermatozoa. Proteasomal inhibitors These same cell-medicated immune perturbations might play roles in the pathogenesis of HIV transmission. Evidence has accumulated of the complexity of seminal fluid,

its components that perturb the female reproductive tract, altering its ability to mount an immune response against spermatozoa (foreign invading cells of another individual), and facilitating the implantation of embryos within the endometrium. These same factors that promote the establishment of pregnancy, however, may also make the female reproductive tract susceptible to invasion not only by spermatozoa but viruses, playing a significant role in the male-to-female transmission of HIV. An understanding of the histology, anatomy, and immunology of the male reproductive tract is essential in understanding its role in Amino acid the pathogenesis of HIV. “
“The molecular mechanisms that underlie poor birth outcomes in malaria during pregnancy remain poorly defined. To assess the role of host immune responses, mice known selleck kinase inhibitor to respond differentially

to Plasmodium chabaudi AS infection were studied. Following infection at day 0 of pregnancy, A/J mice developed significantly higher parasitemia than C57BL/6 (B6) mice and succumbed to infection. Both strains had evidence of parasite accumulation in the placenta at mid-gestation and aborted, with significantly higher embryo loss in infected A/J mice on day 9. While infection-induced systemic tumour necrosis factor (TNF) and interleukin (IL)-1β in the latter were significantly higher at day 11, day 10 IL-10 levels were higher in B6 mice. No differences in the levels of splenic lymphocyte subsets, neutrophils or monocytes between infected pregnant A/J and B6 mice were observed, with most cell types expanding in response to infection regardless of pregnancy. Antibody ablation of TNF exacerbated infection in A/J mice and did not ameliorate pregnancy outcome. Thus, malaria induces poor pregnancy outcome in both the mouse strains in the context of quantitatively different systemic inflammatory responses. Further evaluation of the roles of soluble and cellular immune components, particularly at the uteroplacental level, will be required to define the most critical pregnancy-compromising mechanisms.