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PubMed2002

Hemolytic bacteria in water from the dental air-water syringe.

PURPOSE: The purpose of this pilot study was to determine whether aquatic bacteria expressing hemolysis, a classical virulence factor of pathogenic bacteria, could be found in water flowing from the dental air-water syringe (AWS). METHODS: Water samples were collected from the AWS in each of five dental operatories, and a control sample was collected from the cold-water tap in the sink adjacent to one of the dental operatories. Water samples were plated on NWRI agar to enumerate aquatic heterotrophic bacteria and on Tryptic Soy Blood (TSB) agar to enumerate hemolytic bacteria. After incubation, plates were counted to determine total colony-forming units per mL of AWS water. In addition, TSB plates were examined for hemolytic colonies, which were counted if present. RESULTS: AWS water samples contained an average of 9.4 x 10(4) colony-forming units cfu/mL on NWRI agar, and 1.3 x 10(4) cfu/mL on TSB agar. The control sample from the cold-water tap contained 2.5 x 102 and 50 cfu/mL on NWRI and TSB agars, respectively. Four out of five AWS water samples contained hemolytic bacteria, with an average hemolytic count of 3.2 x 10(3) hemolytic cfu/mL on TSB agar. No hemolytic bacteria were detected from tap water. Most hemolytic organisms exhibited alpha-hemolysis although beta-hemolytic colonies were seen. CONCLUSIONS: AWS water can contain hemolytic bacteria--such bacteria express a virulence factor and therefore may be regarded as potential pathogens. According to a Medline search conducted April 23, 2002, this is the first report of hemolytic bacteria from dental unit water.

Bacteria↗
PubMed1985

The fine specificity of IgG antiguanosine antibodies in systemic lupus erythematosus.

The antigen specificity, isotype, and subclass of antinuclear antibodies may be related to their pathogenicity in systemic lupus erythematosus (SLE). Our laboratory found that IgG antibodies that bound the nucleoside, guanosine, occurred frequently in SLE patients. In contrast, sera from healthy subjects contained IgM but not IgG antiguanosine antibodies. The present studies were designed to characterized the fine specificity of IgG antiguanosine antibodies in SLE and compare them with IgM antiguanosine antibodies in normal sera. Serum antinuclear antibodies from six healthy subjects and six SLE patients were isolated by affinity binding to guanosine and measured by an enzyme-linked immunosorbent assay (ELISA). IgM in normal sera, and both IgM and IgG in SLE sera bound guanosine. IgM antiguanosine antibodies in normal sera were polyspecific and bound other nucleosides and 1-methylguanosine but not denatured DNA (ssDNA). In contrast, IgG antiguanosine antibodies from the SLE patients bound guanosine and ssDNA but not other nucleosides or 1-methylguanosine. SLE IgM antiguanosine antibodies had the same fine specificity and bound guanosine and ssDNA but not any of the other nucleosides. These results suggest that SLE IgG and IgM antiguanosine antibodies have fine specificity in contrast to the polyspecific IgM antibodies in normal sera. In addition, subclass analysis indicated that all SLE patients had either IgG1 or IgG3 subclass of antiguanosine antibodies that bind complement. Characterizing the isotype, subclass, and fine antigen specificity of antiguanosine antibodies should assist in evaluating their potential pathogenicity in SLE.

Antibodies, Antinuclear↗
PubMed1993

Approaches for studying the pathogenic T cells in autoimmune patients.

Our provisional conclusions from this work are as follows. (1) For screening responses of established lines, native human AChR is not prohibitively scarce, especially if it is concentrated onto beads, and class II-transfected TE671 cells may be useful too; both may give vital evidence of AChR-specificity, but it is still crucial to confirm that with synthetic peptides. (2) For mapping epitopes, panels of full-length and shorter recombinant human polypeptides, and of synthetic peptides, are invaluable complementary material: longer peptides tend to stimulate particularly strongly. (3) Initial selection with pooled synthetic peptides can easily generate interesting lines from both patients and controls, but they may depend on the artificial processing sites that are an inevitable consequence of arbitrarily chosen start and stop points. Of course, these might conceivably be employed in unusual antigen-presenting cells (such as thymic myoid cells), so we cannot totally dismiss such "cryptic" epitopes. This system can sometimes select T cells responding to "natural" epitopes too, as now reported for tetanus toxin. Nevertheless, for these and other reasons, at present, we strongly favor using the longest human recombinant material possible, because it is apparently processed more naturally. This must be combined with rigorous screening for reactivity to E. coli-derived contaminants plus concomitant mapping of epitopes as above. Use of intact AChR for initiating lines may yet become feasible. (4) The T cells thus isolated and characterized so far are proving to be heterogeneous in the epitopes and presenting class II molecules they recognize, and in their T-cell receptor gene usage. It is premature to claim key myasthenogenic epitopes or clonotypes, but HLA-DR3 and the linked -DQw2 do not appear to monopolize presentation. (5) Assessing the disease-relevance of these T cells is a separate problem, highlighted by their apparent similarity in healthy controls. In the meantime, to test their potential pathogenicity, we are assaying their cytokine profiles and ability to help specific antibody production in vitro. In the hope that they do prove to be relevant, we are also using some of them to test possible therapeutic strategies that might prove applicable in the patients.

Amino Acid Sequence↗
PubMed1990

Epidemiology of bacterial pathogens associated with infectious diarrhea in Djibouti.

During a survey examining the causes of diarrhea in the East African country of Djibouti, 140 bacterial pathogens were recovered from 209 diarrheal and 100 control stools. The following pathogens were isolated at comparable frequencies from both diarrheal and control stools: enteroadherent Escherichia coli (EAEC) (10.6 versus 13%), enterotoxigenic E. coli (ETEC) (11 versus 10%), enteropathogenic E. coli (EPEC) (7.7 versus 12%), Salmonella spp. (2.9 versus 3%), and Campylobacter jejuni-C. coli (3.3 versus 5%). Surprisingly, the EAEC strains isolated did not correspond to well-recognized EPEC serogroups. No Yersinia spp., enteroinvasive E. coli, or enterohemorrhagic E. coli were isolated during the course of this study. Only the following two genera were recovered from diarrheal stools exclusively: Shigella spp. (7.7%) and Aeromonas hydrophila group organisms (3.3%). Shigella flexneri was the most common Shigella species isolated. Patients with Shigella species were of a higher average age than were controls (27 versus 13 years), while subjects with Campylobacter or Salmonella species belonged to younger age groups (2.6 and 1.6 years, respectively). Salmonella cases were more often in females. Shigella diarrhea was associated with fecal blood or mucus and leukocytes. ETEC was not associated with nausea or vomiting. Anorexia, weight loss, and fever were associated with the isolation of Salmonella and Aeromonas species. EAEC, ETEC, EPEC, and Shigella species were resistant to most drugs used for treating diarrhea in Africa, while the antibiotic most active against all bacteria tested was norfloxacin. We conclude that in Djibouti in 1989, Shigella and Aeromonas species must be considered as potential pathogens whenever they are isolated from diarrheal stools and that norfloxacin should be considered the drug of choice in adults for treating severe shigellosis and for diarrhea prophylaxis in travelers.

Diarrhea↗
PubMed2002

Proatherogenic and proinflammatory properties of immune complexes prepared with purified human oxLDL antibodies and human oxLDL.

Immune complexes (IC) prepared with human low density lipoprotein (LDL) and rabbit LDL antibodies induce foam cell transformation of human macrophages and activate the release of proinflammatory mediators by human macrophages and THP-1 cells. Because the affinity of human oxidized LDL (oxLDL) antibodies is lower than that of rabbit antibodies, IC formed with human antibodies could have limited pathogenic potential. Immune complexes prepared with human oxidized LDL (oxLDL) and purified human oxLDL antibodies (predominantly of the IgG1 and IgG3 isotypes) were presented to THP-1 cells using two protocols previously described in studies of the properties of LDL-IC prepared with rabbit antibodies. OxLDL/human oxLDL antibody IC immobilized by adsorption to red blood cells (RBC) induced the release of significantly higher levels of TNF from THP-1 cells (872-313 pg/ml) than oxLDL adsorbed to RBC (461-75.6 pg/ml) and caused a higher degree of cholesterol ester accumulation in the same cells (5.4-0.77 in cells incubated with IC-coated RBC vs 1.99-1.16 in oxLDL-coated RBC). Insoluble IC prepared with oxLDL/human oxLDL antibody were even more effective in promoting intracellular accumulation of cholesterol in THP-1 cells (total cholesterol = 53.8-13.5 and cholesterol esters = 24.0-7.2 mg/l in THP-1 cells incubated with insoluble IC (200 micrograms) vs total cholesterol = 32.4-8.2 and cholesterol esters = 7.7 +/- 2.8 micrograms/l in THP-1 cells incubated with an identical concentration of oxLDL) and also induced the release of TNF. Thus we have demonstrated that IC prepared with human oxLDL and human oxLDL antibodies have the same atherogenic and proinflammatory properties as IC prepared with human LDL and rabbit LDL antibodies. This strongly supports the concept that modified LDL-IC present in circulation and/or tissues play an important pathogenic role in arteriosclerosis.

Adult↗
PubMed1996

Isolation and characterization of human antioxidized LDL autoantibodies.

Autoantibodies to oxidized LDL have been reported in normal subjects and in patients with arteriosclerosis, but their possible pathogenic role is not yet well defined. One important problem is the existence of contradictory data reported by different groups concerning the associations between antioxidized LDL autoantibodies and the presence or progression of arteriosclerotic lesions. Such contradictions led us to decide to isolate and characterize antioxidized LDL antibodies by affinity chromatography with the use of oxidized LDL cross-linked to Sepharose. Antioxidized LDL antibodies were isolated from selected serum samples obtained from eight subjects. Seven of them (six patients and one control subject) had high levels of antioxidized LDL antibody during screening. The other subject, a healthy volunteer, had a low level of antibody. All purified antibodies contained IgG (of subclasses 1 and 3) as the predominant isotype and were primarily specific for oxidized LDL but showed some cross-reactivity with malondialdehyde-modified LDL and native LDL. Two of the purified antibodies cross-reacted with cardiolipin. We determined average dissociation constants for the antioxidized LDL antibodies purified from five individuals, which varied between 2.4 x 10(-7) and 7.5 x 10(-7) mol/L, whereas the average dissociation constant of rabbit hyperimmune anti-LDL antibody was determined to be 2.7 x 10(-8) mol/L. In conclusion, we have purified human autoantibodies reactive with oxidized LDL that appear to be predominantly of moderate-to-low affinity and of variable cross-reactivity. The predominance of IgG1 and IgG3 antibodies is significant from the standpoint of potential pathogenicity, since these two subclasses activate the classic complement pathway system and have the highest binding affinities for Fc gamma receptors on phagocytic cells.

Adult↗
PubMed1991

Ammonium decreases human polymorphonuclear leukocyte cytoskeletal actin.

Ammonium, a weak base produced as a metabolic by-product of urea metabolism by bacterial pathogens, inhibits a variety of motile polymorphonuclear leukocyte (PMN) functions. It was initially assumed that the mechanism of leukocyte inhibition was due to cytoplasmic alkalinization. However, while it is clear that ammonium can effect cytoplasmic alkalinization, current data indicate that alterations in chemotaxis, degranulation, and receptor recycling occur independently of cytoplasmic alkalinization. Since these are motility-related events, we examined the possibility that alterations in cytoskeletal actin may account for the effects of ammonium on PMN function. The results indicate that ammonium can inhibit degranulation, decrease cytoskeletal actin, and increase actin depolymerization rates. These findings are supported by five lines of evidence. First, formylmethionyl-leucyl-phenylalanine (fMLP)-induced elastase release was inhibited by 85% +/- 3% in the presence of ammonium, and ammonium by itself did not stimulate elastase release. Second, ammonium treatment of resting PMNs caused a rapid 38% +/- 6% decrease in cytoskeletal actin. Third, ammonium treatment accelerated the fMLP-induced depolymerization phase of the cytoskeletal actin transient by 150% +/- 12%. Fourth, in resting PMNs treated with cytochalasin B or D, ammonium induced a 21% +/- 4% and a 25% +/- 5% decrease in cytoskeletal actin, respectively. Conversely, ammonium did not affect the ability of the cytochalasins to inhibit an fMLP-induced cytoskeletal actin transient. Fifth, pertussis toxin treatment of neutrophils did not affect the ammonium-stimulated decrease in cytoskeletal actin. These results suggest that ammonium can inhibit neutrophil function by altering cytoskeletal actin and therefore provide new information regarding potential pathogenic mechanisms for bacterial pathogens.

Actins↗
PubMed2002

Depletion of Vbeta5.2/5.3 T cells with a humanized antibody in patients with multiple sclerosis.

A potentially pathogenic expansion of T cells expressing T cell receptor (TCR) Vbeta5.2/5.3 has been demonstrated in patients with multiple sclerosis (MS). A humanized antibody (ATM-027) directed against these T cells has been developed to further investigate the role of this subpopulation of T cells in MS. The pharmacokinetics/dynamics and safety of ATM-027 (0.3-300 mg intravenously over 30 min) were investigated in 14 patients with MS. The effect of treatment on cytokine expression and autoreactivity to peptides of myelin basic protein (MBP) was also studied. ATM-027 was well tolerated and raised no safety concerns. Clearance of the antibody was low and elimination half-life was approximately 3 weeks. The majority of the target Vbeta5.2/5.3 expressing T cells were depleted for at least 18 months. The small remaining fraction of target cells showed a marked decrease in their TCR expression, which was recovered within 8 months. The numbers of peripheral blood mononuclear cells (PBMCs) with spontaneous expression of IFN-gamma was decreased at 72 h and 8 weeks after treatment, whilst no clear effects on TNF-alpha, IL-4, IL-10, TGF-beta expression were observed. There was also a significant decrease in the number of PBMCs producing IFN-gamma in response to MBP peptide 80-102. We conclude that long-term depletion of T cells expressing defined Vbeta subgroups in MS patients is feasible using selective immunotherapy. The selective depletion of Vbeta5.2/5.3 expressing T cells in this study resulted in a decrease in potentially disease promoting anti-MBP reactivity and pro-inflammatory cytokine production.

Adolescent↗
PubMed1998

Multiplex PCR for the detection of Mycoplasma fermentans, M. hominis and M. penetrans in cell cultures and blood samples of patients with chronic fatigue syndrome.

A multiplex polymerase chain reaction (PCR) was initially developed to detect the presence of mycoplasma genus DNA sequences in cell cultures and to differentiate between three human pathogenic mycoplasma species simultaneously. The assay in turn, proved to be a useful tool for the detection of mycoplasma infection in human DNA samples. One set of oligonucleotide primers which are specific for a highly conserved region among all members of the genus mycoplasma along with three other primer sets which are specific for Mycoplasma fermentans, Mycoplasma hominis andMycoplasma penetrans species were used in this assay. The sensitivity of detection was determined by infecting peripheral blood mononuclear cells (PBMC) of healthy individuals with known bacterial copy numbers from each species, extracting the DNA, and subjecting 1 microgram of DNA from each sample to 40 cycles of amplification. By using agarose gel electrophoresis the detection level was determined to be 7, 7, 9 and 15 mycoplasma cells per microgram of human genomic DNA for M. genus,M. fermentans, M. hominis and M. penetrans, respectively. The assay was applied to DNA extracted from the PBMCs of individuals suffering from chronic fatigue syndrome (CFS) (n=100) as determined by the Center for Disease Control (CDC) criteria, and compared to healthy individuals (n=100). The percentage of M. genus infection was found to be 52% in CFS patients and only 15% in healthy individuals. Mycoplasma fermentans, M. hominis andM. penetrans were detected in 32, 9 and 6% of the CFS patients while they were detected in 8, 3 and 2% of the healthy control subjects, respectively. This assay provides a rapid and cost efficient procedure to screen either cell cultures or clinical samples for the presence of three potentially pathogenic species of mycoplasma with a high level of sensitivity and specificity.

Blood↗
PubMed1998

Biopersistence of synthetic vitreous fibers and amosite asbestos in the rat lung following inhalation.

Fiber biopersistence as a major mechanism of fiber-induced pathogenicity was investigated. The lung biopersistence of 5 synthetic vitreous fibers (SVFs) and amosite asbestos was evaluated using the rat inhalation model. In contrast to several previous studies, this study examined fibers that dissolve relatively slowly in vitro at pH 7.4. Fisher rats were exposed for 5 days by nose-only inhalation to refractory ceramic fiber (RCF1a), rock (stone) wool (MMVF21), 2 relatively durable special application fiber glasses (MMVF32 or MMVF33), HT stonewool (MMVF34), amosite asbestos, or filtered air. Lung burdens were analyzed during 1 year post-exposure. Fiber aerosols contained 150-230 fibers/cc longer than 20 micrometer (>20 micrometer). On post-exposure Day 1, long-fiber lung burdens for the 6 test fibers were similar (12-16 x 10(5) fibers/lung >20 micrometer). After 1 year, the percentage of fibers >20 micrometer remaining in the lung was 0.04-10% for SVFs but 27% for amosite. Lung clearance weighted half-times (WT1/2) for fibers >20 micrometer were 6 days for MMVF34, 50-80 days for the other 4 SVFs, and >400 days for amosite. This study and 3 previous studies demonstrate a broad range of biopersistences for 19 different SVFs and 2 asbestos types. Ten of these fibers also have been (or are being) tested in chronic inhalation studies; in these studies, the very biopersistent fibers were carcinogenic (amosite, crocidolite, RCF1, MMVF32, and MMVF33), while the more rapidly clearing fibers were not (MMVF10, 11, 21, 22, and 34). These studies demonstrate the importance of biopersistence as an indicator of the potential pathogenicity of a wide range of fiber types.

Aerosols↗
PubMedDate not supplied

Gastrointestinal surface protection and mucosa reconditioning.

BACKGROUND: There is increasing evidence that preservation of the ecology of the gastrointestinal tract and the surface protection system--surfactants, mucus, and fiber--is important for the outcome in postoperative trauma patients, patients after bone marrow and liver transplantation, and patients with HIV or AIDS. Approximately 50% of the nourishment of the small intestine and > 80% of the nourishment of the large intestine comes from the lumen. This is especially deleterious to the large intestine. Within less than a week of intestinal starvation--even in the presence of intense parenteral nutrition--a mucosal atrophy is observed, promoting translocation of potentially pathogenic microorganisms. Enteral nutrition is crucial to the outcome in many of these conditions. If however, such a nutrition is based on simple carbohydrates, peptides, amino acids, or fatty acids, most of the nutrition administered will be absorbed in the upper gastrointestinal tract. Complex fibers and proteins can be regarded as nutrients especially destined to the lower gastrointestinal tract. They are fermented by the probiotic flora, normally colonizing the colonic mucosa, and the necessary nutrients: short-chain fatty acids and amino acids such as arginine and glutamine are produced at the level of the colonic mucosa. Careless antibiotic treatment reduces or eliminates this flora, induces local mucosal starvation, and makes the patients vulnerable to opportunistic infections and microbial intestinal translocation. METHODS AND RESULTS: In this review the role of the different ingredients of the surface protection system are discussed. A program to recondition the intestines, particularly the colonic mucosa by resupply of species-specific lactobacilli, surfactants, amino acids (especially glutamine), and oat fiber (beta-glucans) is suggested. Extensive experience in animal models and early experience in a patient population are summarized and discussed. Oat has been chosen as a substrate for fermentation because it contains 100 times more of membrane lipids (surfactants) than any other food, has a favorable amino acid pattern (rich in glutamine), and is rich in water-soluble, fermentable-fiber beta-glucans. More than 1000 isolates of human-specific lactobacilli have been studied. Some strains, especially those of plantarum type, have proven effective in colonizing the colonic mucosa, suppressing the potentially pathogenetic flora, and may have other probiotic effects as well. CONCLUSION: A totally new enteral formula has been designed based on probiotic bacteria and fiber and aimed at colonizing the intestinal mucosa with a local probiotic effect and fermentation of fiber.

Animals↗
PubMed2002

Biofilm production by isolates of Candida species recovered from nonneutropenic patients: comparison of bloodstream isolates with isolates from other sources.

Biofilm production has been implicated as a potential virulence factor of some Candida species responsible for catheter-related fungemia in patients receiving parenteral nutrition. We therefore compared clinical bloodstream isolates representing seven different Candida species to each other and to those from other anatomical sites for the capacity to form biofilms in glucose-containing medium. Potential associations between the capacity to form biofilms and the clinical characteristics of fungemia were also analyzed. Isolates included the following from nonneutropenic patients: 101 bloodstream isolates (35 C. parapsilosis, 30 C. albicans, 18 C. tropicalis, 8 C. glabrata, and 10 other Candida species isolates) and 259 clinical isolates from other body sites (116 C. albicans, 53 C. glabrata, 43 C. tropicalis, 17 C. parapsilosis, and 30 other Candida species isolates). Organisms were grown in Sabouraud dextrose broth (SDB) containing a final concentration of 8% glucose to induce biofilm formation, as published previously. Biofilm production was determined by both visual and spectrophotometric methods. In this medium, biofilm production by C. albicans isolates was significantly less frequent (8%) than that by non-C. albicans Candida species (61%; P < 0.0001). The overall proportion of non-C. albicans Candida species isolates from the blood that produced biofilms was significantly higher than that of non-C. albicans Candida isolates obtained from other sites (79% versus 52%; P = 0.0001). Bloodstream isolates of C. parapsilosis alone were significantly more likely to be biofilm positive than were C. parapsilosis isolates from other sites (86% versus 47%; P = 0.0032). Non-C. albicans Candida species, including C. parapsilosis, were more likely to be biofilm positive if isolates were derived from patients whose candidemia was central venous catheter (CVC) related (95%; P < 0.0001) and was associated with the use of total parenteral nutrition (TPN) (94%; P < 0.005). These data suggest that the capacity of Candida species isolates to produce biofilms in vitro in glucose-containing SDB may be a reflection of the pathogenic potential of these isolates to cause CVC-related fungemia in patients receiving TPN.

Biofilms↗
PubMed1994

Experimental autoimmune panencephalitis and uveoretinitis transferred to the Lewis rat by T lymphocytes specific for the S100 beta molecule, a calcium binding protein of astroglia.

The pathogenic potential of autoimmune T cell responses to nonmyelin autoantigens was investigated in the Lewis rat using the astrocyte-derived calcium binding protein S100 beta, as a model nonmyelin autoantigen. The Lewis rat mounts a vigorous RT1B1 (major histocompatibility complex class II) restricted autoimmune response to an immunodominant S100 beta epitope (amino acid residues 76-91). The adoptive transfer of S100 beta-specific T cell lines induced a severe inflammatory response in the nervous system, but only minimal neurological dysfunction in naive syngeneic recipients. The inability of S100 beta-specific T cell transfer to induce severe disease was associated with a decreased recruitment of ED1+ macrophages into the central nervous system (CNS) in comparison with that seen in severe experimental autoimmune encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein (MBP)-specific T line cells. Moreover, unlike encephalitogenic MBP-specific T cell lines, S100 beta-specific T cell lines exhibited no cytotoxic activity in vitro. Histopathological analysis also revealed striking differences in the distribution of inflammatory lesions in MBP- and S100 beta-specific T cell-mediated disease. In contrast to the MBP paradigm, S100 beta-specific T cell transfer induces intense inflammation not only in the spinal cord, but throughout the entire CNS and also in the uvea and retina of the eye. In view of the distribution of lesions throughout the grey and white matter of the CNS we propose to term this new model experimental autoimmune panencephalomyelitis (EAP) to differentiate it from EAE. These experiments demonstrate for the first time that nonmyelin CNS autoantigens can initiate a pathogenic autoimmune T cell response, although the nature of the target autoantigen profoundly influences the clinical and histopathological characteristics of the resulting autoimmune disease. This is not simply a consequence of the distribution of the autoantigen, as both MBP and S100 beta are coexpressed in many areas of the CNS, but reflects differences in the capacity of different regions of the CNS to process and present specific autoantigens. This new model of T cell-mediated autoimmune CNS disease exhibits a number of similarities to multiple sclerosis (MS), such as its mild clinical course and the involvement of areas of the brain and eye, which are absent in myelin-mediated models of EAE. Nonmyelin autoantigens may therefore play an unexpectedly important role in the immunopathogenesis of inflammatory diseases of the CNS.

Amino Acid Sequence↗
PubMed1996

Myocarditis in mice and guinea pigs experimentally infected with a canine-origin Borrelia isolate from Florida.

OBJECTIVE: To characterize the pathogenic potential of a unique Borrelia isolate obtained from a dog from Florida (FCB isolate). DESIGN: Prospective experimental infection. ANIMALS: 32 preweanling Swiss Webster mice and 12 adult male Hartley guinea pigs were injected intraperitoneally with 10(5) spirochetes. PROCEDURE: Mice were used as controls and blood recipients, and at 3- to 4-day intervals, 1 control mouse and 2 infected mice were necropsied, tissues were cultured, and a recipient mouse was inoculated with blood. Guinea pigs were randomized to 4 groups and inoculated intradermally with 10(0), 10(2), 10(3), or 10(4) spirochetes. For 48 days, clinical, hematologic, serologic, and microbiologic tests were performed on them, after which they were necropsied. RESULTS: In mice, spirochetemia was detectable between postinoculation days (PID) 3 and 13, and seroreactivity to homologous antigen was detectable during PID 10 through 31. Compared with control mice, infected mouse spleens were 2 to 3 times larger. Histologic lesions included lymphoid hyperplasia, neutrophilic panniculitis, epicarditis, and myocarditis, with intralesional spirochetes detected from PID 3 through 6. During PID 10 through 31, nonsuppurative epicarditis developed. Signs of illness and hematologic abnormalities were not observed in guinea pigs, despite isolating spirochetes from blood during PID 7 to 27. When necropsied on PID 48, histologic lesions included lymphoid hyperplasia and lymphocytic plasmacytic epicarditis. CONCLUSIONS: The FCB isolate causes spirochetemia, lymphoid hyperplasia, dermatitis, and myocardial injury in Swiss Webster mice and can be transmitted by blood inoculation. In Hartley guinea pigs, the isolate causes spirochetemia, lymphoid hyperplasia, and epicarditis. Documentation of disease in mice, guinea pigs, and, presumably, dogs raises the level of concern that the FCB isolate might be pathogenic for man and other animal species.

Animals↗
PubMed2006

Probiotic treatment of collagenous colitis: a randomized, double-blind, placebo-controlled trial with Lactobacillus acidophilus and Bifidobacterium animalis subsp. Lactis.

BACKGROUND: Probiotic treatment may be effective in diseases involving gut microflora and intestinal inflammation. In collagenous colitis (CC), a potential pathogenic role of the gut microflora has been proposed. The effect of probiotic treatment in CC is unknown. Our aim was to investigate the clinical effect of treatment with Lactobacillus acidophilus LA-5 and Bifidobacterium animalis subsp. lactis BB-12 (AB-Cap-10) in patients with CC. MATERIALS AND METHODS: Patients with CC and diarrhea were in a double-blind placebo-controlled study randomized (2:1) to AB-Cap-10 or placebo for 12 weeks. The primary end point was reduction in bowel frequency per week of >or=50%. Secondary end points were changes in bowel frequencies, stool consistency, stool weight, histopathology, and abdominal bloating and pain. RESULTS: Twenty-nine patients were randomized: 21 to probiotics and 8 to placebo. Reduction in bowel frequency per week of >or=50% occurred in 6 of 21 (29%) and in 1 of 8 (13%) patients receiving probiotic and placebo, respectively (P = 0.635). No differences between treatments were observed regarding the secondary end points. Post hoc analysis showed a median reduction in bowel frequency per week from 32 (range 18-84) to 23 (range 11-56; P < 0.005), a reduction in number of days with liquid stools per week from 6 days (range 0-7 days) to 1 day (range 0-7 days; P < 0.005), and an increase in number of days with solid stools per week (P < 0.05) in the AB-Cap-10 group. CONCLUSIONS: AB-Cap-10 had no significant effect on the chosen end points. Post hoc analysis demonstrated amelioration of clinical symptoms in the AB-Cap-10 group, indicating that probiotic treatment may potentially influence the disease course of CC.

Adult↗
PubMed1996

Serological IgG, IgM and IgA diagnosis and prognosis of mycobacterial diseases in routine practice.

The routine diagnosis of tuberculosis and other mycobacterial diseases based on organism identification was completed during a period of one year in 730 patients, with serological IgG, IgM and IgA determination of antibodies against antigen 60 from M. bovis , strain BCG. The analysis was performed on 10 groups of patients consisting of 1) inflammatory diseases of the respiratory tract, 2) pericarditis, myocarditis, lymphadenitis and CNS diseases, 3) chronic non-inflammatory diseases of kidneys, liver and pancreas, 4) non-inflammatory diseases of the heart, sarcoidosis and pneumoconiosis, 5) tumor, 6) healthy people with TB contact, 7) inactive TB, 8) culture-positive pulmonary and extra-pulmonary TB, 9) culture-negative TB and extra-pulmonary TB, and 10) potentially pathogenic mycobacteria. The specificity of the test (100% negative cases in Group 6, composed of healthy people) is estimated at about 90%, in accordance with determinations made in other laboratories. In non-tuberculous patients, the specificity varied according to the analysed groups. Group 1 was largely unspecific for IgM (76% positives) but the specificity was acceptable for IgG (6.2% positives ) and IgA (7.4% positives). Group 2 was similar to Group 1. Group 3 was associated with positive IgA titers. Group 4 was only exceptiony seropositive and Group 5 was positive mainly for IgA (11. 4%) associated with lower respiratory tract ailments. This unspecific seropositivity was attributed to inapparent infections by PPM whose colonisation was favored by the particular disease of the patients. The sensitivity of serological measurements applied to the diagnosis of TB patients and PPM patients was similar, regardless if the disease was pulmonary or non-pulmonary, regardless if cultures were positive or not and, in our hands, was low (positivity for IgA about 30 %, for IgM about 10% and for IgG about 30%). This poor sensitivity observed with people presenting for treatment is attributed to an immune depression occuring mainly in elderly patients. The remarkable sensitivity of the serological instrument applied to culture-negative pulmonary and non-pulmonary TB cases as well as PPM cases makes the test a good adjuvant in cases of suspicion of TB. The assessment of the serological status of people under chemotherapy is worth the analysis, a high IgG level being associated with immunocompetence while the absence of IgG antibodies and/or the presence of IgA antibodies denotes an immunologically misdirected response potentially opening the way to chronic infections.

Biomarkers↗
PubMed2006

Rosmarinic acid induces apoptosis of activated T cells from rheumatoid arthritis patients via mitochondrial pathway.

T cells play an important role in the initiation and the progression of rheumatoid arthritis (RA) and depletion of potentially pathogenic T cells was suggested as an important therapeutic protocol. We determined if rosmarinic acid (RosA), known as a secondary metabolite from herbal plants, had apoptotic activity toward T cells from RA patients and further verified target T-cell subsets. CD3(+)CD25(+) activated T-cell subsets from most of the RA patients displayed significantly higher apoptosis rates than did the PBMCs and total CD3(+) T cells. Furthermore, activated and effector CD4(+) T cells, including CD4(+)CD25(+) and CD4(+)CD45RO(+) T cells, had a tendency of being more susceptible to RosA-induced apoptosis than that of resting and naïve T-cell subsets. RosA induced the release of cytochrome c from mitochondria and the blockage of mitochondrial depolarization inhibited apoptosis. Taken together, these results suggest that RosA induces apoptosis of activated T-cell subsets from RA patients via a mitochondrial pathway.

Adult↗
PubMed1999

The intestinal microflora regulates cytokine production positively in spleen-derived macrophages but negatively in bone marrow-derived macrophages.

Besides its role as a barrier against potential pathogens, intestinal flora is presumed to protect the host by priming the immunological defense mechanisms. In this respect, the influence of intestinal flora on macrophage precursors was examined, and its modulating effect was compared on LPS-induced cytokine production by macrophages derived from bone marrow and spleen precursors (BMDM and SDM respectively). The regulation of IL-1, IL-6, TNF-alpha and IL-12 production in macrophages from germ-free and from three groups of flora-associated mice, conventional, conventionalized and E. coli-mono-associated mice, was investigated. The whole flora inhibited IL-1, TNF-alpha and IL-12 secretion by BMDM, whereas it had a stimulatory effect on IL-12 secretion by SDM. Implantation of E. coli alone enhanced cytokine secretion by BMDM but had a more limited effect than whole flora on SDM, enhancing only TNF-alpha and IL-12 secretion. Study of expression of mRNA showed a correlation with protein secretion for IL-6 but not for TNF-alpha and IL-1. IL-12 enhancement in BMDM seemed to be dependent on regulation of p35 mRNA expression while it was correlated to increased p40 mRNA expression in SDM. The results demonstrated that intestinal flora modulated bone marrow and spleen macrophage cytokine production in a differential manner and suggested a role for bacteria other than E. coli among the whole flora. The contrasting effects exerted by the intestinal flora on bone marrow and spleen precursors are an interesting observation in view of the different functions of these organs in immunity. The finding that intestinal flora enhanced IL-12 production in spleen is also potentially important since this cytokine is implicated in the determination of the relative levels of Th1 and Th2 responses and plays a pivotal role in host defense against intracellular microorganisms.

Animals↗