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PubMedDate not supplied

Health survey of house finches (Carpodacus mexicanus) from Wisconsin.

We conducted a health survey of house finches (Carpodacus mexicanus) without evidence of Mycoplasma gallisepticum infection in order to establish baseline population health measures and estimate prevalence of potential pathogens likely to influence host susceptibility to mycoplasmosis. Seasonal changes in several physiologic parameters were observed. Weights were greater in winter compared with the breeding season (P < 0.01), fat scores were greater in winter than during fall migration (P < 0.01) or the breeding season (P < 0.01), and packed cell volume and total plasma protein measures during fall migration (P < 0.05) and winter (P < 0.01) were greater than during the breeding season. Culture of voided fecal material yielded 13 bacterial isolates likely representative of normal gastrointestinal flora. Avian pox lesions and blood and gastrointestinal parasite infections were at low prevalence (< or = 4%) compared with Proctophyllodes spp. feather mite infestations (32%) in the population. All parasites occurred at generally low levels in individual hosts. A logistic regression analysis of our data suggests that greater fat scores, tarsal length, and being male are potential risk factors for mite infestation in house finches.

Animals↗
PubMed2005

Autoantibodies to fibrillin-1 activate normal human fibroblasts in culture through the TGF-beta pathway to recapitulate the "scleroderma phenotype".

Fibroblasts from patients with systemic sclerosis (SSc) are activated producing excessive amounts of extracellular matrix (ECM) components. Recently, we identified a new SSc-specific autoantibody against portions of fibrillin-1, a major component of ECM microfibrils and regulator of TGF-beta1 signaling. To examine a potential pathogenic role of anti-fibrillin-1 autoantibodies, normal human fibroblasts were treated with affinity-purified autoantibodies isolated from SSc sera and then examined for alterations in gene and protein expression levels using microarrays, quantitative RT-PCR, immunoblots, and immunofluorescence. Compared with fibroblasts cultured in normal medium or in medium containing normal human IgG, anti-fibrillin-1 autoantibody-treated normal dermal fibroblasts showed increased expression of COL and several other ECM components characteristically overexpressed in SSc fibroblasts. This was accompanied by phosphorylation and nuclear translocation of Smad3. Neutralization of TGF-beta1 with anti-TGF-beta1 Abs significantly diminished the activation of fibroblasts by anti-fibrillin-1 autoantibodies. These data indicate that anti-fibrillin-1 autoantibodies can induce the activation of normal dermal fibroblasts into a profibrotic phenotype resembling that of SSc by potentially causing the release of sequestered TGF-beta1 from fibrillin-1-containing microfibrils in the ECM.

Active Transport, Cell Nucleus↗
PubMed1998

New acquisitions in Helicobacter pylori characteristics.

The protection of Helicobacter pylori from the gastric acid exerted by urease is based on an increase of the bacterial periplasmic pH and membrane potential. Ammonia generated from urea induces apoptosis of gastric cells in vitro, and inhibits gastric somatostatin release in animals, which could have consequences on the physiology of digestion in general. The type s1/m1 structure of the vacA gene is associated with the production of high levels of cytotoxin. Strains with m2 region type, formerly considered devoid of toxic activity, are fully toxic when assayed with cell lines other than HeLa cells, which possibly lack receptors for m2 VacA type. The enhanced gastric mucosa damage associated with infection by cytotoxic organisms could be explained by the varying of effects exerted by VacA on target cells: extracellular secretion of acidic hydrolases, cytoskeletal alterations, actin rearrangement, reduction of epidermal growth factor binding to its receptor, inhibition of the stimulation of CD4+ T cells proliferation induced by the antigen presenting cells. Organisms that possess the pathogenicity island cag (cag+) induce an increased inflammation and transduction of signals to the host cells; however, they reduce the apoptosis of colonised cells. The results of an investigation on the possible influence of a variable cagA status on the extension of apoptosis have indicated that this kind of programmed death is disengaged from the possession of cagA by Helicobacter pylori organisms colonising the same gastric areas. It is likely that the whole pathogenic potential of cag+ organisms is far from being completely explored, as suggested by the recent finding that the expression of a bacterial adhesin (called BabA) involved in binding to the blood group antigen Lewis b is associated with the presence of cag.

Animals↗
PubMed2003

Adherence to various host cell lines of Mycoplasma bovis strains differing in pathogenic and cultural features.

Mycoplasma bovis is known to be responsible for pneumonia and arthritis in calves, as well as mastitis in dairy cows. Despite clear evidence of its pathogenic potential, little is known about mechanisms of cytadherence and the molecular factors involved. The purpose of this work was to compare adherence rates of M. bovis field strains to different host cell lines and study the effects of cloning and sub-culturing M. bovis strains on their adherence properties. Eighteen metabolically labeled M. bovis strains isolated from different pathological backgrounds were examined in adherence trials using four different host cell lines, i.e. embryonic bovine lung (EBL), embryonic bovine trachea (EBTr), Madin Darby bovine kidney (MDBK) and rabbit kidney (RK) cells. Although large interstrain variations in adherence rates (3.4-19.1%) were measured they could not be correlated to the pathological background (pneumonia, arthritis or mastitis). Adherence rates to the fibroblast cell line (EBTr) were significantly lower than those to the three epithelial cell lines (EBL, MDBK and RK). The only non-pathogenic strain (221/89) exhibited lower adherence rates than three isolates from clinical mastitis. Interestingly, adherence rates were significantly reduced after in vitro passaging. In contrast, no effect of single cloning of strains on adherence was observed. There was no general correlation between expression of variable surface proteins (Vsps) as monitored by immunoblotting and adherence rates, although alterations in Vsp expression profiles were seen as a consequence of passaging. As there is probably a large number of adhesins, variable and non-variable, on the surface of M. bovis cells the issue is very complex, and the most active components have yet to be identified.

Animals↗
PubMedDate not supplied

[The domestic inhalation of the smoke from firewood and of other biological materials. A risk for the development of respiratory diseases].

A high proportion of the world population, especially in developing countries, is exposed to indoor pollutants produced by inefficient biomass stoves. The levels of pollutants, including toxins and carcinogens in the kitchen are usually very high. This potential pathogenic exposure has been scarcely studied. The exposure to biomass smoke has been associated to chronic bronchitis and chronic airflow obstruction in adults and to acute respiratory infections in children. At the National Institute of Pulmonary Diseases in Mexico, we have observed the entire spectrum of diseases associated with tobacco in people who never smoked and who were exposed to wood smoke. Women exposed to wood smoke had a five-fold risk of chronic bronchitis and chronic airflow obstruction, as compared to the non-exposed, according to a recent case-control study done at our Institute. The indoor levels of suspended particles smaller than 10 microns were frequently above 1,000 micrograms/m3 in a rural community in the state of Mexico. This information supports a causal role for biomass smoke for the genesis of several respiratory diseases, representing a potentially public health problem.

Adult↗
PubMed1972

Coagulase and deoxyribonuclease activities of staphylococci isolated from clinical sources.

A total of 504 clinical isolates of the family Micrococcaceae were tested for coagulase, deoxyribonuclease, clumping factor, and phosphatase to determine whether there is a correlation between the results of these tests and the pathogenicity of staphylococci. In the tests for coagulase production, it was found that either human or rabbit plasma could be used with broth cultures, whereas rabbit but not human plasma was satisfactory when microorganisms removed from solid culture medium were used. Deoxyribonuclease production correlated better than the fermentation of mannitol with coagulase production. The use of methyl green, Toluidine Blue O, or acridine orange offered no advantage over the use of HCl for detecting the production of deoxyribonuclease. Neither the presence of clumping factor nor the production of phosphatase correlated well with coagulase production. Strains of staphylococci that did not produce coagulase and deoxyribonuclease were isolated as frequently as, and from a greater variety of clinical sources than, strains which produced these substances. It is concluded that the production of coagulase and deoxyribonuclease are properties of staphylococci which are not necessarily indicative of potential pathogenicity of the organisms for man.

Acridines↗
PubMed2004

Virulence factors of the coagulase-negative staphylococci.

Coagulase-negative staphylococci (CNS) have gained substantial interest as pathogens involved in nosocomial, particularly catheter-related infections. The pathogenic potential of CNS is mainly due to their capacity to form biofilms on indwelling medical devices. In a biofilm, the bacteria are protected against antibiotics and from attacks by the immune system. The factors contributing to biofilm formation are among the best-studied virulence factors of CNS and comprise factors involved in the adhesion to a catheter surface and in cell accumulation. CNS usually persist in the host in relative silence, but may cause sepsis, for which the recently found inflammatory peptides called phenol-soluble modulins are prime candidates. Many CNS also produce several lipases, proteases, and other exoenzymes, which possibly contribute to the persistence of CNS in the host and may degrade host tissue. We are also beginning to understand how regulators of virulence trigger the expression of virulence factors in CNS. A better conception of the mechanisms underlying the pathogenicity and the frequently encountered antibiotic resistance of CNS may help to develop novel, efficient anti-staphylococcal therapeutics.

Animals↗
PubMed2003

[Molecular scanning of candidate mtDNA gene fragment in diabetic pedigrees].

OBJECTIVE: To explore novel pathogenic mutation in the mitochondrial DNA gene in diabetic pedigree. METHODS: Twenty-eight suspected mitochondrial DNA diabetic families were recruited. The gene fragment was produced by PCR, and mutation was detected by direct sequencing. RESULTS: In one pedigree, the proband and her mother were found carrying the most common nt3243 A --> G mutation and another 16S rRNA 3205C --> T mutation. But only 3205C --> T was found in her affected brother. All the two patients were deaf and developed diabetes in early age, characterized by impaired beta cell function and low body mass index (BMI). The proband had relatively higher lactic acid concentration than normal individuals. A novel ND1 gene 3434 A --> G(TAT --> TGT) mutation was explored in another proband with deafness and her affected family members. CONCLUSION: 16SrRNA 3205C --> T mutation was found in a mitochondrial diabetes mellitus pedigree, implying its potential pathogenic role in diabetes. Another novel ND1 3434 A --> G mutation was found in another diabetic pedigree. Because this mutation causes amino acid change (Tyr --> Cys) and is co-segregated with diabetes, it may be diabetogenic.

Adult↗
PubMed2005

Computers in anesthesia and intensive care: lack of evidence that the central unit serves as reservoir of pathogens.

OBJECTIVE: Computers are becoming increasingly visible in operating rooms (OR) and intensive care units (ICU) for use in bedside documentation. Recently, they have been suspected as possibly acting as reservoirs for microorganisms and vehicles for the transfer of pathogens to patients, causing nosocomial infections. The purpose of this study was to examine the microbiological (bacteriological and mycological) contamination of the central unit of computers used in an OR, a surgical and a pediatric ICU of a tertiary teaching hospital. METHODS: Sterile swab samples were taken from five sites in each of 13 computers stationed at the two ICUs and 12 computers at the OR. Sample sites within the chassis housing of the computer processing unit (CPU) included the CPU fan, ventilator, and metal casing. External sites were the ventilator and the bottom of the computer tower. Quantitative and qualitative microbiological analyses were performed according to commonly used methods. RESULTS: One hundred and ninety sites were cultured for bacteria and fungi. Analyses of swabs taken at five equivalent sites inside and outside the computer chassis did not find any significant-number of potentially pathogenic bacteria or fungi. This can probably be attributed to either the absence or the low number of pathogens detected on the surfaces. CONCLUSION: Microbial contamination in the CPU of OR and ICU computers is too low for designating them as a reservoir for microorganisms.

Anesthesiology↗
PubMed1976

Temperature-sensitive mutants of rabies virus in mice: a mutant (ts2) revertant mixture selectively pathogenic by the peripheral route of inoculation.

Analysis of the pathogenic potential in mice of a variety of rabies and rabies serogroup viruses revealed that an apparently revertant population of virus derived from CVS mutant ts 2 had a unique capacity to selectively induce paralytic disease when given by a peripheral [intraplantar (i.pl.)] route of inoculation. Little paralytic disease was induced by high concentrations of virus administered by the intracerebral (i.c.) route, whereas paralytic disease and death were characteristically induced in mice given only a few infectious doses of virus i.c. Disease induced by i.pl. inoculation was dose dependent. Mice frequently survived paralytic disease induced by i. pl. inoculation, with clinical signs often persisting indefinitely; mice surviving i.c. inoculation of high concentrations of virus frequently exhibited chronic nonspecific signs of minor debility. Analysis of the ts 2 virus population indicated that it was composed of a mixture of ts and revertant virions, each with characteristic pathogenic (or nonpatholgnic) propensities, none of which was identical to the original composite ts 2 virus populations. Despite the heterogeneity of the ts 2 virus population, the typical pathogenic pattern of selective pathogenic capicity after i. pl. inoculation at high doses was retained during 11 ocnsecutive passages in suckling mouse brain. ts 2 virus was demonstrated to interfere with the disease-producing capacity of CVS fixed rabies virus when ts 2-CVS mixtures were inoculated i.c. However, attempts to demonstrate a particular propensity for induction in vitro of "autointerference" by ts 2 in serial passage in BHK-21 cell culture inoculated at high multiplicity were unsuccessful.

Animals↗
PubMed2001

Detection and confirmation of reptilian adenovirus infection by in situ hybridization.

Adenovirus infections are documented in at least 12 different species of reptiles. In contrast to their mammalian and avian counterparts reptilian adenoviruses are not well characterized as to their pathogenic potential and their ability to cause primary disease. In the diagnostic setting, fresh tissues are often not available for virus isolation, and the confirmation of reptilian adenovirus infections is dependent largely upon electron microscopy for the identification of intranuclear viral inclusions associated with histopathologic changes. The diagnosis of adenovirus infection in 2 different species of snake was confirmed by the application of DNA in situ hybridization. Using an aviadenovirus specific oligoprobe, adenoviral DNA was observed in the nuclei of hepatocytes, Kupffer cells, endothelial cells, and enterocytes. Electron microscopy of the liver confirmed the presence of intranuclear viral particles morphologically consistent with an adenovirus. DNA in situ hybridization on formalin-fixed tissues can serve as a suitable alternative to electron microscopy in the diagnosis of reptilian adenovirus infections. Both affected snakes had other concurrent diseases, suggesting that the adenovirus may not have been the primary pathogen.

Adenoviridae↗
PubMed1986

Morphologic and physiologic studies of three dematiaceous pathogens.

Uncertainty in identifying a dematiaceous mold from a human bronchial washing precipitated a study of Dactylaria gallopava (Cooke) Bhatt et Kendrick and its relationship to Scolecobasidium constrictum Abbott. Morphologic and physiologic studies were conducted with representative isolates and subcultures derived from the isolates used to prepare the type specimens of these two fungi, as well as a third dark mold, Ochroconis constricta (Abbott) de Hoog et von Arx. All test isolates were morphologically similar in that two-celled, cylindrical blastoconidia with a rhexolytic mode of dehiscence were the predominant and most consistent anamorphic structures. Sympodial development of the conidiophore was too variable to distinguish the isolates. Based on their morphologic similarity, we propose a new combination within the genus Dactylaria as amended by Bhatt and Kendrick, D. constricta (Abbott) Dixon et Salkin. However, D. constricta could be differentiated into two groups on the basis of physiologic tests--a subgroup in which isolates grow at 37 and 45 degrees C, give a delayed positive gelatin reaction, and are inhibited on Mycosel agar; and a second subgroup in which isolates grow on Mycosel agar and give a rapid positive gelatin reaction, but do not grow at 37 or 45 degrees C. We recommend that D. constricta be viewed as a potential pathogen when isolated from clinical specimens.

Culture Media↗
PubMed1987

Lower respiratory tract abnormalities in rheumatoid interstitial lung disease. Potential role of neutrophils in lung injury.

Although the etiology of rheumatoid interstitial lung disease (RILD) remains unknown, bronchoalveolar lavage (BAL) has been useful in studying potentially pathogenic mechanisms in this disorder. Previous investigations in patients with rheumatoid arthritis (RA) and RILD revealed abnormal BAL T-lymphocyte subpopulations and a significant elevation in BAL neutrophils. Because neutrophils have been implicated as important effector cells in inflammatory disorders such as ARDS and idiopathic pulmonary fibrosis, we evaluated BAL fluid in patients with RA for neutrophil chemotactic and activating properties and for evidence of neutrophil activation. The BAL fluid from patients with RILD contained significant neutrophil chemotactic activity derived from both lipid and nonlipid components. Evidence for neutrophil stimulation in the lower respiratory tract of patients with RILD was suggested by elevations in both myeloperoxidase activity and immunologically determined levels of human neutrophil elastase in BAL fluid. Free uninhibited elastolytic activity, however, was not demonstrated, suggesting that adequate protease inhibitor levels were present to inhibit active elastase activity. In addition to elevated myeloperoxidase activity, a potential role for neutrophil-derived oxidant injury was indirectly suggested by the enhanced release of superoxide anion (O2-) from resting normal human blood neutrophils challenged with concentrated BAL fluid from patients with RA and interstitial lung disease. Significant correlations were found between physiologic parameters and the percentage of BAL neutrophils, as well as levels of neutrophil-derived mediators. For example, levels of human neutrophil elastase were strongly correlated with diminished diffusion capacity (r = -0.73, p less than 0.001) and reduced forced vital capacity (r = -0.63, p less than 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMedDate not supplied

[Searching for local similarities between HIV-1 and human proteins. Application to vaccines].

A method for identification of fragments with a high local similarity to human proteins within potentially immunopathogenic regions of HIV-1 proteins was developed. The method is based on the use of an original matrix of antigenic similarity of amino acids. The regions, whose fragments are frequent in human proteins, and regions, exhibiting a high similarity to the proteins responsible for important physiological functions, were identified in HIV-1 proteins. A possibility of participation of such regions in immunopathogenesis of HIV-infection due either to induction of cross-reacting effectors of immune system or through molecular mimicry of physiologically important human proteins, leading to an alteration of homeostasis of the organism, is discussed. Most of regions, identified in HIV-1 proteins, contain either T-cell (CD8+ CTL or CD4+ Th) or B-cell epitopes, or both of them simultaneously. The criteria for the design of safe polyepitopic antiviral vaccines which enable the exclusion of epitopes, having the (immuno)pathogenic potential, are discussed. According to these criteria, polyepitopic immunogens should be free of the virus protein regions, whose fragments are frequent in human proteins, as well as of regions exhibiting a pronounced local similarity to proteins that provide for important physiological functions.

AIDS Vaccines↗
PubMed2005

Understanding carbamoyl phosphate synthetase deficiency: impact of clinical mutations on enzyme functionality.

Carbamoyl phosphate synthetase I (CPSI) deficiency, a recessively inherited error of the urea cycle, causes life-threatening hyperammonaemia. CPSI is a multidomain 1500-residue liver mitochondrial matrix protein that is allosterically activated by N-acetyl-l-glutamate, and which synthesises carbamoyl phosphate (CP) in three steps: bicarbonate phosphorylation by ATP, carbamate synthesis from carboxyphosphate and ammonia, and carbamate phosphorylation by ATP. Several missense mutations of CPSI have been reported in patients with CPSI deficiency, but the actual pathogenic potential and effects on the enzyme of these mutations remain non-characterised. Since the structure of Escherichia coli CPS is known and systems for its overexpression and purification are available, we have constructed and purified eight site-directed mutants of E.coli CPS affecting the enzyme large subunit (A126M, R169H, Q262P, N301K, P360L, V640R, R675L, S789P) that are homologous to corresponding missense mutations found in patients with CPSI deficiency, studying their stability and their ability to catalyse the CPS reaction as well as the partial reactions that reflect the different reactional steps, and analysing the substrate kinetics for the overall and partial reactions. The results show that all the mutations significantly decrease CP synthesis without completely inactivating the enzyme (as reflected in the catalysis of at least one partial reaction), that one of these mutations (Q262P) causes marked enzyme instability, and validate the use of E.coli CPS as a pathogenicity testing model for CPSI deficiency. The causality of the reported clinical mutations is supported and the derangements caused by the mutations are identified, revealing the specific roles of the residues that are mutated. In particular, the findings highlight the importance for carbamate phosphorylation and for allosteric activation of a loop that coordinates K(+), stress the key role of intersubunit interactions for CPS stability, and suggest that lid opening at both phosphorylation sites is concerted.

Adenosine Triphosphate↗
PubMed2003

Human immunodeficiency virus type 1 Nef-mediated downregulation of CD4 correlates with Nef enhancement of viral pathogenesis.

The nef gene products encoded by human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus type 1 (SIV-1) increase viral loads in infected hosts and accelerate clinical progression to AIDS. Nef exhibits a spectrum of biological activities, including the ability to downregulate surface expression of CD4 and major histocompatibility complex (MHC) class I antigens, to alter the state of T-cell activation, and to enhance the infectivity of viral particles. To determine which of these in vitro functions most closely correlates with the pathogenic effects of Nef in vivo, we constructed recombinant HIV-1 NL4-3 viruses carrying mutations within the nef gene that selectively impair these functions. These mutant viruses were evaluated for pathogenic potential in severe combined immunodeficiency (SCID) mice implanted with human fetal thymus and liver (SCID-hu Thy/Liv mice), in which virus-mediated depletion of thymocytes is known to be Nef dependent. Disruption of the polyproline type II helix (Pxx)4 within Nef (required for binding of Hck and p21-activated kinase-like kinases, downregulation of MHC class I, and enhancement of HIV-1 infectivity in vitro but dispensable for CD4 downregulation) did not impair thymocyte depletion in virus-infected Thy/Liv human thymus implants. Conversely, three separate point mutations in Nef that compromised its ability to downregulate CD4 attenuated thymocyte depletion while not diminishing viral replication. These findings indicate that the functional ability of Nef to downregulate CD4 and not MHC class I downregulation, Hck or PAK binding, or (Pxx)4-associated enhancement of infectivity most closely correlates with Nef-mediated enhancement of HIV-1 pathogenicity in vivo. Nef-mediated CD4 downregulation merits consideration as a new target for the development of small-molecule inhibitors.

Alleles↗
PubMed2004

Intronic mutations in the L1CAM gene may cause X-linked hydrocephalus by aberrant splicing.

L1 disease is a clinically heterogeneous X-chromosomal neurodevelopmental disorder that is frequently associated with mental retardation and congenital hydrocephalus in males. It is caused by mutations in L1CAM that encodes a multifunctional transmembrane neuronal cell adhesion molecule. We report our findings on 6 novel intronic L1CAM sequence variants (c.523+5G>A, c.1123+1G>A, c.1547-13delC, c.3323-17dupG, c.3457+3A>T, and c.3457+18C>T), and a recurrent one (c.523+12C>T). While the pathogenic potential of nucleotide changes within the evolutionarily well-conserved splice consensus sequence (c.523+5G>A, c.1123+1G>A, and c.3457+3A>T) is widely accepted, it is not always straight forward to assess the disease relevance of intronic mutations, if they lie outside the consensus. The c.523+12C>T variant co-segregated with X-linked hydrocephalus in two unrelated families. In the mutated allele, a preferentially used novel splice donor site is generated that results in a frame shift due to insertion of the first 10 bp of intron 5 in the mature mRNA, a largely truncated protein, and most likely a functional null allele. The c.1547-13delC mutation creates a new acceptor site resulting in the insertion of 4 additional amino acids at the end of the immunoglobulin like domain 5. In contrast, c.3323-17dupG and c.3457+18C>T seem to be non-pathogenic L1CAM variants.

Base Sequence↗
PubMed2002

The modulation of macrophage activation by tyrosine phosphorylation.

Activated macrophages are a critical component of our antimicrobial armamentarium. Unfortunately, the lipid mediators and free radicals that these cells produce are not only toxic to potential pathogens, but also to the host. Thus the modulation of these activities can mitigate an overzealous immune response and thereby prevent host cell injury. Two families of receptor tyrosine kinases (RTK) in macrophages, the RON/STK and the Tyro3 families of protein kinases, will be examined in this review with an emphasis on their roles in modulating the effector functions of activated macrophages. Both families of receptors are capable of down-regulating the inflammatory response of macrophages to lipopolysaccharide, and both families of RTK's are structurally related. An analysis of the intracellular domains of RON/STK and Tyro3 reveal a common multi-substrate binding site, which can recruit common signaling molecules such as growth factor receptor bound 2 (Grb2) and phosphatidylinositol 3-kinase (PI3-K). The observations relating to a modulation of macrophage effector mechanisms by these receptors open unexplored avenues for the development of pharmacological immunomodulators with the potential to exploit elements of this common pathway.

Animals↗