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PubMed1987

Fimbrial phase variation in Escherichia coli: dependence on integration host factor and homologies with other site-specific recombinases.

Expression of fimA, the structural gene for type 1 fimbriae of Escherichia coli, is phase variable. Significant homologies were identified between the recombinases which control fimbrial phase variation, FimB and FimE, and the integrase class of site-specific recombinases. Normal expression of fimA was shown to require the integration host factor (IHF). Mutations in either the himA-or the himD (hip) gene, which encode the alpha and beta subunits of IHF, respectively, prevented phase variation and locked expression of fimA in either the "on" or "off" phase. In addition, both himA and himD lesions caused a sevenfold reduction in expression of a phi(fimA-lacZ) operon fusion in strains in which fimA was locked in the on phase. Thus, IHF plays a dual role in controlling fimA expression: it is required both for inversion of the fimA control region and for efficient expression from the fimA promoter. A mechanism by which IHF may exert control over fimA expression is discussed.

Amino Acid Sequence↗

PubMed1995

Integration host factor suppresses promiscuous activation of the sigma 54-dependent promoter Pu of Pseudomonas putida.

In the presence of m-xylene, the Pu promoter of the TOL plasmid of Pseudomonas putida is activated by the prokaryotic enhancer-binding protein XylR. The intervening DNA segment between the upstream activating sequences (UASs) and those for RNA polymerase binding contains an integration host factor (IHF) attachment site that is required for full transcriptional activity. In the absence of IHF, the Pu promoter can be cross-activated by other members of the sigma 54-dependent family of regulatory proteins. Such illegitimate activation does not require the binding of the heterologous regulators to DNA and it is suppressed by bent DNA structures, either static or protein induced, between the promoter core elements (UAS and RNA polymerase recognition sequence). The role of IHF in some sigma 54 promoters is, therefore, not only a structural aid for assembling a correct promoter geometry but also that of an active suppressor (restrictor) of promiscuous activation by heterologous regulators for increased promoter specificity.

Bacterial Proteins↗

PubMed1989

Involvement of integration host factor (IHF) in maintenance of plasmid pSC101 in Escherichia coli: characterization of pSC101 mutants that replicate in the absence of IHF.

Escherichia coli mutants defective in the stable maintenance of plasmid pSC101 have been isolated following Tn10 insertion mutagenesis. One class of mutations affecting pSC101 replication was located in the genes himA and himD (hip), which encode the two subunits of integration host factor (IHF), a small histonelike DNA-binding protein that has multiple cellular functions. Mutants of pSC101 that could replicate in the absence of IHF were isolated and characterized; four independent mutational alterations were found to affect the third codon of the pSC101 rep gene, resulting in the replacement of glutamic acid by lysine. The compensating alteration appears to function by altering the activity of the pSC101 rep protein in him mutants.

Bacterial Proteins↗

PubMed1996

Virus and host factors are both important determinants of response to interferon treatment among patients with chronic hepatitis C.

Virus and host factors have both been linked to the response to interferon treatment among patients with chronic hepatitis C but their relative importance and potential interactions are unclear. Hepatitis C virus genotype and level of viraemia were determined in pretreatment sera from 65 Australian patients treated with interferon-alpha 2b (IFN-alpha 2b), 3 MU tiw for 6 months. Hepatitis C viraemia was quantitated by a competitive reverse transcription-polymerase chain reaction (RT-PCR) method and genotype was determined by a line probe assay. By univariate analysis, there were positive associations between initial (short-term) responses to IFN treatment and younger age (P = 0.004), absence of cirrhosis (P = 0.01), and injecting drug use as risk factor for infection (P = 0.05) but not gender, duration of infection, or level of viraemia. Genotype appeared to be important (P = 0.06) but failed to reach statistical significance. By multivariate analysis, absence of cirrhosis was the only significant independent predictor of treatment response (P = 0.01). Among initial responders, the factors associated with long-term response were the pretreatment HCV RNA titre and the duration of infection. There was a close association between viral genotype, but not viral load, and the severity of liver disease. An interplay of factors determines the outcome of a 6-month course of interferon treatment for hepatitis C. Severity of liver disease, but not the viral load, is the most crucial determinant of initial response to interferon, and histological severity appeared to be influenced by the viral genotype. The level of hepatitis C virus (HCV) viraemia and the duration of infection are independent determinants of long-term response by affecting the relapse rate after interferon treatment.

Chronic Disease↗

PubMed2001

Erythrocyte Lewis antigen phenotypes of dyspeptic patients in Taiwan--correlattion of host factor with Helicobacter pylori infection.

BACKGROUND AND AIMS: Because of the molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood-group antigens, Lewis antigen may mediate specific H. pylori binding to surface epithelial cells in gastric mucosa. We, therefore, tested whether different Lewis antigen phenotypes have different prevalence rates of H. pylori infection, and determined the specific H. pylori-related disease entities or histologic features. METHOD: A total of 342 dyspeptic patients without previous anti-H. pylori therapy were enrolled after endoscopy. The Lewis phenotypes, defined as Le(a-b-), Le(a-b+), Le(a+b-), and Le(a+b+) subtypes, were determined from the expression or absence of Lewis antigens (Le(a) and Le(b)) on erythrocytes in each patient using monoclonal antibodies. The H. pylori-specific gastric histology was evaluated using the updated Sydney's system. RESULTS: Of 342 patients, 233 (68.1%) had H. pylori infection. The H. pylori infection rates were significantly higher in patients with Lewis phenotypes Le(a+b-) and Le(a+b+) (p < 0.05). Patients expressing the Le(a) antigen had a higher H. pylori infection rate than those without the Le(a) antigen (80.8 vs 64%, p < 0.005). In H. pylori-infected patients, patients expressing Le(b) antigen had a lower rate of gastroduodenal ulcers than those without Le(b) antigen (46.9 vs 61.4%, p < 0.05). H. pylori-positive patients who expressed the Le(b) antigen had higher bacterial density and inflammation severity in the gastric cardia than those who did not. Patients who expressed the Le(a) antigen had lower bacterial density, less chronic inflammation severity, and lower frequency of lymphoid follicles in the gastric cardia than those who did not (p < 0.05). CONCLUSION: The erythrocyte Lewis phenotype can be a significant host factor related to susceptibility, different histologic patterns, and clinical outcomes of H. pylori infection in Taiwan.

Dyspepsia↗

PubMed1978

A respiratory survey of cedar mill workers. II. Influence of work-related and host factors on the prevalence of symptoms and pulmonary function abnormalities.

The influence of certain work-related and host factors on the prevalence of respiratory symptoms and pulmonary function abnormalities in 405 red cedar workers and 187 control workers was examined. In cedar workers, but not in controls, the prevalence of chest symptoms increased with duration of exposure. The decline in pulmonary function with increasing duration of exposure was also more marked in cedar workers, but in both groups smoking was a more important determinant. Substantial proportions of cedar workers and, to a lesser extent, controls noted improvement of cough and wheeze, and particularly of conjunctivitis and rhinitis, when away from work. No deterioration, however, was found in pulmonary function during the work week in either exposure group. Atopic status was unrelated to the prevalence of chest symptoms or pulmonary function abnormalities; it was more common in workers with conjunctivitis and rhinitis, particularly in the cedar group. Similarly, Pi phenotype did not appear to influence the occurrence of either symptoms or lung function abnormalities.

Adult↗

PubMed1990

Integration host factor plays a role in IS50 and Tn5 transposition.

In Escherichia coli, the frequencies of IS50 and Tn5 transposition are greater in Dam- cells than in isogenic Dam+ cells. IS50 transposition is increased approximately 1,000-fold and Tn5 transposition frequencies are increased about 5- to 10-fold in the absence of Dam methylation. However, in cells that are deficient for both integration host factor (IHF) and Dam methylase, the transposition frequencies of IS50 and Tn5 approximate those found in wild-type cells. The absence of IHF alone has no effect on either IS50 or Tn5 transposition. These results suggest that IHF is required for the increased transposition frequencies of IS50 and Tn5 that are observed in Dam- cells. It is also shown that the level of expression of IS50-encoded proteins, P1 and P2, required for IS50 and Tn5 transposition and its regulation does not decrease in IHF- or in IHF- Dam- cells. This result suggests that the effects of IHF on IS50 and Tn5 transposition are not at the level of IS50 gene expression. Finally, IHF is demonstrated to significantly retard the electrophoretic mobility of a 289-base-pair segment of IS50 DNA that contains a putative IHF protein-binding site. The physiological role of this IHF binding site remains to be determined.

Bacterial Proteins↗

PubMed1988

A host-dependent temperature-sensitive mutant of Rous sarcoma virus: evidence for host factors affecting transformation.

We have characterized a host range mutant of Rous sarcoma virus in order to identify host cell factors involved in transformation. This mutant, tsLA33-1, which was isolated from a stock of the temperature-sensitive mutant tsLA33, is not temperature-sensitive for transformation of chicken embryo fibroblasts, as judged by its ability to induce morphological changes and agar colony formation at both 36 and 41.5 degrees. In Rat-3 cells, however, this mutant induced a temperature-dependent transformation: infected Rat-3 cells were transformed at 34 degrees but not at 39.5 degrees. Retransformants were isolated from tsLA33-1-infected Rat-3 cells by growth in agar suspension at 39.5 degrees. Virus rescued from these retransformants induced a temperature-dependent transformation when reintroduced into rat cells. The level of expression of pp60v-src at 39.5 degrees was unchanged in the retransformants. When the retransformants were treated with herbimycin, an antibiotic which induces turnover of certain protein-tyrosine kinases, they reverted to a normal phenotype, indicating that the transformed phenotype of the retransformants was dependent on continued expression of pp60v-src. The retransformants are therefore pseudorevertants in which a cellular alteration has occurred that allows transformation at 39.5 degrees by the mutant pp60v-src. Thus the temperature-dependence of transformation by tsLA33-1 is affected by the cellular environment, and is suppressed or complemented both in chicken cells and in the rat cell pseudorevertants. No clear correlation between levels of phosphorylation at tyrosine and transformation was observed. In Rat-3 cells the pp60v-src encoded by tsLA33-1 may be defective in its interaction with low abundance substrates that are critical for transformation; alternatively the nonpermissive cells may require a higher threshold dose of pp60v-src for transformation.

Animals↗

PubMed1972

Interferon, antibody, and other host factors in herpes zoster.

The influence of several factors on the course of herpes zoster was studied in 151 patients. Dissemination of zoster was associated with the presence of a concurrent disease, especially Hodgkin's disease, and/or the use of immunosuppressive therapy. Several host-immune parameters, including quantitative immunoglobulins, circulating lymphocyte counts, delayed hypersensitivity to multiple skin test antigens, and lymphocyte transformation to phytohemagglutinin did not correlate with dissemination of disease. Development of virus-specific complement-fixing antibody (CFA) was delayed in some patients with disseminated disease. Vesicle interferon (V-IF) titers were low early in the disease in patients with localized and disseminated zoster and then rose, usually abruptly, to a peak value and declined as pustulation and crusting occurred. However, titers in patients with localized disease rose at an earlier time. This could be seen in terms of time to development of intermediate values of V-IF or by the day on which the sharpest rise occurred. In 15 carefully studied patients with disseminated disease, the development of the maximum V-IF response was followed within 48 hr by cessation of dissemination. Half of the patients in this group had no CFA detectable until after dissemination had ceased. These findings suggest at least two host factors whose interaction might determine host response to zoster; local interferon production (possibly mediated by sensitized lymphocytes) and humoral antibody, acting to prevent or shorten dissemination of an initially local disease.

Antibody Formation↗

PubMed1988

The bacteriophage lambda cohesive end site: isolation of spacing/substitution mutations that result in dependence on Escherichia coli integration host factor.

Substitution, insertion and deletion mutations have been constructed at the XmnI restriction site in cos lambda. The XmnI site is located between cosB, the site where terminase binds lambda DNA; and cosN, the site where terminase introduces staggered nicks to generate cohesive ends. Substitution mutations and deletion of a base pair (a -1 change) do not obviously affect lambda growth and DNA packaging. Changes of -2, +2 and -3 render lambda unable to grow on host cells lacking integration host factor (IHF). The -3 mutant has a reduced burst size in IHF+ cells, due to a defect in the initiation of packaging. A -7 deletion mutation is lethal. Models for the basis of these mutational effects are discussed.

Bacterial Proteins↗

PubMed1994

Host factors in lung carcinogenesis.

The interaction between aetiological factors (e.g. tobacco smoke) and target cells in lung tissues is modulated by host factors, leading to variable risk among individuals. We have studied some of the metabolic properties of the human lung and the effects on them of tobacco smoke. The activity of activating enzymes is induced by recent tobacco smoke exposure, whereas that of inactivating enzymes is depressed, and this effect is greater in patients with lung cancer than in controls. This imbalance between activating and detoxifying enzymes in the lung may be a key factor in determining the genetic damage to the lung. These differences between lung cancer patients and controls in metabolic activities in lung tissues may be documented at a phenotypic level as well as at a genotypic level. Also wide interindividual differences have been shown in deoxyribonucleic acid (DNA) repair enzymes and in the extent of DNA damage.

Carcinogens↗

PubMed1996

Identification of host factors that regulate the influenza virus RNA polymerase activity.

Transcription and replication of the influenza virus RNA genome take place in the nuclei of infected cells. Ribonucleoprotein (RNP) complexes consisting of viral RNA, RNA polymerase, and nucleocapsid protein (NP) are proven to be the catalytic unit for RNA synthesis, while it has been indicated that the viral RNA polymerase activity is modulated by host-derived nuclear factors. Here we have identified such host factors present in nuclear extracts prepared from uninfected HeLa cells with biochemical complementation assays using the in vitro RNA synthesis system. The stimulatory activity was not absorbed to phosphocellulose but was tightly bound to Q-Sepharose. The eluate recovered from Q-Sepharose was able to stimulate the RNA synthesis catalyzed by both RNP complexes and purified RNA polymerase and NP. The stimulatory activity was further separated into two distinct fractions, designated RAF-1 (RNA polymerase activating factor-1) and RAF-2 fractions, through phenyl-Sepharose column chromatography. When these fractions were fractionated through a gel filtration column, RAF-1 and RAF-2 activities were recovered in fractions corresponding to the molecular mass of 350 kDa and 60 kDa, respectively. Furthermore, the RAF-2 fraction was shown to contain an inhibitory activity, tentatively designated RIF-1 (RNA polymerase inhibitory factor-1). RIF-1 sedimented as fast as bovine serum albumin in glycerol density gradient centrifugation. Roles of these host factors are discussed in the context of viral RNA transcription and replication.

Biological Factors↗

PubMed2005

Role of integration host factor in the transcriptional activation of flagellar gene expression in Caulobacter crescentus.

In the Caulobacter crescentus predivisional cell, class III and IV flagellar genes, encoding the extracytoplasmic components of the flagellum, are transcribed in the nascent swarmer compartment. This asymmetric expression pattern is attributable to the compartmentalized activity of the sigma54-dependent transcriptional activator FlbD. Additionally, these temporally transcribed flagellar promoters possess a consensus sequence for the DNA-binding protein integration host factor (IHF), located between the upstream FlbD binding site and the promoter sequences. Here, we deleted the C. crescentus gene encoding the beta-subunit of the IHF, ihfB (himD), and examined the effect on flagellar gene expression. The DeltaihfB strain exhibited a mild defect in cell morphology and impaired motility. Using flagellar promoter reporter fusions, we observed that expression levels of a subset of class III flagellar promoters were decreased by the loss of IHF. However, one of these promoters, fliK-lacZ, exhibited a wild-type cell cycle-regulated pattern of expression in the absence of IHF. Thus, IHF is required for maximal transcription of several late flagellar genes. The DeltaihfB strain was found to express significantly reduced amounts of the class IV flagellin, FljL, as a consequence of reduced transcriptional activity. Our results indicate that the motility defect exhibited by the DeltaihfB strain is most likely attributable to its failure to accumulate the class IV-encoded 27-kDa flagellin subunit, FljL.

Bacterial Proteins↗

PubMed2000

Two roles for integration host factor at an enhancer-dependent nifA promoter.

Control of transcription in prokaryotes often involves direct contact of regulatory proteins with RNA polymerase. For the sigma54 RNA polymerase, regulatory proteins bound to distally located enhancers engage the polymerase via DNA looping. The sigma54-dependent nifA promoter of Herbaspirillum seropedicae (Hs) is activated under nitrogen-limiting growth conditions. Potential enhancers for the nitrogen control activators NTRC and NIFA and binding sites for integration host factor (IHF) and sigma54-holoenzyme were identified. DNA footprinting experiments showed that these sites functioned for protein binding. Their involvement in the promoter regulation was explored. In vitro, activation of the Hs nifA promoter by NTRC is stimulated by the DNA bending protein IHF. In marked contrast, activation by NIFA is greatly reduced by IHF, thus diminishing potentially destabilizing autoactivation of the nifA promoter by NIFA. Additionally, high levels of NIFA appear to limit NTRC-dependent activation. This inhibition is IHF dependent. Therefore, IHF acts positively and negatively at the nifA promoter to restrict transcription activation to NTRC and one signal transduction pathway.

Bacterial Proteins↗

PubMed1997

Integration host factor stimulates both FimB- and FimE-mediated site-specific DNA inversion that controls phase variation of type 1 fimbriae expression in Escherichia coli.

The site-specific DNA inversion that controls phase variation of type 1 fimbriation in E. coli is catalysed by two recombinases, FimB and FimE. Efficient inversion by either recombinase also requires the leucine-responsive regulatory protein (Lrp). In addition, FimB recombination is stimulated by the integration host factor (IHF). The effect of IHF on FimE inversion has not previously been reported. Here it is shown that IHF stimulates FimE recombination; In strain MG1655, mutants containing lesions in either the alpha (ihfA) or beta (ihfB) subunits of IHF show a marked decrease in both FimB- (100-fold) and FimE (15,000-fold)-promoted switching. IHF is shown to bind with high affinity to sites both adjacent to (site I) and within (site II) the fim invertible element. Furthermore, mutations in site I or site II that lower the affinity of IHF binding In vitro were found to lower the frequency of FimE and/ or FimB recombination in vivo. Although site I and site II mutations in combination have an effect on FimB-promoted switching comparable to that of IHF knockout mutations (100-fold), the cis site mutations have a much less marked effect (100-fold) on FimE-promoted switching.

Amino Acid Sequence↗

PubMed1997

Deletion analysis of the fis promoter region in Escherichia coli: antagonistic effects of integration host factor and Fis.

Fis is a small DNA-binding and -bending protein in Escherichia coli that is involved in several different biological processes, including stimulation of specialized DNA recombination events and regulation of gene expression. fis protein and mRNA levels rapidly increase during early logarithmic growth phase in response to a nutritional upshift but become virtually undetectable during late logarithmic and stationary phases. We present evidence that the growth phase-dependent fis expression pattern is not determined by changes in mRNA stability, arguing in favor of regulation at the level of transcription. DNA deletion analysis of the fis promoter (fis P) region indicated that DNA sequences from -166 to -81, -36 to -26, and +107 to +366 relative to the transcription start site are required for maximum expression. A DNA sequence resembling the integration host factor (IHF) binding site centered approximately at -114 showed DNase I cleavage protection by IHF. In ihf cells, maximum cellular levels of fis mRNA were decreased more than 3-fold and transcription from fis P on a plasmid was decreased about 3.8-fold compared to those in cells expressing wild-type IHF. In addition, a mutation in the ihf binding site resulted in a 76 and 61% reduction in transcription from fis P on a plasmid in the presence or absence of Fis, respectively. Insertions of 5 or 10 bp between this ihf site and fis P suggest that IHF functions in a position-dependent manner. We conclude that IHF plays a role in stimulating transcription from fis P by interacting with a site centered approximately at -114 relative to the start of transcription. We also showed that although the fis P region contains six Fis binding sites, Fis site II (centered at -42) played a predominant role in autoregulation, Fis sites I and III (centered at +26 and -83, respectively) seemingly played smaller roles, and no role in negative autoregulation could be attributed to Fis sites IV, V, and VI (located upstream of site III). The fis P region from -36 to +7, which is not directly regulated by either IHF or Fis, retained the characteristic fis regulation pattern in response to a nutritional upshift.

Bacterial Proteins↗

PubMed1987

Two promoter-specific host factors interact with adjacent sequences in an EIA-inducible adenovirus promoter.

We previously reported the identification of a host factor (EIIA-EF) specific for an upstream transcriptional control sequence (-82 to -66) of the EIA-inducible adenovirus EIIA early promoter. The levels of this factor remained unchanged after virus infection of human cells. Another study also identified a factor (EIIF) specific for this same promoter, but the activity of this second factor was shown to increase severalfold after virus infection. We now show that these dramatically different results, both based on gel shift assays on the same promoter, may be explained by variations in protocol details and actually identify two distinct factors. When synthetic DNA copolymers [poly(dI).poly(dC) or poly(dI-dC).poly(dI-dC)] are used as competitors in gel shift assays, a factor specific for DNA sequences between -82 and -66 can be identified, whereas when natural eukaryotic DNAs (salmon sperm or calf thymus) are used as competitors a different factor specific for DNA sequences between -69 and -33 can be identified. We have mapped the DNA-protein contact residues for the EIIF by analyzing a series of linker scan mutants in gel shift assays and methylation interference experiments. The EIIA-EF and EIIF bind to two distinct but adjacent sequences. Competition experiments indicate that these two activities are due to two different factors. Consistent with the earlier reports, the levels of one (EIIA-EF) do not change after virus infection of human cells, whereas the levels of the other (EIIF) are increased severalfold.

Adenoviruses, Human↗

PubMed2000

Transcription from fusion promoters generated during transposition of transposon Tn4652 is positively affected by integration host factor in Pseudomonas putida.

We have previously shown that both ends of the Tn3 family transposon Tn4652 contain integration host factor (IHF) binding sites and that IHF positively regulates expression of the Tn4652 transposase gene tnpA in Pseudomonas putida (R. Hõrak, and M. Kivisaar, J. Bacteriol. 180:2822-2829, 1998). Tn4652 can activate silent genes by creating fusion promoters during the transposition. The promoters are created as fusions between the -35 hexamer provided by the terminal inverted repeats of Tn4652 and the -10 hexamers in the target DNA. Two fusion promoters, PRA1 and PLA1, that contain sequences of the right and left termini of Tn4652, respectively, were chosen for the study of mechanisms of transcription activation. Gel mobility shift analysis using crude extracts from P. putida cells allowed us to detect specific binding of P. putida IHF to the ends of the transposon Tn4652. We found that the rate of transcription from the fusion promoter PRA1 is enhanced by IHF. Notably, the positive effect of IHF on transcription from the promoter PRA1 appeared only when cells of P. putida reached the stationary growth phase. We speculate that the intracellular concentration of IHF might be critical for the in vivo effect of IHF on transcription from the fusion promoters in P. putida. In the case of PLA1, the mechanism of transcription modulation by IHF is different than that observed for PRA1. Our results demonstrate that transcription of neighboring genes from outwardly directed promoters at the ends of a mobile DNA element could be influenced by the same factors that control transposition of the element.

Base Sequence↗