Integration host factor and conjugative transfer of the antibiotic resistance plasmid R100.
Transfer of plasmid R100-1 was reduced 100-fold in the absence of integration host factor.
Bacterial Proteins↗
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Integration host factor interactions with Neisseria gene sequences: correlation between predicted binding sites and in vitro binding of Neisseria -derived IHF protein.
Putative integration host factor (IHF) binding sites are frequently being identified in Neisseria gene sequences on the basis of similarity to a degenerate Escherichia coli -derived consensus binding sequence. In this report, three different Neisseria genetic systems that contain predicted IHF binding sites were assessed for IHF binding through gel retardation analysis. The results show a positive correlation between the identification of a predicted Neisseria IHF binding site and in vitro binding of Neisseria -derived IHF protein.
Base Sequence↗
The role of host factors for the chemotherapy of BCG infection in inbred strains of mice.
Host factors have previously been considered to play a role in the efficacy of "incomplete" antituberculous chemotherapy. We investigated this aspect using a model of intravenous infection with M. bovis-BCG in three inbred strains of mice. Viable splenic counts of bacilli (CFU) were monitored following a three week regimen of rifampicin (R) and isoniazid (H) given either immediately or from three weeks after infection. At the end of the immediate (0-3 weeks) therapy the spleens of all mice were sterile and only a minority of animals had demonstrable CFU's at 23 weeks after infection. However, following the delayed-onset (3-6 weeks) therapy we found a pronounced relapse of BCG growth which was about 10 times higher in CBA/Ca and BALB/C than in C57B1/6 mice. These results indicated that host immunity which developed during the first three weeks after infection may have aggravated the relapse of bacterial growth following chemotherapy. This interpretation was corroborated by the finding that the immunosuppressive drug cyclosporin given concurrently with R/H reduced the splenic viable counts of BCG.
Animals↗
Host factors in chronic obstructive pulmonary disease in an upper Midwest rural community. Design, case selection, and clinical characteristics in a matched-pair study.
A series of 111 index subjects with chronic obstructive pulmonary disease (COPD) who had forced expiratory volume in 1 second (FEV1) of 70% or less of that predicted were matched on the basis of age, sex, occupation, and smoking history with control subjects who had an FEV1 of 85% or more of that predicted. Index and control subjects with seasonal or reversible airway disease were excluded. Men outnumbered women by a ratio of 4.5 to 1. Thirty-five percent of the women and 2% of the men were nonsmokers (0 pack-years). There were three PiZ phenotypes in the index group (two nonsmokers) and none in the controls. PiMZ phenotypes in the index group outnumbered those in the controls by 8 to 5. Host factors that might be important in these closely matched pairs were sought by history, physical examination, and a large battery of laboratory tests. A standard respiratory questionnaire revealed the anticipated significantly higher frequency of cough, phlegm, noisy respiration, and all grades of dyspnea in index subjects. Previous lower respiratory tract infections also were more frequent in index subjects than in controls. There were no detectable differences between groups in the frequency of upper airway infections, nasal polyps, sinus surgery, or reported allergy to any substance. If the British Medical Research Council's definition of chronic bronchitis were applied to our study, about two-thirds of our index subjects and almost one-third of our controls would be considered to have chronic bronchitis. Pack-years of smoking were not significantly associated with the amount and duration of cough and expectoration in male or female index subjects or controls. Significant differences between index and control groups on physical examination included the audible forced expiratory flow time over the trachea, the estimated maximal midexpiratory flow, breath sounds, rales, and total excursion of the hemidiaphragms. An endocrine questionnaire and measurement of blood sex hormones did not give any clues as to the propensity of males to develop COPD. Women with airway obstruction similar to that of men had histories of significantly fewer pack-years than did the men, and there was a much larger proportion of women who never smoked. Further studies, specifically on genetic and immunologic characteristics, are under way to identify potential host factors.
Bronchitis↗
Integration host factor is required for 1,2-propanediol-dependent transcription of the cob/pdu regulon in Salmonella typhimurium LT2.
We show that integration host factor (IHF) is required for the activation of transcription of the cobalamin biosynthetic (cob) and 1,2-propanediol (1,2-PDL) utilization (pdu) operons in Salmonella typhimurium LT2. A lack of IHF affected transcription of the cob/pdu regulon in at least two ways. First, the level of the regulatory protein PocR was decreased in ihfB (formerly himD) mutants, as judged by Western blot analysis with polyclonal antiserum raised against PocR. Second, even when PocR was available, in the absence of IHF, PocR was unable to activate transcription of cob/pdu in response to 1,2-PDL. This result suggested an additional role for IHF in PocR-dependent transcription activation. Consistent with these findings, ihfB mutants of this bacterium were unable to use 1,2-PDL as a carbon or energy source.
Apoproteins↗
Co-regulation by bent DNA. Functional substitutions of the integration host factor site at sigma 54-dependent promoter Pu of the upper-TOL operon by intrinsically curved sequences.
The role of integration host factor (IHF) in the regulation of the sigma 54-dependent promoter Pu of the TOL plasmid of Pseudomonas putida has been examined. We have selected in vivo insertions of intrinsically curved DNA that restore the responsiveness of an IHF-binding site deletion variant of Pu to the cognate activator of the system, XylR. We found five Pu derivatives which had inserted a core sequence with 6 phased [A]6 tracts, flanked by different lengths of DNA at the location of the former IHF site. They displayed 40-100% of the activity of Pu, were independent of IHF, and maintained the overall geometry of the wild-type promoter. The induction patterns of Pu, compared to those of hybrid promoters, were virtually indistinguishable. This supports the notion that, in native conditions, IHF co-regulates the system by providing a structural aid for promoter architecture and not by interacting directly with the RNA polymerase, as it has been suggested with other known IHF-dependent promoters.
Bacterial Proteins↗
Structural distortions induced by integration host factor (IHF) at the H' site of phage lambda probed by (+)-CC-1065, pluramycin, and KMnO4 and by DNA cyclization studies.
Integration Host Factor (IHF) is a sequence-specific DNA-bending protein that is proposed to interact with DNA primarily through the minor groove. We have used various chemical probes [(+)-CC-1065, a minor-groove-specific agent that alkylates N3 of adenine and traps bends into the minor groove; pluramycin, a minor-major-groove threading intercalator that alkylates N7 of guanine; KMnO4, which reacts more strongly with bases in denatured DNA] to gain more information on the interaction of IHF with the H' site of phage lambda. In addition to the 13-bp core consensus recognition element present at all IHF binding sites, the H' site also has an upstream AT-rich element that increases the affinity of IHF for this site. Our results reveal new details of IHF-DNA interaction at this site. Results with (+)-CC-1065 modification suggest that IHF interacts with the adenines on the 3'-side of the AT-rich element and likely induces a minor-groove bend in its vicinity, which in turn stabilizes the interaction. Pluramycin modification experiments suggest the presence of both short- and long-range structural perturbations (possible DNA unwinding events) on either side of the IHF contact region. Although IHF is known to induce a large bend in DNA at the H' site, no separation of base pairs was detected when the bent DNA was probed with KMnO4. DNA cyclization studies indicate a large magnitude (approximately 180 degrees) for the IHF-induced bend at the H' site, consistent with > 140 degrees bend estimated by gel electrophoresis methods. These studies suggest that IHF-induced DNA bending is accompanied by the introduction of a DNA node, DNA unwinding, and/or by some other DNA distortion. An enhanced binding and stability of IHF was observed on small circular DNA.
Adenine↗
In vivo UV laser footprinting of the Pseudomonas putidasigma 54Pu promoter reveals that integration host factor couples transcriptional activity to growth phase.
The occupation of the final sigma(54)-dependent Pu promoter of Pseudomonas putida by the integration host factor (IHF) under different growth conditions has been monitored in its native state and stoichiometry (i.e. monocopy) with UV laser footprinting technology. We present evidence that an abrupt change in intracellular IHF concentrations occurs when P. putida cells enter stationary phase. This change results in enhanced binding of the factor to the promoter and in the ensuing bending of the target DNA. Since Pu activity depends rigorously on DNA bending, promoter occupation is in turn translated into a much higher transcriptional output when cells leave exponential growth. Inspection of the residual activity of Pu in an IHF(-) strain reveals that IHF predominantly locks the capacity of the promoter to specific growth stages and also that additional physiological signals are entered in the system through final sigma(54)-RNA polymerase. The results substantiate the notion that final sigma(54) promoters process metabolic co-regulation signals through factor-induced changes in the architecture of the cognate DNA region. Further, they validate UV laser technology as a suitable tool to visualize nondisruptive alterations of DNA shape in vivo.
Bacterial Proteins↗
Host factor I, Hfq, binds to Escherichia coli ompA mRNA in a growth rate-dependent fashion and regulates its stability.
The stability of the ompA mRNA depends on the bacterial growth rate. The 5' untranslated region is the stability determinant of this transcript and the target of the endoribonuclease, RNase E, the key player of mRNA degradation. An RNA-binding protein with affinity for the 5' untranslated region ompA was purified and identified as Hfq, a host factor initially recognized for its function in phage Qbeta replication. The ompA RNA-binding activity parallels the amount of Hfq, which is elevated in bacteria cultured at slow growth rate, a condition leading to facilitated degradation of the ompA mRNA. In hfq mutant cells with a deficient Hfq gene product, the RNA-binding activity is missing, and analysis of the ompA mRNA showed that the growth-rate dependence of degradation is lost. Furthermore, the half-life of the ompA mRNA is prolonged in the mutant cells, irrespective of growth rate. Hfq has no affinity for the lpp transcript whose degradation, like that of bulk mRNA, is not affected by bacterial growth rate. Compatible with our results, we found that the intracellular concentration of RNase E and its associated degradosome components is independent of bacterial growth rate. Thus our results suggest a regulatory role for Hfq that specifically facilitates the ompA mRNA degradation in a growth rate-dependent manner.
Bacterial Outer Membrane Proteins↗
Requirement of integration host factor (IHF) for growth of Escherichia coli deficient in HU protein.
Escherichia coli mutants deficient in histone-like protein, HU, and integration host factor (IHF) were constructed and their growth characteristics were examined. Mutants deficient in both HU and IHF grew slowly and were filamentous at both 30 degrees C and 37 degrees C. These mutants scarcely grew in LB broth at 42 degrees C. They formed minute colonies on LB plates at 42 degrees C and no colonies at 46 degrees C, indicating temperature-sensitive (ts) growth. On the contrary, mutants deficient in either HU or IHF were not ts for growth. These results indicate that IHF compensates for the absence of HU and permits normal cell growth; this suggests functional similarity between HU and IHF.
Bacterial Proteins↗
Influence of host factors on immunoglobulin G concentration in oral fluid specimens.
The influence of host factors (tobacco use, dentition, bleeding gums, oral rinsing, nasal medications, and time since the last meal) on immunoglobulin G (IgG) concentration in oral fluids (OF) was determined by univariate and multivariate analysis. Significant differences in IgG concentration were found to be associated with human immunodeficiency virus (HIV) status (HIV antibody positive, +16.60 microg/ml, P = 0.0001), sex (female, +1.23 microg/ml, P = 0.004), dentition (+2.83 microg/ml, edentulous versus dentulous, P = 0.0001), bleeding gums (+6.35 microg/ml, P = 0.0001), and time since the last meal (+3.55 microg/ml, >6 h, P = 0.0001). These factors could impact diagnostic methods that rely on the immunoglobulin concentration in OF specimens.
Adolescent↗
Host factors affecting longitudinal decline in lung spirometry among grain elevator workers.
The host factors affecting the longitudinal decline in lung function among 267 white male grain elevator workers who were still working in the industry and did not change their smoking habits over a period of six years were studied. Spirometric measures declined more rapidly in older grain handlers as compared with younger workers. Smokers had slightly greater decline in spirometry compared to nonsmokers, but the differences failed to reach the level of statistical significance. Acute changes in lung function over the course of one work week during the initial study were also positively correlated with subsequent decline in lung function, as was bronchial hyperreactivity determined during the follow-up study. Positive immediate skin reactivity to common allergens, presence and absence of respiratory symptoms, and initial lung function did not appear to influence the subsequent decline in lung function in this group.
Adult↗
Host factors and efficacy of antiretroviral treatment.
It has been proposed that some host factors may affect the intracellular drug concentration leading to the inability of drug regimens to inhibit human immunodeficiency virus (HIV) replication in cells. Among them, two factors, whose description is the main aim of this review, have been considered during the last years with particular emphasis. They are: i) altered uptake and reduced activation of nucleoside reverse transcriptase inhibitors (NRTIs) in target cells, and ii) efflux of NRTIs and protease inhibitors (PIs) by cellular transporter molecules. In fact, several authors have shown that: changes in the activity of various purine and pyrimidine biosynthetic enzymes may occur in lymphocytes of HIV-infected patients; HIV-infected patients on prolonged treatment with nucleoside analogs, such as zidovudine, show significantly decreased activity of thymidine kinase compared to untreated HIV-infected persons; NRTI and PIs are substrates for the so-called multidrug membrane transporters. With regard to the latter issue, it is known that the ATP-binding cassette transporter proteins such as the P glycoprotein, and the newly discovered family of multidrug resistance-associated proteins (MRP 1-9) promote the active extracellular efflux of a wide variety of therapeutics and overexpression of some of them lowers intracellular concentration of PIs. In the very near future such mechanisms, called by most authors "cellular drug-resistance", might be taken into account, together with other immunological, virological and behavioral factors, to explain "drug failure" and/or the variability of response in HIV patients undergoing an antiretroviral treatment.
ATP-Binding Cassette Transporters↗
The RNA-binding protein HF-I, known as a host factor for phage Qbeta RNA replication, is essential for rpoS translation in Escherichia coli.
The rpoS-encoded sigma(S) subunit of RNA polymerase in Escherichia coli is a global regulatory factor involved in several stress responses. Mainly because of increased rpoS translation and stabilization of sigma(S), which in nonstressed cells is a highly unstable protein, the cellular sigma(S) content increases during entry into stationary phase and in response to hyperosmolarity. Here, we identify the hfq-encoded RNA-binding protein HF-I, which has been known previously only as a host factor for the replication of phage Qbeta RNA, as an essential factor for rpoS translation. An hfq null mutant exhibits strongly reduced sigma(S) levels under all conditions tested and is deficient for growth phase-related and osmotic induction of sigma(S). Using a combination of gene fusion analysis and pulse-chase experiments, we demonstrate that the hfq mutant is specifically impaired in rpoS translation. We also present evidence that the H-NS protein, which has been shown to affect rpoS translation, acts in the same regulatory pathway as HF-I at a position upstream of HF-I or in conjunction with HF-I. In addition, we show that expression and heat induction of the heat shock sigma factor sigma(32) (encoded by rpoH) is not dependent on HF-I, although rpoH and rpoS are both subject to translational regulation probably mediated by changes in mRNA secondary structure. HF-I is the first factor known to be specifically involved in rpoS translation, and this role is the first cellular function to be identified for this abundant ribosome-associated RNA-binding protein in E. coli.
Allolevivirus↗
Host factors influencing the response to antimicrobial agents.
When the desired clinical response to an antibiotic therapeutic regimen is not achieved, despite appropriate antibiotic selection and organism sensitivity, the clinician must be aware that several host factors exist that may influence the outcome. Examples of the influence of host-related factors on drug disposition have been briefly reviewed in this article. It should be noted, however, that further investigation is needed to determine whether these factors truly exert a significant influence on the outcome of antibiotic utilization.
Anti-Bacterial Agents↗
Primary structure of the hip gene of Escherichia coli and of its product, the beta subunit of integration host factor.
We describe the isolation and sequencing of the hip gene of Escherichia coli and show that it encodes the beta subunit of integration host factor (IHF beta). In order to locate the coding region, we constructed a set of deletion mutants by exonucleolytic digestion of a fragment containing hip, determined which mutants were hip+ and which hip- by complementation, and then sequenced the ends of the critical deletions. The 5' end of the coding region was located precisely by comparing the deduced amino acid sequence to the actual N-terminal amino acid sequence of IHF. Our assignment of the coding region was further substantiated by the nucleotide sequences of a hip point mutant and of internal replacement mutations. We found a probable promoter for hip located about 85 base-pairs upstream from the initial AUG codon and about 75 base-pairs downstream from the 3' end of the neighboring gene, rpsA, and we constructed an IHF beta overproducer by fusing the coding sequences to the lambda pL promoter. A survey of known protein sequences revealed a close relationship between IHF beta and the type II prokaryotic DNA binding proteins (the "histone-like" proteins). This relationship is shared to a considerable extent by the other subunit of IHF, IHF alpha. A hip missense mutation that replaces a completely conserved glycine with aspartate has a null phenotype, suggesting that the conserved regions are functionally important.
Amino Acid Sequence↗
Integration host factor, a histone-like Escherichia coli protein, binds to at least four sites of the DNA fragment containing the recA gene.
The integration host factor (IHF) is a sequence-specific, histone-like, multifunctional DNA-binding and -bending protein of Escherichia coli. The characterization and functional analysis of this protein has been carried out mainly in bacteriophage lambda and other mobile genetic elements. Less is known concerning the role of IHF in E. coli, although it has been implicated in a number of processes in this organism including DNA replication, site-specific recombination, and gene expression. In this paper we report data concerning the binding of IHF protein to the recA gene region. IHF binds to at least four sites of the DNA fragment containing the recA gene, as shown by gel mobility shift assays. On the basis of the ihf consensus sequences published, we have been able to identify two sequences of putative ihf sites (ihf 1 and ihf2) into the 1390 bp long sequence containing the recA gene, but only the ihf2 site was able to bind IHF, as measured by gel mobility shift experiments. The nonfunctional ihf1 sequence was found to overlap the -35 region of the recA promoter and the functional ihf2 sequence was found within the recA gene structure at nt +780 to +807 (both with three mismatches according to the consensus sequence of Kur et al., 1989). This confirms our earlier results that the IHF-DNA interaction does not depend on any very rigid sequence, but also on the suitable sequences of the neighbouring regions, together with the proper DNA conformation.(ABSTRACT TRUNCATED AT 250 WORDS)
Bacterial Proteins↗
Involvement of integration host factor (IHF) in maintenance of plasmid pSC101 in Escherichia coli: mutations in the topA gene allow pSC101 replication in the absence of IHF.
Integration host factor (IHF), encoded by the himA and himD genes, is a histonelike DNA-binding protein that participates in many cellular functions in Escherichia coli, including the maintenance of plasmid pSC101. We have isolated and characterized a chromosomal mutation that compensates for the absence of IHF and allows the maintenance of wild-type pSC101 in him mutants, but does not restore IHF production. The mutation is recessive and was found to affect the gene topA, which encodes topoisomerase I, a protein that relaxes negatively supercoiled DNA and acts in concert with DNA gyrase to regulate levels of DNA supercoiling. A previously characterized topA mutation, topA10, could also compensate for the absence of IHF to allow pSC101 replication. IHF-compensating mutations affecting topA resulted in a large reduction in topoisomerase I activity, and plasmid DNA isolated from such strains was more negatively supercoiled than DNA from wild-type strains. In addition, our experiments show that both pSC101 and pBR322 plasmid DNAs isolated from him mutants were of lower superhelical density than DNA isolated from Him+ strains. A concurrent gyrB gene mutation, which reduces supercoiling, reversed the ability of topA mutations to compensate for a lack of him gene function. Together, these findings indicate that the topological state of the pSC101 plasmid profoundly influences its ability to be maintained in populations of dividing cells and suggest a model to account for the functional interactions of the him, rep, topA, and gyr gene products in pSC101 maintenance.
Bacterial Proteins↗