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At least 307 records · Page 17Linked to original sources
PubMed2004

Integration host factor is involved in transcriptional regulation of the Brucella abortus virB operon.

Type IV secretion systems (T4SSs) are multicomponent machineries that play an essential role in pathogenicity of many facultative intracellular bacteria. The virB operon of Brucella abortus codes for a T4SS essential for virulence and intracellular multiplication. Here, virB expression analyses carried out using lacZ transcriptional fusions showed that virB promoter (PvirB) is temporally activated within J774 cells. Primer extension experiments revealed that virB transcription starts at 27 bp upstream of the first gene of the virB operon. Structural analyses showed that PvirB and regulatory sequences involved in intracellular regulation span 430 bp upstream of the transcription start site. A protein able to bind PvirB was isolated and identified. This protein, homologue to integration host factor (IHF), specifically interacts with PvirB and induces a DNA bending with an angle of 50.36 degrees . DNAse I footprinting experiments showed that IHF protects a 51 bp region that contains two overlapped IHF binding consensus motifs. VirB expression experiments carried out with PvirB-lacZ fusions showed that in B. abortus IHF participates in the regulation of PvirB activity during the intracellular and vegetative growth in different media. A mutant strain with a 20 bp IHF binding site replacement failed to turn on the virB operon during the initial stages of macrophage infection and displayed severe intracellular multiplication defects. These data indicate that IHF plays a key role during intracellular virB operon expression being required for the biogenesis of the endoplasmic reticulum-derived replicative vacuole.

Animals↗
PubMed1976

Role of host factors in the pathogenesis of Salmonella-associated arthritis in rats.

To evaluate the roles of the infectious agent and the host in the pathogensis of Salmonella-associated arthritis (SAA), 1O(3) to 10(6) heat-killed Salmonella enteritidis were injected directly into involved carpal joints in normal and actively immunized rats and in hosts adoptively immunized by the intravenous transfer of spleen cells from syngeneic donors with ongoing SAA. As many as 10(6) living Salmonellae invariably failed to generate more than a transient inflammatory response in normal rats. The regression of acute joint swelling was accelerated in both types of immunized hosts. The intensity and duration of acute inflammation evoked in normal rats by 10(6) and 10(9) heat-killed Salmonellae did not exceed the response elicited by 10(3) living organisms. In sharply contrasting results, however, a chronic arthritis became established in a significant number of actively and adoptively sensitized rats after the intra-articular injection of 10(9) heat-killed organisms. No Salmonellae were recovered from these adoptively sensitized rats although small numbers of organisms has been present among the spleen cells in the transfer inocula. Taken together, these results indicate the obligatory involvement of host factors in the mediation of this chronic arthritis and virtually eliminate any likelihood that joint damage in SAA is due to the directly destructive effects of intra-articular infection.

Animals↗
PubMed1991

Use of monoacetyl-4-hydroxyaminoquinoline 1-oxide to probe contacts between guanines and protein in the minor and major grooves of DNA. Interaction of Escherichia coli integration host factor with its recognition site in the early promoter and transposition enhancer of bacteriophage Mu.

Monoacetyl-4-hydroxyaminoquinoline 1-oxide (Ac-HAQO) reacts with DNA to form adducts at the C8- and N2-positions of guanine and with the N6-position of adenine. Only the N2-guanine adduct blocks the 3'-5' exonuclease action of phage T4 DNA polymerase. Piperidine treatment cleaves the DNA at sites bearing C8-guanine adducts. The N2-position of guanine lies in the minor groove of DNA, whereas the C8-position of guanine occupies the major groove. We have taken advantage of these characteristics to employ Ac-HAQO in conjunction with either T4 DNA polymerase or piperidine in a footprinting technique to probe the interaction of the Escherichia coli integration host factor (IHF) with its binding site. We show that when IHF binds to its recognition site both the N2- and C8-positions of guanines are protected from modification by AcHAQO. In addition, the binding of IHF to DNA was prevented when either an N2- or a C8-AQO adduct was present in the binding site. When dimethylsulfate was used as the footprinting reagent, IHF protected against methylation of the N3 position of adenine in the minor groove but not the N7 position of guanine in the major groove. The difference in results obtained with the two reagents is ascribed to their relative sizes. Both DMS and AcHAQO are excluded by IHF from the minor groove, but only the larger AcHAQO molecule is excluded from the major groove.

Aminoquinolines↗
PubMed1986

Positive and negative regulation of the Mu operator by Mu repressor and Escherichia coli integration host factor.

Bacteriophage Mu utilizes two converging promoters to regulate the lytic and lysogenic pathways. Messenger RNA encoding the repressor gene is synthesized leftward from a promoter (PcM) located 1066 base pairs from the Mu left end. This transcript overlaps and is complementary to RNA synthesized rightward from the early promoter (PE) for transposase and replication proteins which initiates transcription at base pair 1028. Purified Mu repressor binds to three distinct operator sites (O1, O2, and O3); repressor binding at O2 blocks RNA polymerase binding at PE and repressor binding at O3 blocks RNA polymerase binding at PcM. O1 and O2 have higher affinity for repressor than O3, and transcription from PE is blocked at repressor concentrations that do not affect PcM. Thus, maintenance of the lysogenic state and autoregulation of the repressor gene is achieved by RNA polymerase transcription through DNA-repressor ensembles at O1 and O2. Integration host factor (IHF) encoded by the Escherichia coli him A and him D genes binds to Mu operator DNA between sites O1 and O2. IHF enhances transcription from PE 3-5-fold on supercoiled plasmid substrates in vitro and in Mu monolysogens in vivo. In vitro, IHF simultaneously decreases transcription from PcM 5-10-fold which results in a 25-fold change in lytic transcription relative to repressor transcription. A model for regulating the Mu lysis-lysogeny decision is presented.

Bacterial Proteins↗
PubMed2003

Chapter 5: Viral and host factors in human papillomavirus persistence and progression.

Understanding the interdependent roles that host and viral factors play in cervical cancer pathogenesis is important for distinguishing women at the highest risk of human papillomavirus (HPV) persistence and progression to cervical cancer. Ongoing research on viral factors such as viral variants is providing important clues regarding HPV oncogenesis; the comprehensive characterization of the HPV genome and the function of viral genes by HPV type and variant will further this understanding. Although the biologic importance of viral integration and viral load measurements in cervical neoplasia is still being debated, available data are difficult to interpret because of methodologic limitations; to sufficiently address the importance of these events will require further methods validation and subsequent application in epidemiologic studies. Continued and expanded investigation of host immune responses-humoral, cellular, and innate immunity-should specifically address the outcomes of HPV persistence and progression to cervical cancer. Molecularly based assays paired with functional assays will be integral toward the identification and validation of key immune pathways and genes specifically relevant to cervical cancer pathogenesis. Novel technologies such as gene expression microarrays will further allow comprehensive identification of relevant genes that are important at various stages of cervical pathogenesis. The study of viral and host factors will undoubtedly lead to markers that may hold diagnostic and/or prognostic value; the clinical validity and utility of these molecular events will, therefore, need to be carefully assessed before implementation in a population setting.

Cell Transformation, Neoplastic↗
PubMed2000

Regulation of the Escherichia coli K5 capsule gene cluster: evidence for the roles of H-NS, BipA, and integration host factor in regulation of group 2 capsule gene clusters in pathogenic E. coli.

The expression of Escherichia coli group 2 capsules (K antigens) is temperature dependent, with capsules only being expressed at temperatures above 20 degrees C. Thermoregulation is at the level of transcription, with no detectable transcription at 20 degrees C. Using the E. coli K5 capsule gene cluster as a model system, we have shown that the nucleoid-associated protein H-NS plays a dual role in regulating transcription of group 2 capsule gene clusters at 37 and 20 degrees C. At 37 degrees C H-NS is required for maximal transcription of group 2 capsule gene clusters, whereas at 20 degrees C H-NS functions to repress transcription. The BipA protein, previously identified as a tyrosine-phosphorylated GTPase and essential for virulence in enteropathogenic E. coli, was shown to play a similar role to H-NS in regulating transcription at 37 and 20 degrees C. The binding of integration host factor (IHF) to the region 1 promoter was necessary to potentiate transcription at 37 degrees C and IHF binding demonstrated by bandshift assays. The IHF binding site was 3' to the site of transcription initiation, suggesting that sequences in the 5' end of the first gene (kpsF) in region 1 may play a role in regulating transcription from this promoter at 37 degrees C. Two additional cis-acting sequences, conserved in both the region 1 and 3 promoters, were identified, suggesting a role for these sequences in the coordinate regulation of transcription from these promoters. These results indicate that a complex regulatory network involving a number of global regulators exists for the control of expression of group 2 capsules in E. coli.

Bacterial Capsules↗
PubMed1975

Experimental immune arthritis: host factors.

An experimental chronic mono-arthritis was induced in rabbits using adjuvants and bovine serum albumin. The results suggest that unidentified host factors (possibly genetic) influence the induction of delayed hypersensitivity to the antigen. The data further show a clear correlation between systemic cell mediated immunity and chronic synovitis. When this condition is absent, there is a poor correlation between the humoral response and the arthritis. The results make difficult the interpretation of local immune complex deposition as the sole, chronic phlogistic stimulus. (J Rheumatol 2: 373-383, 1975).

Adjuvants, Immunologic↗
PubMed1981

Analysis of an in vivo model to study the interaction of host factors with Candida albicans.

Conditions were established under which membrane diffusion chambers surgically implanted into mice could be used to study interactions between host defense factors and Candida albicans within the chambers. Depending on the size of membrane pores, soluble host substances and phagocytic cells entered the chambers during the first 24 h after chamber implantation. By 7 days in vivo, the membranes of chambers appeared impermeable to these host factors. Mouse phagocytic cells were found to be functional within the in vivo chambers whether the cells emigrated to the chambers on their own accord or were placed there before chamber implantation. Opsonic factors such as antibody and complement appeared to be biologically functional within the in vivo chambers. Conditions suitable for harvesting C. albicans from the chambers also were determined.

Animals↗
PubMed2001

Activation from a distance: roles of Lrp and integration host factor in transcriptional activation of gltBDF.

The leucine-responsive regulatory protein (Lrp) binds to three sites centered 252, 216, and 152 bp upstream of the transcription start site of the Escherichia coli glutamate synthase operon (gltBDF) and activates transcription. Activators of sigma(70)-dependent promoters usually bind closer to the -35 hexamer of the core promoter sequence. To study the mechanism by which Lrp-dependent activation occurs over this relatively large distance, the gltBDF upstream region was sequentially replaced with corresponding portions from the well-characterized sigma(70)-dependent promoter lacZYAp. The glt-lac promoter hybrids were placed upstream of lacZ, allowing transcriptional activity to be monitored via beta-galactosidase assays. Even replacing all gltBDF sequences downstream of and including the -35 hexamer did not eliminate Lrp-dependent activation of transcription. When a 91-bp region between the -35 hexamer and the proximal Lrp binding site (-48 to -128) was replaced with heterologous DNA of the same length, transcription was reduced nearly 40-fold. Based on the presence of a consensus binding sequence, this region seemed likely to be a binding site for integration host factor (IHF). Experiments to study the effects of a himD mutant on expression of a gltB::lacZ transcriptional fusion, gel mobility shift analyses, and DNA footprinting assays were used to confirm the direct participation of IHF in gltBDF promoter regulation. Based on these results, we suggest that IHF plays a crucial architectural role, bringing the distant Lrp complex in close proximity to the promoter-bound RNA polymerase.

Bacterial Proteins↗
PubMed1991

Activation of the Pseudomonas TOL plasmid upper pathway operon. Identification of binding sites for the positive regulator XylR and for integration host factor protein.

Expression of the Pseudomonas putida TOL plasmid upper pathway operon requires a promoter that belongs to the -12/-24 class. Stimulation of transcription from this promoter is positively controlled by the effector-activated XylR protein and requires a form of RNA-polymerase holoenzyme containing the RpoN-encoded sigma factor, sigma 54. XylR-dependent stimulation of transcription from the Pseudomonas TOL upper pathway promoter was examined using deletions, insertions, and in vivo dimethyl sulfate footprinting. Two upstream activator sequences were identified in the -160 (UAS1) and -130 (UAS2) regions. Deletion of these two regions abolished transcription activation, although conservation of the UAS2 element alone allowed limited transcription stimulation. Separation of UAS1 from UAS2 by half a turn or a full turn significantly reduced XylR stimulation of transcription from the upper pathway operon promoter. An inverted repeated ATTTGN2CAAAT (where N is any nucleoside), which most likely represented the XylR recognition sequence, was identified. Binding of XylR was observed in vivo in the absence of effector, but changes in the binding pattern were induced in the presence of m-methylbenzyl alcohol, a XylR effector. In vivo footprinting analysis revealed that changes in the methylation pattern of G and T also occurred in the -50 to -90 region, which is probably occupied by integration host factor (IHF) protein. IHF was required for maximal expression from the TOL upper pathway operon promoter in Escherichia coli. Separation of the IHF site from UAS2 by a full helix turn did not significantly affect stimulation of transcription, which is consistent with this region playing a conformational role, rather than a regulatory one, in promoter function.

Autoradiography↗
PubMed1983

Risk factors for childhood respiratory disease. The effect of host factors and home environmental exposures.

Standardized respiratory disease questionnaires (ATS-DLD-78-C) were completed by the parents of 4,071 children 5 to 14 yr of age, and risk factors for respiratory symptoms were evaluated by logistic analysis. Younger age, male sex, and lower socioeconomic status (SES) were independent risk factors for most respiratory symptoms and illnesses. All respiratory outcomes were significantly more prevalent in children with a physician's diagnosis of asthma. Asthma was more prevalent in male (4.5%) than in female (2.6%) children, and the greater prevalence of most respiratory symptoms in males did not persist in children with the same asthma status. Children whose questionnaires were completed by their fathers were reported to have significantly fewer respiratory symptoms than children with mother-completed questionnaires. We postulate that fathers underreport symptoms for their children. A positive parental history of allergy or respiratory illness was an independent predictor of respiratory symptoms and illnesses in the children. Chest illness before 2 yr of age and chest illness in the past year showed a significant positive linear trend with the number of parental smokers, and these effects of passive smoking were confirmed in the logistic analysis. The use of gas cooking stoves, inversely associated with SES, was not an independent risk factor for any respiratory symptoms or illnesses.

Adolescent↗
PubMed1994

Identification of the integration host factor genes of Erwinia chrysanthemi 3937.

Two Erwinia chrysanthemi homologues of the himA and himD genes of Escherichia coli which encode the integration host factor (IHF) were cloned, sequenced and compared to their homolog in other enterobacteria (EMBL accession nos X74749 and X74750). Both genes were inactivated by the insertion of an antibiotic resistance cassette, allowing for the isolation of IHF- mutants of E chrysanthemi.

Amino Acid Sequence↗
PubMed1994

Host factors and environmental determinants associated with skin test reactivity and eosinophilia in a community-based population study.

We examined the relationship of host factors (age, gender) and environmental determinants (smoking status, area of residence) to indicators of allergy (skin test reactivity and eosinophil count) in a random population sample in the Netherlands. Positive skin test reactivity was associated with age (decreasing with increasing age), with male gender (versus female gender), and with urban residence (versus rural residence). Positive skin test reactivity was not associated with smoking. Elevated eosinophil counts were associated with male gender (versus female gender), with urban residence (versus rural residence), and with current smoking (versus never smoking). Elevated eosinophil counts were not clearly associated with age (if adjusted for the age-related effects of skin test reactivity). Additionally, this study specifically demonstrates that skin test reactivity increases with increasing eosinophil count and vice versa, indicating that the two traits are interrelated. Furthermore, this interrelationship was demonstrated to be age-dependent (decreasing with increasing age).

Adolescent↗
PubMed2001

Host factors influencing the preferential localization of sterically stabilized liposomes in Klebsiella pneumoniae-infected rat lung tissue.

PURPOSE: To gain insight into the host factors influencing liposome localization at sites of bacterial infection. METHODS: In a unilateral Klebsiella pneumoniae pneumonia rat model, capillary permeability and number of circulating leukocytes was quantified and related to the degree of liposome target localization. RESULTS: Liposome localization was highest in the hemorrhagic zone of infection, a zone characterized by markedly increased capillary permeability and high bacterial numbers. Both liposome localization and capillary permeability correlated positively with severity of infection. Lung instillation of other inflammatory stimuli, such as lipopolysaccharide or 0.1 M HCl inducing increased capillary permeability, also promoted liposome localization. As liposomal target localization in leukopenic rats was similar to that in immunocompetent rats, contribution of circulating leukocytes seems limited. Intrapulmonary distribution of liposomes shows that leukocytes at the target site are involved in liposome uptake after extravasation. CONCLUSIONS: Increased capillary permeability plays a crucial role in liposome localization at the infected site, whereas contribution of leukocytes is limited. These results suggest inflammatory conditions that could benefit from liposomal drug delivery. The involvement of leukocytes in liposome uptake at the target site could be important information in the selection of appropriate drugs.

Animals↗
PubMed1996

Host factors and the pathogenesis of HIV-induced disease.

The level of human immunodeficiency virus (HIV) replication in patients reflects a balance between stimulatory and inhibitory host factors (particularly endogenous cytokines). New information concerning the cellular co-receptors for HIV and the cellular tropism of different strains of virus will advance our understanding of HIV-induced pathogenesis and suggests new therapeutic and preventive strategies.

Animals↗
PubMed1984

Importance of host factors in human salmonellosis caused by multiresistant strains of Salmonella.

Antimicrobial resistance patterns of Salmonella isolates from persons in randomly selected urban and rural counties in the United States were examined along with clinical and epidemiological characteristics of the host. Multiresistant strains, isolated from 66 (12.2%) of 542 persons evaluated, were associated with five of 20 variables in univariate analyses: serotype heidelberg, host of Hispanic origin, host exposure to penicillins within four weeks before stool culture, age greater than or equal to 60 years, and regular antacid use. By multiple linear regression, the first three variables were each significantly associated with infections due to multiresistant Salmonella. One or more of the last three variables, thought to be host factors that may promote disease, were present for persons yielding 38% of multiresistant strains but only 12% of sensitive strains (P less than .001). The relatively large proportion of multiresistant Salmonella among isolates from persons with these risk factors suggests that to cause disease, resistant organisms are more dependent than are sensitive organisms on host characteristics.

Adolescent↗
PubMed1992

Host factors versus virulence-associated bacterial characteristics in neonatal and infantile bacteraemia and meningitis caused by Escherichia coli.

Possession of P fimbriae, virulence-associated O and K antigens, haemolysin and aerobactin production, and susceptibility to 10 antimicrobial agents were studied in 63 Escherichia coli strains isolated from blood or CSF of infants who were grouped according to their clinical characteristics. These isolates were compared with 35 faecal E. coli strains from healthy infants. Individual virulence factors showed a relatively weak association with invasive infection except for P fimbriae in urosepsis and aerobactin production in meningitis. Combinations of factors were generally more predictive for defining virulent clones, particularly in infants defined as being at normal risk of developing septicaemia. Thus, 62% of isolates from such infants had characteristics typical of previously described uropathogenic or meningitis-associated clones of E. coli, compared with 32% of the isolates from high-risk infants (i.e., those defined as being at high risk of developing septicaemia) and only 9% of the faecal isolates (p less than 0.001 and less than 0.05, respectively). Overall, 45% of the episodes of invasive infection were caused by such clones, whereas risk factors (conditions considered to be associated with increased risk of invasive infection) were present in 59% of the infected infants (39% in meningitis and urosepsis, 78% in cryptogenic septicaemia and untreated bacteraemia). The results indicated that bacterial factors played a significant causative role in neonatal meningitis and urosepsis, particularly in normal-risk infants, whereas predisposing host factors contributed greatly to cryptogenic septicaemia and untreated bacteraemia.

Antigens, Bacterial↗