Biomedical subjects

B Jiang

Publications and source records attributed to B Jiang.

At least 145 records · Page 8Linked to original sources

PubMed1996

CWH41 encodes a novel endoplasmic reticulum membrane N-glycoprotein involved in beta 1,6-glucan assembly.

CWH41 encodes a novel type II integral membrane N-glycoprotein located in the endoplasmic reticulum. Disruption of the CWH41 gene leads to a K1 killer toxin-resistant phenotype and a 50% reduction in the cell wall beta 1,6-glucan level. CWH41 also displays strong genetic interactions with KRE1 and KRE6, two genes known to be involved in the beta 1,6-glucan biosynthetic pathway. The cwh41 delta kre6 delta double mutant is nonviable; and the cwh41 delta kre1 delta double mutation results in strong synergistic defects, with a severely slow-growth phenotype, a 75% reduction in beta 1,6-glucan level, and the secretion of a cell wall glucomannoprotein, Cwp1p. These results provide strong genetic evidence indicating that Cwh41p plays a functional role, possibly as a new synthetic component, in the assembly of cell wall beta 1,6-glucan.

Amino Acid Sequence↗

PubMed1996

Development of type-specific PCR for typing Pneumocystis carinii f. sp. hominis based on nucleotide sequence variations of internal transcribed spacer region of rRNA genes.

The nucleotide sequence variations in the internal transcribed spacer region 1 (ITS1) and region 2 (ITS2) of rRNA genes were found to be useful for typing Pneumocystis carinii isolates that infect humans. Two types of ITS1 (A and B) and three types of ITS2 (a, b, and c) sequences have been found, and P. carinii isolates are classified based on sequence types of ITS1 and ITS2 as Ax or Bx (where x may be a, b, or c). Type determination has been achieved by sequencing the ITS regions or by reacting the ITS regions amplified by PCR with type-specific oligonucleotide (TSO) probes. However, TSO typing alone does not work on a specimen from an individual who is infected by more than one strain of P. carinii where different ITS1 types are present in the same specimen. In this study, type-specific PCR assays were developed to supplement TSO typing. Type-specific PCR primers were made so that they differ at their 3' ends by the two nucleotides which distinguish type A from type B of ITS1 plus an additional "A" residue at the extreme 3' ends of the primers. These two primers were paired separately with a general primer which anneals to a region downstream from ITS2 to specifically amplify Ax or Bx. The amplified products were then reacted separately with ITS2-specific probes 2-a, 2-b, and 2-c to identify their types.

Base Sequence↗

PubMed1996

Parathyroid hormone-related protein inhibits indothelin-1 production.

The effect of human parathyroid hormone-related protein, a powerful vasodilator, on endothelin-1 production in cultured bovine pulmonary arterial endothelial cells was studied. Treatment with parathyroid hormone-related protein(1-34) at concentrations of 10(-9) to 10(-6) mol/L for 24 hours caused dose-dependent suppression of the secretion of endothelin-1, with maximal suppression at 10(-7) mol/L to 74% of the control value. This inhibitory effect was completely abolished by coincubation with 100 ng/mL pertussis toxin, an inhibitor of GTP binding protein. Furthermore, addition of Ng-monomethyl-L-arginine, an inhibitor of nitric oxide synthase, at 10(-3) mol/L significantly blocked the suppressive effect of parathyroid hormone-related protein (1-34) on endothelin-1 secretion, and further addition of 5x10(-3) mol/L L-arginine significantly attenuated the blocking effect of N(G)-monomethyl-L-arginine. Parathyroid hormone-related protein (1-34) at 10(-7) mol/L resulted in an approximately fivefold increase in intracellular cGMP level. Northern blot analysis revealed that parathyroid hormone-related protein (1-34) inhibited both basal and thrombin-induced endothelin-1 gene expression. These findings suggest that the vasodilating property of parathyroid hormone-related protein may be mediated in part through its inhibitory effect on endothelin-1 production, which is probably mediated through nitric oxide and cGMP in endothelial cells. Thus, a feedback regulatory mechanism may exist between parathyroid hormone-related protein and endothelin-1 in the vascular wall.

Animals↗

PubMed1996

[Accelerated streptokinase dose regimens for coronary thrombolysis].

Forty patients entering our hospital up to 12 hours (5.1 +/- 2.8 hours) after the onset of definite acute myocardial infarction were treated with accelerated streptokinase dose regimens (1.5 million U/30 min) intravenously. The reperfusion rate of infarct-related arteries determined by clinical evidence of reperfusion was 77.5% (31/40). There was significant difference in reperfusion rates: 89.3% (25/28) among patients within 6 hours versus 50% (6/12) among patients within 6-12 hours after the onset of chest pain. Five cases (12.5%) experienced mild bleeding complications. One patient had chill. Three patients (7.5%) had hypotension (BP < or = 10.7/6.67 kPa, 1 kPa = 7.5 mmHg). The 5 week mortality was 2.5% (1/40). In conclusion, intravenous accelerated streptokinase dose regimen for coronary thrombolysis seems to improve reperfusion rate markedly without increasing adverse events such as allergic reactions, severe bleeding and hypotension.

Adult↗

PubMed1995

Regulation of cell wall beta-glucan assembly: PTC1 negatively affects PBS2 action in a pathway that includes modulation of EXG1 transcription.

Analysis of genes involved in yeast cell wall beta-glucan assembly has led to the isolation of EXG1, PBS2 and PTC1. EXG1 and PBS2 were isolated as genes that, when expressed from multicopy plasmids, led to a dominant killer toxin-resistant phenotype. The PTC1 gene was cloned by functional complementation of the calcofluor white-hypersensitive mutant cwh47-1. PTC1/CWH47 is the structural gene for a type 2C serine/threonine phosphatase, EXG1 codes for an exo-beta-glucanase, and PBS2 encodes a MAP kinase kinase in the Pbs2p-Hog1p signal transduction pathway. Overexpression of EXG1 on a 2 mu plasmid led to reduction in a cell wall beta 1,6-glucan and caused killer resistance in wild type cells; while the exg1 delta mutant displayed modest increases in killer sensitivity and beta 1,6-glucan levels. Disruption of PTC1/CWH47 and overexpression of PBS2 gave rise to similar beta-glucan related phenotypes, with higher levels of EXG1 transcription, increased exo-beta-glucanase activity, reduced beta 1,6-glucan levels, and resistance to killer toxin. Genetic analysis revealed that loss of function of the PBS2 gene was epistatic to PTC1/CWH47 disruption, indicating a functional role for the Ptc1p/Cwh47p phosphatase in the Pbs2p-Hog1p signal transduction pathway. These results suggest that Ptc1p/Cwh47p and Pbs2p play opposing regulatory roles in cell wall glucan assembly, and that this is effected in part by modulating Exg1p activity.

Cell Wall↗

PubMed1995

Induction of apoptosis by enediyne antitumor antibiotic C1027 in HL-60 human promyelocytic leukemia cells.

C1027, a new macromolecular antitumor antibiotic with an enediyne chromophore, displays extremely potent cytotoxicity against cancer cells. HL-60 human promyelocytic leukemia cells treated with C1027 (0.1-10 nM) for 2 hours resulted in morphological changes, including Hoechst 33342-stained condensed nuclei, condensation of nuclear chromatin, and nuclear fragmentation. Agarose gel electrophoresis of C1027-treated HL-60 cells showed a typical ladder-like pattern of DNA fragments. In addition, the apoptotic DNA peak of propidium iodide-stained nuclei was revealed by flow cytometry. Treatment of HL-60 cells with C1027 (5 nM) induced apoptosis in up to 79% of the cells. The results suggest that C1027 may exert antitumor activity by triggering apoptosis.

Aminoglycosides↗

PubMed1995

Lysophosphatidylcholine causes Ca2+ influx, enhanced DNA synthesis and cytotoxicity in cultured vascular smooth muscle cells.

The effects of lysophosphatidylcholine (LPC), a vasoactive phospholipid, on intracellular free calcium concentration ([Ca2+]i), DNA synthesis and cytotoxicity of vascular smooth muscle cells (VSMC) were studied. LPC from 10(-7) to 10(-5) mol/l dose-dependently induced a sustained increase in [Ca2+]i. In contrast to the response of [Ca2+]i induced by angiotensin II, that induced by LPC was totally abolished when extracellular Ca2+ was removed, was not affected by pretreatment of the cells with islet-activating protein, and was not desensitized by repeated addition. 8-(N,N-Diethylamino)octyl 3,4,5-trimethoxybenzoic acid (TMB-8), an inhibitor of Ca2+ release from intracellular Ca2+ stores, 1-(5-isoquinolinesulfonyl)-2-methylpiperadine dihydrochloride (H-7), an inhibitor of protein kinase C, KT5823, an inhibitor of protein kinase G, and Ca2+ channel blockers failed to suppress the LPC-induced increase in [Ca2+]i. LPC at 10(-5) mol/l caused significant stimulation of [3H]thymidine incorporation into VSMC, and at concentrations of 10(-5) mol/l and higher dose-dependently stimulated release of lactate dehydrogenase in cell culture supernatants. Moreover, digitonin mimicked the effects of LPC on [Ca2+]i, and also caused similar effects to those of LPC on DNA synthesis and cytotoxicity in VSMC. These observations suggest that LPC causes both cell growth and cell injury of VSMC, at least partly, through its detergent action, causing membrane leakiness and resultant [Ca2+]i overload in vitro, thus indicating the possible participation of LPC in atherosclerosis and/or injury of the vascular wall.

Animals↗

PubMed1995

Astrocytes modulate retinal vasculogenesis: effects on endothelial cell differentiation.

In the developing retina, the microvessels form by differentiation of endothelial precursor cells in a process referred to as vasculogenesis. Experiments using in vivo and in vitro model systems were designed to determine the specific influence of astrocytes on this process. Immunolocalization analyses of retinal vasculogenesis in vivo showed that astrocytes spread within the nerve fiber layer of the neonatal rat retina just ahead of the forming vessels. Then, endothelial precursor cells align themselves in register with the astrocytes. In contact with astrocytes, precursor cells differentiate as vascular endothelium, as indicated by lumen formation and patency to red blood cells. Experiments in vitro using cell culture and conditioned medium approaches showed that cell-cell contact between rat brain astrocytes and bovine retinal endothelial cells results in release of soluble factors, inhibiting endothelial cell growth and inducing morphological differentiation in capillary-like structures. Thus, it is suggested that astrocytes lay down the pattern for vasculogenesis and induce the elongation and alignment of endothelial precursor cells into a prevascular meshwork. In contact with astrocytes, precursor cells differentiate as vascular endothelium. Furthermore, this cell-cell contact with astrocytes apparently inhibits endothelial cell growth and stimulates their elongation, alignment, and morphogenic differentiation by means of the release or activation of soluble, growth factor-like substances.

Animals↗

PubMed1995

Angiostatic role of astrocytes: suppression of vascular endothelial cell growth by TGF-beta and other inhibitory factor(s).

Our previous in vivo analyses have suggested that astrocytes play a key role in retinal vascularization by inducing endothelial cell differentiation. Here we demonstrate that medium conditioned by cultured rat brain astrocytes (ACM) contains factors, including transforming growth factor-beta (TGF-beta), that inhibit endothelial cell growth. Serum-free medium conditioned for 1-3 days was tested on exponentially growing bovine retinal microvascular endothelial, aortic endothelial, mink lung epithelial CCL-64, and Swiss mouse 3T3 fibroblast cells. The growth of all four cell types was inhibited in a dose- and time-dependent manner. CCL cells, which are used as a model for assaying TGF-beta activity, were more sensitive than the endothelial cells, suggesting that ACM contains TGF-beta. Moreover, acid treatment significantly increased the inhibitory activity of ACM, indicating that TGF-beta in ACM is predominantly in the latent form. Mouse fibroblasts, which are not affected by TGF-beta treatment under the same conditions, were also inhibited by ACM. This suggests that other inhibitory factors in addition to TGF-beta may be involved. Adsorption by an anti-TGF-beta polyclonal antibody column substantially reduced but did not eliminate the inhibitory activity of ACM for CCL and endothelial cells. Western blot analysis of ACM and proteins eluted from the affinity column revealed a 25 kDa band that co-migrates with TGF-beta. Comparative densitometry of the 25 kDa bands on Western blot indicated that the amount of TGF-beta in ACM is not sufficient to account for the total growth-inhibitory activity. These experiments demonstrate directly that rat brain astrocytes express TGF-beta. They also indicate that astrocytes may produce other growth-inhibitory factor(s) yet to be identified.

Adsorption↗

PubMed1995

Effect of reversible dorsal cold block on the persistence of inhibition generated by spinal reflexes.

The effects of bilateral focal cooling of dorsolateral thoracic spinal cord on segmental reflex pathways to the triceps surae muscles were assessed in decerebrate cats from the reflex forces produced by single shocks or trains of electrical stimuli applied to the ipsilateral caudal cutaneous sural and the contralateral tibial nerves. The validity of the dorsal cold block technique as a substitute for acute surgical dorsal hemisection was established by showing that focal cooling reliably reproduced the stretch-induced "clasp knife" inhibition of triceps surae reflexive force seen following dorsal hemisection. Under control (warm) conditions, the inhibitory components of electrically evoked ipsilateral sural and contralateral tibial reflexes faded rapidly during sustained trains, with a resultant production of large-amplitude reflex force as measured from either the entire triceps surae or from the medial gastrocnemius muscle alone. Dorsal cold block greatly reduced the amplitude of reflexive force evoked by sustained electrical stimulation of either nerve. Indeed, the cold block completely reversed the sign of train-evoked reflexes to a net inhibition of reflex force output in one-half of the sural and one-half of the contralateral tibial stimulation experiments. Peak transient forces evoked by single shocks to the sural or contralateral tibial nerves were also sometimes reduced, but this result was more variable than for prolonged nerve stimulation. The persistence of activity in segmental inhibitory pathways during dorsal cold block, as indicated by instances of reflex sign reversal, suggests that descending bulbospinal pathways traversing the dorsolateral funiculi may be responsible for "fading" of segmental inhibitory reflex components in decerebrate cats with intact spinal cords during sustained afferent input. The possibility that the enhanced magnitude and duration of segmental inhibition during cold block will increase the likelihood of disruption of the size principle for motoneuron recruitment is also discussed.

Animals↗

PubMed1995

Correlation between presence of clonal rearrangements of immunoglobulin heavy chain genes and B-cell antigen expression in Hodgkin's disease.

Southern blot analysis of Hodgkin's disease (HD), although often compromised by the small number of abnormal cells present in the tissue, have tended to favor a B-cell derivation of the Hodgkin's and Reed-Sternberg (HRS) cells in cases of nodular sclerosis (NS) and mixed cellularity (MC) Hodgkin's disease. Eighteen frozen and 29 paraffin-embedded sections of lymph node specimens from 29 patients with pretreatment HD (22 NSHD and 7 MCHD) were studied by molecular analysis and immunohistochemistry to determine the phenotype of HRS cells. All cases were reviewed and showed typical morphology and CD45-, CD30+, CD15+, BLA.36+ HRS cells. In 11 of 29 (38%) cases, HRS cells were reactive with at least one B-cell marker (CD20, CD79a, MB2), 7 of 29 (24%) cases showed reactivity with the T-cell marker CD3, and 11 of 29 (38%) cases displayed a "null" phenotype. By using a polymerase chain reaction (PCR) and consensus primers for the V and J regions of the immunoglobulin heavy chain (IgH) gene, the authors were able to detect B-cell clonality in 9 of 18 (50%) frozen samples of HD analyzed. IgH gene rearrangement was present in 8 of 15 (53%) NSHD and in 1 of 3 (33%) MCHD. In five of nine (56%) of these cases, HRS cells were reactive with at least one B-cell marker, whereas one case expressed the T-cell marker CD3. The other three cases with IgH gene rearrangement showed a "null" immunophenotype. IgH gene analysis was negative in all remaining CD3+ cases and in two other cases that expressed B-cell markers by immunohistology. Southern blotting failed to detect rearrangement of the T-cell receptor beta-chain gene and immunoglobulin heavy and light genes in any of these cases. The results show that PCR represents a specific and sensitive technique for the detection of IgH gene rearrangements in cases of Hodgkin's disease. The results also suggest a lymphoid B-cell derivation of HRS cells in a high proportion of the cases.

Antigens, Neoplasm↗

PubMed1995

First detection of group C rotavirus in fecal specimens of children with diarrhea in the United States.

Group C rotaviruses cause sporadic cases and outbreaks of acute diarrhea in children and adults in many countries but have never been identified from patients in the United States. Fecal specimens from children with diarrhea who were hospitalized in Providence, Rhode Island, were screened for group C rotaviruses if rotavirus was detected by electron microscopy but the specimens were negative for group A rotavirus by ELISA. Of 16 specimens examined, 3 were positive for group C rotavirus by ELISA using reagents specific to the Cowden strain of porcine group C rotavirus and all 16 were positive using a more sensitive assay: reverse transcriptase-polymerase chain reaction. Group C rotavirus infections occurred primarily among infants in winter in 4 of the 5 years examined and were acquired both in community and nosocomial settings. Future clinical and epidemiologic studies with group C rotavirus will require development of assays that are more sensitive and simpler to perform.

Animals↗

PubMed1995

Diagnosis of Pneumocystis carinii pneumonia in AIDS patients by using polymerase chain reactions on serum specimens.

A polymerase chain reaction (PCR) that amplifies the internal transcribed spacers of rRNA genes of Pneumocystis carinii (Pc-ITS-PCR) was compared with dihydrofolate reductase (DHFR) gene PCR to determine its usefulness in the diagnosis of Pneumocystis carinii pneumonia. All specimens from non-P. carinii pneumonia AIDS patients were both Pc-ITS-PCR- and DHFR PCR-negative. Twenty-six (96%) of 27 bronchoalveolar lavage specimens from P. carinii pneumonia patients were Pc-ITS-PCR-positive, and all 27 of these patients had at least 1 serum sample positive by Pc-ITS-PCR. In contrast, DHFR PCR detected P. carinii in only 4 (17%) of 24 P. carinii-positive lavage specimens and 2 (10%) of the 20 sera from P. carinii pneumonia patients. These results suggest that serum Pc-ITS-PCR may be useful for the diagnosis of P. carinii pneumonia.

AIDS-Related Opportunistic Infections↗

PubMed1995

Association of a 33-kilodalton cysteine proteinase found in corn callus with the inhibition of fall armyworm larval growth.

Protein patterns of callus from corn (Zea mays L.) inbreds that are either resistant or susceptible to fall armyworm (Spodoptera frugiperda [J.E. Smith]) were analyzed by two-dimensional electrophoresis. Fall armyworm larvae reared on callus initiated from resistant inbreds were significantly smaller than those reared on callus of susceptible inbreds. A 33-kD protein found in callus from the resistant inbreds Mp704 and Mp708 was absent in callus from the susceptible inbreds Tx601 and Ab24E. However, a 36-kD protein found in Ab24E callus immunoreacted with polyclonal antibody raised against the 33-kD protein. When Mp704 nonfriable callus changed to friable, larval growth was not inhibited and the 33-kD protein was absent. There was a significant negative correlation between the concentration of the 33-kD protein in the callus and the weight of the larvae feeding on the callus in the F2 progeny of Mp704 x Tx601. The N-terminal amino acid sequence of the 33-kD protein suggested that it was cysteine proteinase. Purification of the 33- (Mp708) and 36-kD (Ab24E) proteins indicated that they were both cysteine proteinases. The 33-kD cysteine proteinase had 7-fold higher specific activity than the 36-kD enzyme.

Amino Acid Sequence↗

PubMed1995

Human fiber size and enzymatic properties after 5 and 11 days of spaceflight.

Biopsies from the vastus lateralis muscle were obtained from three astronauts before and after two 5-day flights and from five astronauts before and after one 11-day flight (space shuttle flights: STS-32, -33, and -34). Muscle fibers from two separate samples from each biopsy were classified as type I and II or as type I, IIA, and IIB by using qualitative myofibrillar adenosinetriphosphatase (ATPase) staining. Cross-sectional area (CSA), number of capillaries per fiber, and the activities of succinate dehydrogenase (SDH), alpha-glycerophosphate dehydrogenase (GPD), and myofibrillar ATPase were determined from one sample of fibers of each myofibrillar ATPase type. Postflight biopsies had 6-8% fewer type I fibers than preflight. Mean fiber CSAs were 16-36% smaller after the 11-day flight with the relative effect being type IIB > IIA > I. Mean fiber CSAs were 11 and 24% smaller in type I and II fibers after 5 days of flight. Myofibrillar ATPase activities increased in type II but not in type I fibers after flight, whereas SDH activity was unaffected in either fast or slow fibers. GPD activity in type I fibers was approximately 80% higher (P > 0.05) postflight compared with preflight. Myofibrillar ATPase/SDH ratios in type II fibers were higher after than before flight, suggesting that some fast fibers were more susceptible to fatigue after flight. The GPD/SDH ratios were elevated in some type I fibers after spaceflight. The number of capillaries per fiber was 24% lower after than before flight, whereas the number of capillaries per unit CSA of muscle tissue was unchanged. These data suggest that adaptations in the size, metabolic properties, and vascularity of muscle fibers can occur rapidly in the space environment. These adaptations were qualitatively similar to those observed in animals after actual or simulated spaceflight conditions for short periods.

Adenosine Triphosphatases↗

PubMed1995

Myofibrillar ATPase activity of feline muscle fibers expressing slow and fast myosin heavy chains.

The interrelationships among myofibrillar ATPase activity (Quant-mATPase), qualitative myofibrillar ATPase staining after acid (Acid-mATPase) and alkaline (Alk-mATPase) preincubations, and myosin heavy chain (MHC) composition were determined in frozen sections of soleus (Sol) and medial gastrocnemius (MG) muscle fibers from adult control cats and cats 6 months after complete spinal cord transection (Sp). Fibers were categorized as either fast, slow, or fast and slow (Fast-Slow) based on monoclonal antibody labeling. Slow fibers had low Quant-mATPase activity and stained lightly with Alk-mATPase and darkly with Acid-mATPase. Fast fibers had high Quant-mATPase activity (approximately twice that of slow fibers) and stained darkly with Alk-mATPase and lightly with Acid-mATPase. Fast-Slow fibers had intermediate Quant-mATPase activity and stained intermediately for Acid-mATPase and darkly for Alk-mATPase. There was a positive linear relationship between Alk-mATPase and Quant-mATPase for all fibers of Sol and MG from control and Sp cats. There was a negative linear relationship between Acid-mATPase and Quant-mATPase for all fibers of Sol and MG. However, within the fast fiber population of the MG there was a positive relationship between these two measures of mATPase. In summary, quantitative and qualitative measures of mATPase are highly correlated with the types of MHC expressed by single fibers from control and Sp cat muscles.

Animals↗

PubMed1995

Role of parathyroid hormone-related protein in the proliferation of vascular smooth muscle cells.

Human parathyroid hormone-related protein(1-34) [hPTHrP(1-34)] inhibited [3H]thymidine incorporation into DNA of cultured vascular smooth muscle cells (VSMC) and increased intracellular cAMP accumulation, both in a concentration-dependent manner. The potency of hPTHrP(1-34) was similar to that of human parathyroid hormone(1-34) [hPTH(1-34)], but their antagonists, hPTHrP(7-34) and hPTH(3-34), showed no effect on VSMC DNA synthesis. The inhibitory effect of PTHrP on VSMC DNA synthesis was mimicked by dibutyryl-cAMP but not by dibutyryl-cGMP. These results suggest that PTHrP, as an autocrine and/or paracrine regulator, may inhibit VSMC DNA synthesis mediated at least partly by cAMP, a second messenger which has also been proposed to mediate vascular relaxation.

Animals↗

PubMed1995

The adhesion of Helicobacter pylori extract to four mammalian cell lines.

OBJECTIVE: To study the adherence of acid-glycine extract (AGE) from Helicobacter pylori to four mammalian cell lines: KATO III, CCL17, CCL156 and Neuro-2A. DESIGN: In vitro assays to assess H. pylori adherence were based on the principle of the affinity of the bacterial antigens to mammalian cells in culture. Protein extracts from mammalian cells were either coated onto 96-well microtitre plates or electrophoretically resolved and blotted onto immobilon-P membranes. When the adhesive proteins derived from the AGE of H. pylori adhered to the mammalian cell proteins, these adhesive antigens were detected by rabbit anti-H. pylori AGE antibodies. METHODS: The adhesive proteins in H. pylori NCTC11637 AGE were detected by enzyme-linked immunosorbent assay (ELISA) and Western blot under non-denaturing conditions. RESULTS: Adhesive proteins constitute 5% H. pylori AGE proteins. The adhesive proteins adhered more readily to mammalian cell extracts than to bovine serum albumin. Modified Western blot analysis showed their affinity to a number of mammalian proteins ranging in molecular weight from 40 to 900 kDa, and in particular to the 140-230 kDa proteins. CONCLUSIONS: The two in vitro adherence assays used effectively demonstrated the adherence of H. pylori to different mammalian cell lines. The 5% adhesive proteins from H. pylori may play an essential role in infection and colonization by H. pylori. Furthermore, adhesive proteins have similar adherence properties to mammalian cell components and may play an important role in the pathogenesis of H. pylori infection.

Adhesins, Bacterial↗