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PubMed2005

The Rac activator Tiam1 is required for (alpha)3(beta)1-mediated laminin-5 deposition, cell spreading, and cell migration.

The Rho-like guanosine triphosphatase Rac1 regulates various signaling pathways, including integrin-mediated adhesion and migration of cells. However, the mechanisms by which integrins signal toward Rac are poorly understood. We show that the Rac-specific guanine nucleotide exchange factor Tiam1 (T-lymphoma invasion and metastasis 1) is required for the integrin-mediated laminin (LN)-5 deposition, spreading, and migration of keratinocytes. In contrast to wild-type keratinocytes, Tiam1-deficient (Tiam1-/-) keratinocytes are unable to adhere to and spread on a glass substrate because they are unable to deposit their own LN5 substrate. Both Tiam1 and V12Rac1 can rescue the defects of Tiam1-/- keratinocytes, indicating that these deficiencies are caused by impaired Tiam1-mediated Rac activation. Tiam1-/- cells are unable to activate Rac upon alpha3beta1-mediated adhesion to an exogenous LN5 substrate. Moreover, Tiam1 deficiency impairs keratinocyte migration in vitro and reepithelialization of excision wounds in mouse skin. Our studies indicate that Tiam1 is a key molecule in alpha3beta1-mediated activation of Rac, which is essential for proper production and secretion of LN5, a requirement for the spreading and migration of keratinocytes.

Animals↗
PubMed1972

Do morphogenetic tissue rearrangements require active cell movements? The reversible inhibition of cell sorting and tissue spreading by cytochalasin B.

Previous studies have indicated that cell sorting and tissue spreading are caused by cell combination-specific differences in intercellular adhesive energies, acting in a system of motile cells. We wished to determine whether these adhesive energies could drive cell rearrangements as well as guide them. Accordingly, aggregates of intermixed embryonic cells were cultured in solutions of the drug cytochalasin B (CCB) at a concentration shown to inhibit the locomotion of cells on a solid surface. In addition, spherical aggregates of several kinds were cultured in mutual contact under similar conditions. Both cell sorting and tissue spreading were found to be inhibited. The prompt release of this inhibition upon removal of the CCB showed that the inhibited cells were not merely injured. Moreover, aggregation experiments showed that CCB did not prevent cells of several kinds from initiating mutual adhesions. In fact, heart cell aggregation was enhanced by CCB. We conclude that interfacial forces, originating outside the cell, act together with forces originating inside it in bringing about the morphogenetic movements of cell sorting and tissue spreading. We propose the term "cooperative cell locomotion" to describe translational movements of cells arising from such a combination of intrinsic and extrinsic forces.

Animals↗
PubMed1973

Manganese stimulates adhesion and spreading of mouse sarcoma I ascites cells.

Adhesion of Sarcoma I cells (SaI) to untreated or to serum-treated glass was examined by layering (51)Cr-labeled cells on the substrate for 20 min at 34 degrees C and determining the glass-bound radioactivity after the monolayers were rinsed. Adhesion to untreated glass proceeded in sodium chloride-imidazole-potassium medium (SIK) without added divalent cations, whereas SaI adhered maximally to the serum-coated substrate only in the presence of 50 microM or more Mn. Divalent Mg, Ca, Co, Ni, or Zn were inactive or minimally active. Mn-stimulated adhesion was sharply temperature dependent, reversible upon removal of Mn, and inhibited by Ca as well as by cytochalasin B, vinblastine, or tetracaine. Adhesion of SaI in SIK did not ensue when cells or the coated substrate were pretreated with Mn and washed in SIK before the adhesion assays. Microscope observations showed that Mn induced the formation of cell processes, ruffles, and veils, and that SaI spread on the uncoated or serum-coated substrate when exposed to Mn. Cells withdrew veils and processes and rounded up when postincubated in Mn-free medium. Formation of cell processes and spreading was inhibited by cytochalasin B, vinblastine, or tetracaine. Manganese-induced adhesion seems to require the participation of microtubules and microfilaments and may be mediated by an effect of Mn on Ca fluxes. The results support the role of cell processes and spreading in cell-to-substrate adhesion.

Animals↗
PubMed1975

Laser-induced spreading arrest of Mytilus gill cilia.

Using a "slit camera" recording technique, we have examined the effects of local laser irradiation of cilia of the gill epithelium of Mytilus edulis. The laser produces a lesion which interrupts epithelial integrity. In artificial sea water that contains high K+ or is effectively Ca++ free, metachronism of the lateral cilia continues to either side of the lesion with only minor perturbations in frequency synchronization and wave velocity, such as would be expected if metachronal wave coordination is mechanical. However, in normal sea water and other appropriate ionic conditions (i.e., where Ca++ concentration is elevated), in addition to local damage, the laser induces distinct arrest responses of the lateral cilia. Arrest is not mechanically coordinated, since cilia stop in sequence depending on stroke position as well as distance from the lesion. The velocity of arrest under standard conditions is about 3 mm/s, several orders of magnitude faster than spreading velocities associated with diffusion of materials from the injured region. Two responses can be distinguished on the basis of the kinetics of recovery of the arrested regions. These are (a) a nondecremental response that resembles spontaneous ciliary stoppage in the gills, and (b) a decremental response, where arrest nearer the stimulus point is much longer lasting. The slower recovery is often periodic, with a step size approximating lateral cell length. Arrest responses with altered kinetics also occur in laterofrontal cilia. The responses of Mytilus lateral cilia resemble the spreading ciliary arrest seen in Elliptio and arrest induced by electrical and other stimuli, and the decremental response may depend upon electrotonic spread of potential change produced at the stimulus site. If this were coupled to transient changes in Ca++ permeability of the cell membrane, a local rise in Ca++ concentration might inhibit ciliary beat at a sensitive point in the stroke cycle to produce the observed arrest.

Animals↗
PubMed1973

Prevention of cell-to-cell spread of herpes simplex virus by leukocytes.

Antibody to herpes simplex virus (HSV) plus complement destroyed HSV-infected cells but did not stop the spread of the infection. Studies on the relationship between the time of appearance of viral antigens on the cell surface, immunological destruction of the cells by antiviral antibody and complement, and transfer of the virus to adjacent cells showed that the virus spread from infected to uninfected cells before the infected cells were susceptible to immunological destruction. Incubation of infected monolayers with leukocytes, however, stopped the spread of the virus by nonspecifically damaging both infected and uninfected cells and by presumably breaking intercellular bridges. When leukocytes were removed from infected monolayers, viral plaques developed. If, however, antiviral antibody and complement were added to monolayers before the leukocytes were removed, the development of plaques was prevented. These findings suggest that both antibody and leukocytes are needed to cure HSV infections.

Animals↗
PubMed1995

Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis.

The role of epitope spreading in the pathology of relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) was examined. Using peripherally induced immunologic tolerance as a probe to analyze the neuropathologic T cell repertoire, we show that the majority of the immunopathologic reactivity during the acute phase of R-EAE in SJL/J mice induced by active immunization with the intact proteolipid (PLP) molecule is directed at the PLP139-151 epitope and that responses to secondary encephalitogenic PLP epitopes may contribute to the later relapsing phases of disease. Intermolecular epitope spreading was demonstrated by showing the development of T cell responses to PLP139-151 after acute disease in mice in which R-EAE was initiated by the transfer of T cells specific for the non-cross-reactive MBP84-104 determinant. Intramolecular epitope spreading was demonstrated by showing that endogenous host T cells specific for a secondary encephalitogenic PLP epitope (PLP178-191) are demonstrable by both splenic T cell proliferative and in vivo delayed-type hypersensitivity responses in mice in which acute central nervous system damage was initiated by T cells reactive with the immunodominant, non-cross-reactive PLP139-151 sequence. The PLP178-191-specific responses are activated as a result of and correlate with the degree of acute tissue damage, since they do not develop in mice tolerized to the initiating epitope before expression of acute disease. Most importantly, we show that the PLP178-191-specific responses are capable of mediating R-EAE upon adoptive secondary transfer to naive recipient mice. Furthermore, induction of tolerance to intact PLP (which inhibits responses to both the initiating PLP139-151 epitope and to the PLP178-191 epitope) after the acute disease episode is sufficient to prevent relapsing disease. These results strongly support a contributory role of T cell responses to epitopes released as a result of acute tissue damage to the immunopathogenesis of relapsing clinical episodes and have important implications for the design of antigen-specific immunotherapies for the treatment of chronic autoimmune disorders in humans.

Acute Disease↗
PubMed1997

Determinant spreading of T helper cell 2 (Th2) responses to pancreatic islet autoantigens.

The nature (Th1 versus Th2) and dynamics of the autoimmune response during the development of insulin-dependent diabetes mellitus (IDDM) and after immunotherapy are unclear. Here, we show in nonobese diabetic (NOD) mice that the autoreactive T cell response starts and spreads as a pure Th1 type autoimmunity, suggesting that a spontaneous Th1 cascade underlies disease progression. Surprisingly, induction of antiinflammatory Th2 responses to a single beta cell antigen (betaCA) resulted in the spreading of Th2 cellular and humoral immunity to unrelated betaCAs in an infectious manner and protection from IDDM. The data suggest that both Th1 and Th2 autoimmunity evolve in amplificatory cascades by generating site-specific, but not antigen-specific, positive feedback circuits. Determinant spreading of Th2 responses may be a fundamental mechanism underlying antigen-based immunotherapeutics, explaining observations of infectious tolerance and providing a new theoretical framework for therapeutic intervention.

Animals↗
PubMed2003

The role of intramolecular epitope spreading in the pathogenesis of endemic pemphigus foliaceus (fogo selvagem).

We report here a relationship between intramolecular epitope spreading and the clinical onset of the endemic form of pemphigus foliaceus in a Brazilian community with a high prevalence and incidence of the disease. Also known as Fogo Selvagem (FS), this disease is characterized by severe skin blistering and pathogenic anti-desmoglein-1 (Dsg1) autoantibodies. These autoantibodies bind the Dsg1 ectodomain and trigger keratinocyte cell detachment, the hallmark of FS. We show that (a) sera from FS patients in the preclinical stage recognized epitopes on the COOH-terminal EC5 domain of Dsg1, (b) disease onset was associated with the emergence of antibodies specific for epitopes on the NH2-terminal EC1 and EC2 domains, (c) all sera from FS patients with active disease recognized the EC1 and/or EC2 domains, and (d) sera from FS patients in remission showed reactivity restricted to EC5. These results suggest that anti-Dsg1 autoantibodies in FS are initially raised against the COOH-terminal EC5 domain of Dsg1 in individuals without skin disease; in genetically predisposed subjects the autoimmune response may then undergo intramolecular epitope spreading toward epitopes on the NH2-terminal EC1 and EC2 domains of Dsg1 leading to disease onset. Moreover, intramolecular epitope spreading may also modulate remissions and relapses of FS.

Antibody Specificity↗
PubMed1959

Spread of directly evoked responses in the cat's cerebral cortex.

A study has been made of the electrical responses to direct stimulation of the exposed cerebral cortex of cats that had been immobilized with neuromuscular blocking drugs, and whose muscle and skin wounds had been locally anesthetized. The characteristics and spread of the first and second surface-negative responses are described. It was found that the first surface-negative response to weak stimuli decays linearly to zero at 3 to 6 mm. from the point of stimulation. Intermediate stimuli cause farther and non-linear spread: responses are re-initiated, or reinforced, at 6 to 10 mm.; and supramaximal stimulation produces reinforcement both at 5 and at 10 mm. The conduction velocity of these responses is uniform for linear spread (0.7 to 2.0 m./sec.), but reinforced responses occur 1 to 3 msec. earlier than would be expected for simple conduction. The phenomenon of re-initiation, or reinforcement, depends upon the excitatory state of the brain; circulation and previous stimulation are important factors. Connections outside the gyrus matter only in so far as they provide other sources of general excitation. It is concluded that two types of transmission: slow and fast, can lead to generation of similar surface-negative responses. The suggestion is made that the slowly conducted surface-negative potentials are due to direct or to synaptic excitation of pyramidal cells; while the responses with shortened latency are initiated synaptically on other pyramidal cells after fast conduction at about 10 m./sec. in tangential fibres.

Animals↗
PubMed1967

The mode of transverse spread of contraction initiated by local activation in single frog muscle fibers.

Isolated single frog muscle fibers were locally activated by applying negative current pulses to a pipette whose tip was in contact with the fiber surface. In contrast to the graded inward spread of contraction initiated by a moderate depolarization, the contraction in response to a strong negative current was observed to spread transversely around the whole perimeter but not through the center of the fiber. This response was elicited only with pipettes of more than 6 micro diameter. The response was still present if the sodium of the Ringer solution was replaced by choline, or the chloride was replaced by nitrate or propionate. The duration of the response appeared to be independent of the duration of stimulating current in fresh fibers, while the contraction lasted as long as the current went on in deteriorated fibers. The contraction was first initiated at the area of fiber surface covered by the pipette, and spread around the perimeter of the fiber with a velocity of 0.8-6 cm/sec. Possible mechanisms of the response are discussed in connection with the properties of the transverse tubular system, the possibility of some self-propagating process along the walls of the tubules being suggested.

Action Potentials↗
PubMed2001

Development and spread of bacterial resistance to antimicrobial agents: an overview.

Resistance to antimicrobial agents is emerging in a wide variety of nosocomial and community-acquired pathogens. The emergence and spread of multiply resistant organisms represent the convergence of a variety of factors that include mutations in common resistance genes that extend their spectrum of activity, the exchange of genetic information among microorganisms, the evolution of selective pressures in hospitals and communities that facilitate the development and spread of resistant organisms, the proliferation and spread of multiply resistant clones of bacteria, and the inability of some laboratory testing methods to detect emerging resistance phenotypes. Twenty years ago, bacteria that were resistant to antimicrobial agents were easy to detect in the laboratory because the concentration of drug required to inhibit their growth was usually quite high and distinctly different from that of susceptible strains. Newer mechanisms of resistance, however, often result in much more subtle shifts in bacterial population distributions. Perhaps the most difficult phenotypes to detect, as shown in several proficiency testing surveys, are decreased susceptibility to beta-lactams in pneumococci and decreased susceptibility to vancomycin in staphylococci. In summary, emerging resistance has required adaptations and modifications of laboratory diagnostic techniques, empiric anti-infective therapy for such diseases as bacterial meningitis, and infection control measures in health care facilities of all kinds. Judicious use is imperative if we are to preserve our arsenal of antimicrobial agents into the next decade.

Anti-Bacterial Agents↗
PubMed2002

Exploiting circuit-specific spread of pseudorabies virus in the central nervous system: insights to pathogenesis and circuit tracers.

The neurotropic alpha-herpesviruses are common mammalian pathogens that invade the peripheral and central nervous system of their hosts. Their ability to invade and spread in the nervous system in a directional manner has been exploited to develop them as neuronal circuit tracers. Tracing viruses spread among synaptically connected neurons and, by assaying brain sections for viral antigen or reporter genes expressed from the viruses, chains of synaptically connected neurons can be visualized. Virulent field strains generally are not good tracers, but some attenuated strains perform well. Live attenuated vaccine strains of pseudorabies virus (PRV), such as PRV Bartha, are among the most popular virus circuit tracers. It may be counterintuitive that attenuation results in improved neural tracing that requires extensive replication and spread in the brain. This report summarizes two lines of experiments directed to resolving this apparent paradox and introduces a new paradigm for tracing viruses.

Animals↗
PubMed2005

Prevalence and nosocomial spread of methicillin-resistant Staphylococcus aureus in a long-term-care facility in Slovenia.

OBJECTIVES: To determine the prevalence and incidence of methicillin-resistant Staphylococcus aureus (MRSA) colonization among residents and healthcare workers (HCWs) of a long-term-care facility (LTCF), to assess possible routes of nosocomial spread, and to determine genetic relatedness of the isolates. SETTING: A 351-bed community LTCF for the elderly. DESIGN AND PARTICIPANTS: Study investigators made two visits, approximately 3 months apart, to the facility. Samples for cultures were obtained from 107 residents during the first visit, 91 residents during the second visit, and 38 HCWs. RESULTS: The prevalence of MRSA colonization among residents was 9.3% during the first visit and 8.8% during the second visit. During the first visit, two HCWs were colonized. During the second visit, no HCWs were colonized. The colonization of HCWs suggested a potential role in the transmission of MRSA. Molecular typing showed that two of three roommates in one room had the same strain, whereas two in another room differed from one another. All isolates, except one, belonged to two related clonal groups. It seems that the clonal group to which most isolates belonged had the greatest potential for spreading among both residents and HCWs. CONCLUSIONS: Similar prevalence rates of MRSA colonization have been found in other European countries, but such studies have usually involved residents with better functional status than that of the participants in this study. Nosocomial spread of MRSA occurred in the facility examined, but not frequently. More attention should be focused on the hand hygiene of HCWs.

Aged↗
PubMed1999

Preventing the spread of antimicrobial resistance among bacterial respiratory pathogens in industrialized countries: the case for judicious antimicrobial use.

The spread of antimicrobial resistance is an important emerging health threat in developed countries. Widespread outpatient antimicrobial use leads to the spread of resistance among community-acquired pathogens such as Streptococcus pneumoniae. The Centers for Disease Control and Prevention and partner organizations have initiated a national campaign promoting more judicious antimicrobial use to decrease the spread of resistance. The initial focus is to improve management of respiratory tract infections, which account for most outpatient antimicrobial use. Survey and focus group results indicate that patient pressure and suboptimal diagnosis and treatment contribute to antibiotic overuse. To educate physicians, a series of "principles of judicious antibiotic use" have been developed that identify optimal approaches to management of common respiratory infections. Patient education materials and strategies to improve doctor-patient communication also have been developed. Several studies currently under way will evaluate the impact of intervention on antibiotic use practices and resistant carriage or infection.

Anti-Infective Agents↗
PubMed1997

Modeling the spread of resistant nosocomial pathogens in an intensive-care unit.

OBJECTIVES: To show the value of mathematical modeling in simulating the spread of nosocomial pathogens in an intensive-care unit (ICU), to provide a framework for listing available knowledge; to predict the benefits of various control measures; and to supplement the epidemiological assessment of these measures. DESIGN: Simulated outbreak of a nosocomial pathogen in an ICU, based on a deterministic compartmental model describing both person-to-person spread and indirect spread between patients through staff members. INTERVENTIONS: Stimulation of three typical colonization control measures: effective handwashing compliance among staff members, ICU antimicrobial policy, and curtailing ICU admission of colonized patients. RESULTS: In controlling colonization, effective handwashing compliance reduced staff member colonization, but only moderately limited patient colonization unless the ICU was isolated strictly by curtailing the admission of colonized patients. The impact of antibiotic policy was very slight. CONCLUSIONS: In the field of nosocomial infection, mathematical modeling appears to be valuable tool that can be used to evaluate the magnitude of the expected effects of control strategies and to guide the selection of the best randomized clinical trials to pursue.

Cross Infection↗
PubMed1998

Spread of vancomycin-resistant enterococci: why did it happen in the United States?

The question of why vancomycin-resistant enterococci (VRE) became epidemic in the United States can be answered on at least three basic levels: (1) molecular and genetic, (2) factors affecting host-microbe interactions, and (3) epidemiological. This article will address the epidemiological issues and seek to defend the assertion that, once VRE had evolved, its spread throughout hospitals in the United States was all but assured. Nosocomial VRE outbreaks were reported first in the mid- and late-1980s. Since that time, scientific reports of VRE have increased over 20-fold. Among hospitals participating in the National Nosocomial Infection Surveillance System from 1989 to 1997, the percentage of enterococci reported as resistant to vancomycin increased from 0.4% to 23.2% in intensive-care settings and from 0.3% to 15.4% in non-intensive-care settings. Factors leading to the spread of VRE in US hospitals include (1) antimicrobial pressure, (2) sub-optimal clinical laboratory recognition and reporting, (3) unrecognized "silent" carriage and prolonged fecal carriage, (4) environmental contamination and survival, (5) intrahospital and interhospital transfer of colonized patients, (6) introduction of unrecognized carriers from community settings such as nursing homes, and (7) inadequate compliance with hand washing and barrier precautions. Guidelines developed by the Centers for Disease Control and Prevention's Hospital Infection Control Practices Advisory Committee address each of these factors. The impact of these guidelines on the spread of VRE within individual institutions has been variable, and the overall impact of the guidelines nationally is unknown.

Anti-Bacterial Agents↗
PubMed1999

An equation describing spread of membrane potential changes in a short segment of blood vessel.

The spread of membrane potential changes throughout certain cells and tissues plays an important role in their physiology. The attenuation of such changes in any tissue is usually characterized by the cable length constant lambda, which can be determined experimentally if the equations describing membrane potential spread in the tissue are known. Here we derive an equation describing spread of membrane potential changes in a short cable, which is an appropriate model for short segments of blood vessels. This equation is more general than those already published in that the positions of both the current source that gives rise to a potential change, and the point at which the change is measured, can be anywhere along the cable.

Animals↗
PubMed2003

Time-series observation of the spreading out of microvessel endothelial cells with atomic force microscopy.

The spreading out of microvessel endothelial cells plays a key role in angiogenesis and the post-injury healing of endothelial cells. In our study, a physical force applied with an atomic force microscopic (AFM) cantilever tip in contact mode partly broke the peripheral adhesion that just-confluent cultured rat cerebral microvessel endothelial cells had formed with basal structures and resulted in the cells actively withdrawing from the stimulated area. Time-series changes in cell extension were imaged using tapping mode AFM, in conjunction with total internal reflection fluorescence microscopy, intensified charge-coupled device and field emission scanning electron microscopy. We also interpreted phase images of living endothelial cells. The results showed that formation of a fibronectin molecule monolayer is key to the spreading out of the cells. Lamellipods as well as filopods would spread out in temporal and spatial distribution following the formation of fibronectin layer. In addition, a lattice-like meshwork of filopods formed in the regions leading lamellipods, which would possibly provide a fulcrum for the filaments of the cytoskeleton within the leading cell body periphery.

Animals↗