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Journal articles on the topic 'Chemoattractants'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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1

Heit, Bryan, Samantha Tavener, Eko Raharjo, and Paul Kubes. "An intracellular signaling hierarchy determines direction of migration in opposing chemotactic gradients." Journal of Cell Biology 159, no. 1 (October 7, 2002): 91–102. http://dx.doi.org/10.1083/jcb.200202114.

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Neutrophils must follow both endogenous and bacterial chemoattractant signals out of the vasculature and through the interstitium to arrive at a site of infection. By necessity, in the setting of multiple chemoattractants, the neutrophils must prioritize, favoring end target chemoattractants (e.g., fMLP and C5a) emanating from the site of infection over intermediary endogenous chemoattractants (e.g., IL-8 and LTB4) encountered en route to sites of infection. In this study, we propose a hierarchical model of two signaling pathways mediating the decision-making process of the neutrophils, which allows end target molecules to dominate over intermediary chemoattractants. In an under agarose assay, neutrophils predominantly migrated toward end target chemoattractants via p38 MAPK, whereas intermediary chemoattractant-induced migration was phosphoinositide 3-kinase (PI3K)/Akt dependent. When faced with competing gradients of end target and intermediary chemoattractants, Akt activation was significantly reduced within neutrophils, and the cells migrated preferentially toward end target chemoattractants even at 1/1,000th that of intermediary chemoattractants. End target molecules did not require chemotactic properties, since the p38 MAPK activator, LPS, also inhibited Akt and prevented migration to intermediary chemoattractants. p38 MAPK inhibitors not only reversed this hierarchy, such that neutrophils migrated preferentially toward intermediary chemoattractants, but also allowed neutrophils to be drawn out of a local end target chemoattractant environment and toward intermediary chemoattractants unexpectedly in an exaggerated (two- to fivefold) fashion. This was entirely related to significantly increased magnitude and duration of Akt activation. Finally, end target chemoattractant responses were predominantly Mac-1 dependent, whereas nondominant chemoattractants used primarily LFA-1. These data provide support for a two pathway signaling model wherein the end target chemoattractants activate p38 MAPK, which inhibits intermediary chemoattractant-induced PI3K/Akt pathway, establishing an intracellular signaling hierarchy.
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2

King, Danielle, Hakan Başağaoğlu, Hoa Nguyen, Frank Healy, Melissa Whitman, and Sauro Succi. "Effects of Advective-Diffusive Transport of Multiple Chemoattractants on Motility of Engineered Chemosensory Particles in Fluidic Environments." Entropy 21, no. 5 (May 4, 2019): 465. http://dx.doi.org/10.3390/e21050465.

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Motility behavior of an engineered chemosensory particle (ECP) in fluidic environments is driven by its responses to chemical stimuli. One of the challenges to understanding such behaviors lies in tracking changes in chemical signal gradients of chemoattractants and ECP-fluid dynamics as the fluid is continuously disturbed by ECP motion. To address this challenge, we introduce a new multiscale numerical model to simulate chemotactic swimming of an ECP in confined fluidic environments by accounting for motility-induced disturbances in spatiotemporal chemoattractant distributions. The model accommodates advective-diffusive transport of unmixed chemoattractants, ECP-fluid hydrodynamics at the ECP-fluid interface, and spatiotemporal disturbances in the chemoattractant concentrations due to particle motion. Demonstrative simulations are presented with an ECP, mimicking Escherichia coli (E. coli) chemotaxis, released into initially quiescent fluids with different source configurations of the chemoattractants N-methyl-L-aspartate and L-serine. Simulations demonstrate that initial distributions and temporal evolution of chemoattractants and their release modes (instantaneous vs. continuous, point source vs. distributed) dictate time histories of chemotactic motility of an ECP. Chemotactic motility is shown to be largely determined by spatiotemporal variation in chemoattractant concentration gradients due to transient disturbances imposed by ECP-fluid hydrodynamics, an observation not captured in previous numerical studies that relied on static chemoattractant concentration fields.
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3

Mahadeo, Dana C., Mirkka Janka-Junttila, Rory L. Smoot, Pavla Roselova, and Carole A. Parent. "A Chemoattractant-mediated Gi-coupled Pathway Activates Adenylyl Cyclase in Human Neutrophils." Molecular Biology of the Cell 18, no. 2 (February 2007): 512–22. http://dx.doi.org/10.1091/mbc.e06-05-0418.

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Neutrophils and Dictyostelium use conserved signal transduction pathways to decipher chemoattractant gradients and migrate directionally. In both cell types, addition of chemoattractants stimulates the production of cAMP, which has been suggested to regulate chemotaxis. We set out to define the mechanism by which chemoattractants increase cAMP levels in human neutrophils. We show that chemoattractants elicit a rapid and transient activation of adenylyl cyclase (AC). This activation is sensitive to pertussis toxin treatment but independent of phosphoinositide-3 kinase activity and an intact cytoskeleton. Remarkably, and in sharp contrast to Gαs-mediated activation, chemoattractant-induced AC activation is lost in cell lysates. Of the nine, differentially regulated transmembrane AC isoforms in the human genome, we find that isoforms III, IV, VII, and IX are expressed in human neutrophils. We conclude that the signal transduction cascade used by chemoattractants to activate AC is conserved in Dictyostelium and human neutrophils and is markedly different from the canonical Gαs-meditated pathway.
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4

Geiger, Jeremy, Deborah Wessels, Shawn R. Lockhart, and David R. Soll. "Release of a Potent Polymorphonuclear Leukocyte Chemoattractant Is Regulated by White-Opaque Switching in Candida albicans." Infection and Immunity 72, no. 2 (February 2004): 667–77. http://dx.doi.org/10.1128/iai.72.2.667-677.2004.

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ABSTRACT Previous studies employing transmembrane assays suggested that Candida albicans and related species, as well as Saccharomyces cerevisiae, release chemoattractants for human polymorphonuclear leukocytes (PMNs). Because transmembrane assays do not definitively distinguish between chemokinesis and chemotaxis, single-cell chemotaxis assays were used to confirm these findings and test whether mating-type or white-opaque switching affects the release of attractant. Our results demonstrate that C. albicans, C. dubliniensis, C. tropicalis, C. parapsilosis, and C. glabrata release bona fide chemoattractants for PMNs. S. cerevisiae, however, releases a chemokinetic factor but not a chemoattractant. Characterization of the C. albicans chemoattractant revealed that it is a peptide of approximately 1 kDa. Whereas the mating type of C. albicans did not affect the release of chemoattractant, switching did. White-phase cells released chemoattractant, but opaque-phase cells did not. Since the opaque phase of C. albicans represents the mating-competent phenotype, it may be that opaque-phase cells selectively suppress the release of chemoattractant to facilitate mating.
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5

Goldman, G., R. Welbourn, J. M. Klausner, L. Kobzik, C. R. Valeri, D. Shepro, and H. B. Hechtman. "Intravascular chemoattractants inhibit diapedesis by selective receptor occupancy." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (February 1, 1991): H465—H472. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h465.

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An extravascular chemoattractant leads to migration of polymorphonuclear neutrophils (PMN) to that site, whereas intravascular administration leads to PMN oxidative activity and sequestration in microvessels but no diapedesis. This study examines the inhibitory role of intravascular chemoattractants. Rabbits (n = 37) were pretreated with zymosan-activated plasma (ZAP), leukotriene (LT) B4, or thromboxane (Tx) mimic. These agents were given intra-arterially, topically into plastic chambers taped atop sites of dermabrasion on the back, or into a lobar bronchus (n = 35). Intra-arterial injection of each chemoattractant resulted, 10 min later, in a 29-42% increase in intracellular PMN H2O2. In saline-infused animals, topical administration of the chemoattractants into dermabrasion chambers resulted in PMN accumulation per cubic millimeter after 3 h of 600 with ZAP, 536 with LTB4, and 643 with Tx mimic; all values higher than 46 with saline and 63 with normal plasma (all P less than 0.05). In other saline-infused animals, lobar lung aspiration of chemoattractants led to diapedesis as measured in bronchoalveolar lavage (BAL) fluid (PMN x 10(4)/ml) after 3 h: 19.0 with ZAP, 11.2 with LTB4 and 14.5 with Tx mimic, all greater than aspiration with saline or normal plasma 4.0 and 4.9, respectively (all P less than 0.05). Intra-arterial chemotactic administration inhibited subsequent PMN diapedesis in response to that same chemoattractant, both in dermabrasion chambers and in BAL fluid. When different intra- and extra-vascular chemoattractants were used diapedesis was promoted. Thus Tx infused intra-arterially and ZAP applied to a blister or lobar bronchus led to rapid cell migration and increased cell numbers.(ABSTRACT TRUNCATED AT 250 WORDS)
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6

Ho, Y. S., W. M. Lee, and R. Snyderman. "Chemoattractant-induced activation of c-fos gene expression in human monocytes." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1524–38. http://dx.doi.org/10.1084/jem.165.6.1524.

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Human monocytes use the products of phosphoinositide hydrolysis (1,2-diacylglycerol and inositol 1,4,5-triphosphate) as second messengers to trigger rapid cellular activation during the occupancy of chemoattractant receptors. The effect of chemoattractants on modulation of gene expression in monocytes was examined in this study. The chemoattractants FMLP and platelet-activating factor induced the progressive increase of c-fos RNA to 6-15-fold over those of control within 30 min after treatment. Similar kinetics of c-fos gene activation was also observed when cells were treated with PMA or sn-1,2-dioctanoylglycerol, but not with the calcium mobilizer ionomycin, suggesting a role for protein kinase C in gene regulation by chemoattractant receptors. Activation of c-fos gene expression by FMLP is mediated through a pertussis toxin-sensitive G protein, since pertussis toxin treatment of the cells blocked the induction of the c-fos gene by FMLP but not PMA. The level of c-myc RNA was slightly decreased after 1 h of treatment with chemoattractants, but not with PMA or diacylglycerol. This implies that chemoattractant receptor occupancy generates signals beyond protein kinase C activation that are capable of selectively downregulating monocyte gene expression. The effect of FMLP and PMA on the accumulation of c-fos RNA appears to result from altering both the rate of transcription and message stability. These observations indicate that signals generated through chemoattractant receptor occupancy may regulate monocyte function at the genetic level.
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7

Shutt, D. C., L. M. Jenkins, E. J. Carolan, J. Stapleton, K. J. Daniels, R. C. Kennedy, and D. R. Soll. "T cell syncytia induced by HIV release. T cell chemoattractants: demonstration with a newly developed single cell chemotaxis chamber." Journal of Cell Science 111, no. 1 (January 1, 1998): 99–109. http://dx.doi.org/10.1242/jcs.111.1.99.

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A chemotaxis chamber has been developed to analyze both the velocity and the directionality of individual T cells in gradients of high molecular mass molecules over long periods of time. Employing this chamber, it is demonstrated that syncytia induced by HIV in SUP-T1 cell cultures release two T cell chemoattractants with approximate molecular masses of 30 and 120 kDa. Neither uninfected single cells nor polyethylene glycol-induced syncytia release detectable chemoattractant, suggesting that these chemoattractants are linked to HIV infection. Soluble gp120 functions as a T cell chemoattractant and the addition of anti-gp120 antibody to syncytium-conditioned medium blocks the high molecular mass chemoattractant activity but not the low molecular mass activity. The addition of anti-CD4 antibody to syncytium-conditioned medium also blocks the high molecular mass chemoattractant activity but not the low molecular mass activity. These results demonstrate that HIV-induced T cell syncytia release a low and a high molecular mass T cell chemoattractant, and suggest that the high molecular mass factor is gp120 and that it functions through the CD4 receptor.
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8

Takeyama, Kiyoshi, Carlos Agustí, Iris Ueki, James Lausier, Lars Olaf Cardell, and Jay A. Nadel. "Neutrophil-dependent goblet cell degranulation: role of membrane-bound elastase and adhesion molecules." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (August 1, 1998): L294—L302. http://dx.doi.org/10.1152/ajplung.1998.275.2.l294.

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We examined the effect of the neutrophil chemoattractants interleukin (IL)-8 and N-formyl-methionyl-leucyl-phenylalanine on goblet cell (GC) degranulation in guinea pigs. Chemoattractants caused time-dependent neutrophil recruitment and GC degranulation in vivo. NPC 15669 (an inhibitor of leukocyte infiltration) prevented both responses, implicating neutrophils. ICI 200,355 (an inhibitor of neutrophil elastase and proteinase-3) or secretory leukocyte protease inhibitor (an inhibitor of elastase but not of proteinase-3) abolished IL-8-induced GC degranulation, implicating elastase. Incubating tracheal segments with IL-8 plus neutrophils caused GC degranulation in vitro, an effect due to activation of the neutrophils themselves (and not an effect present in the supernatant). Chemoattractant increased surface staining of elastase and the cleavage of elastase-specific fluorogenic substrate by neutrophils. Pretreatment with anti-intercellular adhesion molecule-1, anti-CD18, or anti-CD11b antibody inhibited the chemoattractant-induced GC degranulation in vitro, implicating adhesion molecules. These studies suggest that chemoattractants cause neutrophil-dependent GC degranulation involving adhesive interactions between cells, with elastase activity occurring at the cell interface, causing GC secretion. The findings, reproduced in human airways, suggest novel methods of therapeutic intervention.
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9

Kim, Chang H., and Hal E. Broxmeyer. "In Vitro Behavior of Hematopoietic Progenitor Cells Under the Influence of Chemoattractants: Stromal Cell–Derived Factor-1, Steel Factor, and the Bone Marrow Environment." Blood 91, no. 1 (January 1, 1998): 100–110. http://dx.doi.org/10.1182/blood.v91.1.100.

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Abstract How multiple chemoattractants cooperate in directing the migration of hematopoietic progenitor cells (HPC) for homing and peripheral blood mobilization has not yet been established. We report here the behavior of HPC under the influence of two different chemoattractants, stromal cell-derived factor (SDF)-1 and steel factor (SLF), and the chemotactic nature of the bone marrow (BM) environment using a two-chamber in vitro migration system. Various formulae were adopted to quantitate these effects. Based on these quantitations, SDF-1 showed only chemotactic activity, while SLF showed both chemotactic and chemokinetic activities on factor-dependent MO7e cells. SLF, like SDF-1, attracted human HPC from a population of CD34+ cells and induced actin polymerization in MO7e cells. SLF and SDF-1 cooperated in attracting MO7e cells, as well as cord blood (CB) and BM CD34+cells. A negative concentration gradient of SLF and SDF-1, formed by the presence of chemoattractants in the upper chamber, showed potent inhibitory effects on MO7e cell migration induced by either of these chemoattractants in the lower chamber, and SDF-1 and SLF were synergistic in mobilizing cells to the lower chamber from this negative chemoattractant gradient. Plasma obtained from BM aspirates, but not CB or peripheral blood, showed strong chemotactic effects on BM and CB CD34+ cells, and an inhibitory effect in a negative gradient on SDF-1–dependent CD34+ cell migration. These in vitro migration experiments suggest that chemoattractants such as SDF-1 and SLF with other unidentified BM chemoattractants may be involved cooperatively in the migration of HPC to the BM and in preventing spontaneous mobilization of HPC out of the BM.
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10

Kim, Chang H., and Hal E. Broxmeyer. "In Vitro Behavior of Hematopoietic Progenitor Cells Under the Influence of Chemoattractants: Stromal Cell–Derived Factor-1, Steel Factor, and the Bone Marrow Environment." Blood 91, no. 1 (January 1, 1998): 100–110. http://dx.doi.org/10.1182/blood.v91.1.100.100_100_110.

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How multiple chemoattractants cooperate in directing the migration of hematopoietic progenitor cells (HPC) for homing and peripheral blood mobilization has not yet been established. We report here the behavior of HPC under the influence of two different chemoattractants, stromal cell-derived factor (SDF)-1 and steel factor (SLF), and the chemotactic nature of the bone marrow (BM) environment using a two-chamber in vitro migration system. Various formulae were adopted to quantitate these effects. Based on these quantitations, SDF-1 showed only chemotactic activity, while SLF showed both chemotactic and chemokinetic activities on factor-dependent MO7e cells. SLF, like SDF-1, attracted human HPC from a population of CD34+ cells and induced actin polymerization in MO7e cells. SLF and SDF-1 cooperated in attracting MO7e cells, as well as cord blood (CB) and BM CD34+cells. A negative concentration gradient of SLF and SDF-1, formed by the presence of chemoattractants in the upper chamber, showed potent inhibitory effects on MO7e cell migration induced by either of these chemoattractants in the lower chamber, and SDF-1 and SLF were synergistic in mobilizing cells to the lower chamber from this negative chemoattractant gradient. Plasma obtained from BM aspirates, but not CB or peripheral blood, showed strong chemotactic effects on BM and CB CD34+ cells, and an inhibitory effect in a negative gradient on SDF-1–dependent CD34+ cell migration. These in vitro migration experiments suggest that chemoattractants such as SDF-1 and SLF with other unidentified BM chemoattractants may be involved cooperatively in the migration of HPC to the BM and in preventing spontaneous mobilization of HPC out of the BM.
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11

Owen, C. A., M. A. Campbell, S. S. Boukedes, and E. J. Campbell. "Monocytes recruited to sites of inflammation express a distinctive proinflammatory (P) phenotype." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 6 (December 1, 1994): L786—L796. http://dx.doi.org/10.1152/ajplung.1994.267.6.l786.

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Only a minor proportion of monocytes responds to chemoattractants. To test the possibility that chemoattractant-responsive monocytes have distinctive functional characteristics, we enriched or depleted monocyte preparations for cells having a proinflammatory (P) phenotype and tested their responses to biologically relevant chemoattractants. We prepared monocyte subpopulations by one of three independent techniques to minimize the chances of artifacts: 1) depletion of P monocytes by adherence to fibronectin; 2) enrichment for P monocytes by negative selection for HLA-DR antigen; and 3) flow cytometric sorting. We measured responsiveness of monocyte subpopulations to N-formyl-Met-Leu-Phe, C5a, zymosan-activated serum, and monocyte chemoattractant protein-1 by three parameters: 1) polarization, 2) actin polymerization, and 3) directed migration. With each chemoattractant and each parameter, there was a striking direct relationship between the responsiveness of the monocyte preparations and their content of P monocytes. Our data indicate that the capacity of monocytes to be recruited rapidly from the vasculature into sites of inflammation is a property of a subpopulation of monocytes with a distinctive, neutrophil-like proinflammatory phenotype.
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12

Wu, D., C. K. Huang, and H. Jiang. "Roles of phospholipid signaling in chemoattractant-induced responses." Journal of Cell Science 113, no. 17 (September 1, 2000): 2935–40. http://dx.doi.org/10.1242/jcs.113.17.2935.

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Chemoattractants, including chemokines, play a central role in regulation of inflammatory reactions by attracting and activating leukocytes. These molecules have been found to regulate metabolism of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)) via phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K). Recent studies of mouse lines that lack PLC-(beta)2, PLC-(beta)3, or PI3K(gamma) demonstrate that chemoattractants act through PLC-(beta)2 and PLC-(beta)3 to hydrolyze PtdIns(4,5)P(2) and through PI3K(gamma) to phosphorylate PtdIns(4,5)P(2) in mouse neutrophils. These studies also confirmed the importance and revealed new roles of these signaling pathways in chemoattractant-induced responses.
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13

Southwick, F. S., G. A. Dabiri, M. Paschetto, and S. H. Zigmond. "Polymorphonuclear leukocyte adherence induces actin polymerization by a transduction pathway which differs from that used by chemoattractants." Journal of Cell Biology 109, no. 4 (October 1, 1989): 1561–69. http://dx.doi.org/10.1083/jcb.109.4.1561.

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Nitrobenzoxadiazole-phallacidin in combination with quantitative fluorescent microscopy have been used to measure F-actin concentrations in human polymorphonuclear leukocytes (PMN) as they adhere to a plastic surface. Like stimulation with chemoattractants, adherence is associated with a twofold rise in F-actin content. However unlike the rapid rise in F-actin induced by chemoattractants which peaks within 30 s, actin assembly induced by adherence is slower, maximum F-actin values not being observed until 10 min. Furthermore the rise in F-actin induced by adherence is persistent, remaining constant over 60 min while F-actin returns to near basal levels after 20 min exposure to chemoattractant. The combination of adherence (5 min) followed by chemoattractant (FMLP 5 x 10(-8) M for 40 s) resulted in an additive rise in F-actin content to greater than threefold over unstimulated values. Unlike chemoattractant induced actin assembly, adherence-associated PMN actin polymerization was not inhibited by pertussis toxin, but was markedly reduced by lowering extracellular Ca2+. Fluorescent micrographs of adherent PMN stained with nitrobenzoxadiazole-phallacidin revealed F-actin in the lamellipodia and in small foci on the adherent surface. These findings suggest that the transduction mechanisms by which adherence induces PMN actin polymerization differ from those used by chemoattractant receptors.
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14

Liao, Xin-Hua, Jonathan Buggey, Yun Kyung Lee, and Alan R. Kimmel. "Chemoattractant stimulation of TORC2 is regulated by receptor/G protein–targeted inhibitory mechanisms that function upstream and independently of an essential GEF/Ras activation pathway in Dictyostelium." Molecular Biology of the Cell 24, no. 13 (July 2013): 2146–55. http://dx.doi.org/10.1091/mbc.e13-03-0130.

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Global stimulation of Dictyostelium with different chemoattractants elicits multiple transient signaling responses, including synthesis of cAMP and cGMP, actin polymerization, activation of kinases ERK2, TORC2, and phosphatidylinositide 3-kinase, and Ras-GTP accumulation. Mechanisms that down-regulate these responses are poorly understood. Here we examine transient activation of TORC2 in response to chemically distinct chemoattractants, cAMP and folate, and suggest that TORC2 is regulated by adaptive, desensitizing responses to stimulatory ligands that are independent of downstream, feedback, or feedforward circuits. Cells with acquired insensitivity to either folate or cAMP remain fully responsive to TORC2 activation if stimulated with the other ligand. Thus TORC2 responses to cAMP or folate are not cross-inhibitory. Using a series of signaling mutants, we show that folate and cAMP activate TORC2 through an identical GEF/Ras pathway but separate receptors and G protein couplings. Because the common GEF/Ras pathway also remains fully responsive to one chemoattractant after desensitization to the other, GEF/Ras must act downstream and independent of adaptation to persistent ligand stimulation. When initial chemoattractant concentrations are immediately diluted, cells rapidly regain full responsiveness. We suggest that ligand adaptation functions in upstream inhibitory pathways that involve chemoattractant-specific receptor/G protein complexes and regulate multiple response pathways.
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Pike, MC, L. Jakoi, LC McPhail, and R. Snyderman. "Chemoattractant-mediated stimulation of the respiratory burst in human polymorphonuclear leukocytes may require appearance of protein kinase activity in the cells' particulate fraction." Blood 67, no. 4 (April 1, 1986): 909–13. http://dx.doi.org/10.1182/blood.v67.4.909.909.

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Abstract Low doses of aliphatic alcohols produce divergent effects on the function of chemoattractant receptors on human polymorphonuclear leukocytes (PMNs) since they enhance chemotaxis but inhibit stimulation of superoxide production by chemoattractants. As such, alcohols can provide useful pharmacologic tools to probe the mechanisms of stimulus- response coupling in leukocytes. A role for protein kinase C has been implicated in the activation of the respiratory burst in PMNs. Although the vast majority of this enzyme activity is located in the cytosolic fraction of unactivated PMNs, protein kinase C activity appears in the particulate fraction of the cells when they are stimulated to produce superoxide by either chemoattractants or by phorbol myristate acetate (PMA). Doses of the alcohols that selectively inhibited stimulation of superoxide production by chemoattractants also inhibited the appearance of protein kinase C activity as well as an undefined protein kinase activity in the particulate fraction of the cells. In contrast, the alcohols did not affect either the ability of PMA to stimulate the production of superoxide in PMNs nor the appearance of protein kinase activity in the cells' particulate fraction. PMA is known to bind and activate protein kinase C directly, thus bypassing receptor-mediated events. These data suggest that alcohols inhibit the stimulation of the respiratory burst by chemoattractants in PMNs by blocking the ability of receptor occupancy to induce the appearance of protein kinase activity in particulate fractions. These results moreover suggest that the appearance of protein kinase activity in the particulate fraction may be required for activation of the respiratory burst in PMNs.
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Pike, MC, L. Jakoi, LC McPhail, and R. Snyderman. "Chemoattractant-mediated stimulation of the respiratory burst in human polymorphonuclear leukocytes may require appearance of protein kinase activity in the cells' particulate fraction." Blood 67, no. 4 (April 1, 1986): 909–13. http://dx.doi.org/10.1182/blood.v67.4.909.bloodjournal674909.

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Low doses of aliphatic alcohols produce divergent effects on the function of chemoattractant receptors on human polymorphonuclear leukocytes (PMNs) since they enhance chemotaxis but inhibit stimulation of superoxide production by chemoattractants. As such, alcohols can provide useful pharmacologic tools to probe the mechanisms of stimulus- response coupling in leukocytes. A role for protein kinase C has been implicated in the activation of the respiratory burst in PMNs. Although the vast majority of this enzyme activity is located in the cytosolic fraction of unactivated PMNs, protein kinase C activity appears in the particulate fraction of the cells when they are stimulated to produce superoxide by either chemoattractants or by phorbol myristate acetate (PMA). Doses of the alcohols that selectively inhibited stimulation of superoxide production by chemoattractants also inhibited the appearance of protein kinase C activity as well as an undefined protein kinase activity in the particulate fraction of the cells. In contrast, the alcohols did not affect either the ability of PMA to stimulate the production of superoxide in PMNs nor the appearance of protein kinase activity in the cells' particulate fraction. PMA is known to bind and activate protein kinase C directly, thus bypassing receptor-mediated events. These data suggest that alcohols inhibit the stimulation of the respiratory burst by chemoattractants in PMNs by blocking the ability of receptor occupancy to induce the appearance of protein kinase activity in particulate fractions. These results moreover suggest that the appearance of protein kinase activity in the particulate fraction may be required for activation of the respiratory burst in PMNs.
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17

Fitzpatrick, John L., Charlotte Willis, Alessandro Devigili, Amy Young, Michael Carroll, Helen R. Hunter, and Daniel R. Brison. "Chemical signals from eggs facilitate cryptic female choice in humans." Proceedings of the Royal Society B: Biological Sciences 287, no. 1928 (June 10, 2020): 20200805. http://dx.doi.org/10.1098/rspb.2020.0805.

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Mate choice can continue after mating via chemical communication between the female reproductive system and sperm. While there is a growing appreciation that females can bias sperm use and paternity by exerting cryptic female choice for preferred males, we know surprisingly little about the mechanisms underlying these post-mating choices. In particular, whether chemical signals released from eggs (chemoattractants) allow females to exert cryptic female choice to favour sperm from specific males remains an open question, particularly in species (including humans) where adults exercise pre-mating mate choice. Here, we adapt a classic dichotomous mate choice assay to the microscopic scale to assess gamete-mediated mate choice in humans. We examined how sperm respond to follicular fluid, a source of human sperm chemoattractants, from either their partner or a non-partner female when experiencing a simultaneous or non-simultaneous choice between follicular fluids. We report robust evidence under these two distinct experimental conditions that follicular fluid from different females consistently and differentially attracts sperm from specific males. This chemoattractant-moderated choice of sperm offers eggs an avenue to exercise independent mate preference. Indeed, gamete-mediated mate choice did not reinforce pre-mating human mate choice decisions. Our results demonstrate that chemoattractants facilitate gamete-mediated mate choice in humans, which offers females the opportunity to exert cryptic female choice for sperm from specific males.
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18

BISMARA, CLAUDIO, GIAN MARIA BONORA, CLAUDIO TONIOLO, ELMER L. BECKER, and RICHARD J. FREER. "Synthetic homo-oligomethionine chemoattractants." International Journal of Peptide and Protein Research 26, no. 5 (January 12, 2009): 482–92. http://dx.doi.org/10.1111/j.1399-3011.1985.tb01015.x.

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19

Schröder, J. M. "Inflammatory mediators and chemoattractants." Clinics in Dermatology 13, no. 2 (March 1995): 137–50. http://dx.doi.org/10.1016/0738-081x(95)93820-e.

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20

Moore, J. P., and R. A. Koup. "Chemoattractants attract HIV researchers." Journal of Experimental Medicine 184, no. 2 (August 1, 1996): 311–13. http://dx.doi.org/10.1084/jem.184.2.311.

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21

Fay, F. S., R. Brundage, K. Perry, and S. H. Gilbert. "The dynamics of local chemical changes underlying white-cell chemotaxis measured with digital imaging microscopy." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (August 1992): 422–23. http://dx.doi.org/10.1017/s0424820100122514.

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The ability of cells to polarize and move towards or away from a chemical stimulus is a fundamental property of virtually all cell types at some stage in their development. This process is important for biological processes ranging from morphogenesis, to wound healing, to the attack by leukocytes of invading organisms in our body. Despite the importance of this phenomenon, surprisingly little is known regarding the mechanism whereby an external chemical gradient is converted into an intracellular gradient of 2° messengers, how the local chemistry of the cell is compared and how the result of that comparison gives rise to the polarized organization of the cell and the resulting directional migration of the cells. In order to obtain insights into this fundamental cellular process, we have been investigating the local chemical changes underlying the response of newt eosinophils to chemoattractants. This cell system is particularly well suited for asking such questions as the cells are large (30 microns wide, 70 microns long), thereby facilitating micro-injection of various fluorescent compounds as well as the imaging of local differences in the concentration of important species involved in responses to chemoattractants. Furthermore, these cells respond in seconds to gradients of serum chemoattractants, thereby facilitating an analysis of the sequence of events linking the gradient of chemoattractant to the generation of local chemical signals ultimately leading to the polarization and directed migration of these cells.
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22

Weisbart, RH, L. Kwan, DW Golde, and JC Gasson. "Human GM-CSF primes neutrophils for enhanced oxidative metabolism in response to the major physiological chemoattractants." Blood 69, no. 1 (January 1, 1987): 18–21. http://dx.doi.org/10.1182/blood.v69.1.18.18.

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Abstract Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a T cell- derived lymphokine which induces hematopoietic precursor cells to proliferate in vitro and differentiate to neutrophils and macrophages. GM-CSF also inhibits the motility of mature neutrophils (NIF-T activity), and primes neutrophils to enhance oxidative metabolism in response to the bacterial chemoattractant, N-formyl-methionyl-leucyl- phenylalanine (f-MLP). The present study was designed to determine whether this lymphokine also enhances neutrophil oxidative metabolism in response to the other major physiological chemoattractants which include complement-derived C5a, and the 5-lipoxygenation product of arachidonic acid, leukotriene B4 (LTB4). Superoxide anion production was measured as superoxide dismutase-inhibitable cytochrome C reduction. Purified biosynthetic GM-CSF enhanced superoxide anion production by neutrophils in response to f-MLP, C5a desArg, and LTB4. In contrast to several other factors which prime neutrophils, GM-CSF did not prime for an enhanced oxidative response to phorbol myristate acetate (PMA). These results suggest that GM-CSF may be an endogenous regulator of neutrophil inflammatory responses induced by the major physiological chemoattractants.
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23

Weisbart, RH, L. Kwan, DW Golde, and JC Gasson. "Human GM-CSF primes neutrophils for enhanced oxidative metabolism in response to the major physiological chemoattractants." Blood 69, no. 1 (January 1, 1987): 18–21. http://dx.doi.org/10.1182/blood.v69.1.18.bloodjournal69118.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a T cell- derived lymphokine which induces hematopoietic precursor cells to proliferate in vitro and differentiate to neutrophils and macrophages. GM-CSF also inhibits the motility of mature neutrophils (NIF-T activity), and primes neutrophils to enhance oxidative metabolism in response to the bacterial chemoattractant, N-formyl-methionyl-leucyl- phenylalanine (f-MLP). The present study was designed to determine whether this lymphokine also enhances neutrophil oxidative metabolism in response to the other major physiological chemoattractants which include complement-derived C5a, and the 5-lipoxygenation product of arachidonic acid, leukotriene B4 (LTB4). Superoxide anion production was measured as superoxide dismutase-inhibitable cytochrome C reduction. Purified biosynthetic GM-CSF enhanced superoxide anion production by neutrophils in response to f-MLP, C5a desArg, and LTB4. In contrast to several other factors which prime neutrophils, GM-CSF did not prime for an enhanced oxidative response to phorbol myristate acetate (PMA). These results suggest that GM-CSF may be an endogenous regulator of neutrophil inflammatory responses induced by the major physiological chemoattractants.
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24

Miyabe, Yoshishige, Chie Miyabe, Vinidhra Mani, Thorsten R. Mempel, and Andrew D. Luster. "Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation." Science Immunology 4, no. 35 (May 10, 2019): eaav5951. http://dx.doi.org/10.1126/sciimmunol.aav5951.

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Chemoattractant-induced arrest of circulating leukocytes and their subsequent diapedesis is a fundamental component of inflammation. However, how tissue-derived chemoattractants are transported into the blood vessel lumen to induce leukocyte entry into tissue is not well understood. Here, intravital microscopy in live mice has shown that the “atypical” complement C5a receptor 2 (C5aR2) and the atypical chemokine receptor 1 (ACKR1) expressed on endothelial cells were required for the transport of C5a and CXCR2 chemokine ligands, respectively, into the vessel lumen in a murine model of immune complex–induced arthritis. Transported C5a was required to initiate C5aR1-mediated neutrophil arrest, whereas transported chemokines were required to initiate CXCR2-dependent neutrophil transdendothelial migration. These findings provide new insights into how atypical chemoattractant receptors collaborate with “classical” signaling chemoattractant receptors to control distinct steps in the recruitment of neutrophils into tissue sites of inflammation.
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25

Bacon, K. B., and R. D. R. Camp. "Lipid lymphocyte chemoattractants in psoriasis." Prostaglandins 40, no. 6 (December 1990): 603–14. http://dx.doi.org/10.1016/0090-6980(90)90005-g.

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26

Loike, J. D., J. el Khoury, L. Cao, C. P. Richards, H. Rascoff, J. T. Mandeville, F. R. Maxfield, and S. C. Silverstein. "Fibrin regulates neutrophil migration in response to interleukin 8, leukotriene B4, tumor necrosis factor, and formyl-methionyl-leucyl-phenylalanine." Journal of Experimental Medicine 181, no. 5 (May 1, 1995): 1763–72. http://dx.doi.org/10.1084/jem.181.5.1763.

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We have examined the capacity of four different chemoattractants/cytokines to promote directed migration of polymorphonuclear leukocytes (PMN) through three-dimensional gels composed of extracellular matrix proteins. About 20% of PMN migrated through fibrin gels and plasma clots in response to a gradient of interleukin 8 (IL-8) or leukotriene B4 (LTB4). In contrast, < 0.3% of PMN migrated through fibrin gels in response to a gradient of tumor necrosis factor alpha (TNF) or formyl-methionyl-leucyl-phenylalanine (FMLP). All four chemoattractants stimulated PMN to migrate through gels composed of collagen IV or of basement membrane proteins (Matrigel), or through filters to which fibronectin or fibrinogen had been adsorbed. PMN stimulated with TNF or FMLP adhered and formed zones of close apposition to fibrin, as measured by the exclusion of a 10-kD rhodamine-polyethylene glycol probe from the contact zones between PMN and the underlying fibrin gel. By this measure, IL-8- or LTB4-treated PMN adhered loosely to fibrin, since 10 kD rhodamine-polyethylene glycol permeated into the contact zones between these cells and the underlying fibrin gel. PMN stimulated with FMLP and IL-8, or FMLP and LTB4, exhibited very little migration through fibrin gels, and three times as many of these cells excluded 10 kD rhodamine-polyethylene glycol from their zones of contact with fibrin as PMN stimulated with IL-8 or LTB4 alone. These results show that PMN chemotaxis is regulated by both the nature of the chemoattractant and the composition of the extracellular matrix; they suggest that certain combinations of chemoattractants and matrix proteins may limit leukocyte movements and promote their localization in specific tissues in vivo.
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27

Rainard, P. "Consequences of Interference of Milk with Chemoattractants for Enzyme-Linked Immunosorbent Assay Quantifications." Clinical and Vaccine Immunology 17, no. 5 (March 17, 2010): 848–52. http://dx.doi.org/10.1128/cvi.00447-09.

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ABSTRACT Concentrations of the chemoattractants CXCL1, CXCL2, CXCL3, CXCL8, and C5a in milk were reduced by the preparation of milk whey by high-speed centrifugation or with rennet. About half of the chemoattractants (35 to 65%) were associated with the casein micelle sediment, except when whey was prepared by acidification. Consequently, quantification of chemoattractants should be carried out preferentially with skimmed milk samples or, whenever whey is needed, with acidic whey samples. The interference of milk or milk whey with the enzyme-linked immunosorbent assays (ELISAs) used to quantify the chemoattractants was moderate, as long as tetramethylbenzidine (TMB), not ABTS [2,2′-azino-bis-(3-ethylbenzthiazoline-sulfonate)], was used as the substrate of peroxidase. These considerations will help to assess more precisely a component of the immune response of the mammary gland to infection.
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28

Foxman, Ellen F., Eric J. Kunkel, and Eugene C. Butcher. "Integrating Conflicting Chemotactic Signals." Journal of Cell Biology 147, no. 3 (November 1, 1999): 577–88. http://dx.doi.org/10.1083/jcb.147.3.577.

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Leukocytes navigate through complex chemoattractant arrays, and in so doing, they must migrate from one chemoattractant source to another. By evaluating directional persistence and chemotaxis during neutrophil migration under agarose, we show that cells migrating away from a local chemoattractant, against a gradient, display true chemotaxis to distant agonists, often behaving as if the local gradient were without effect. We describe two interrelated properties of migrating cells that allow this to occur. First, migrating leukocytes can integrate competing chemoattractant signals, responding as if to the vector sum of the orienting signals present. Second, migrating cells display memory of their recent environment: cells' perception of the relative strength of orienting signals is influenced by their history, so that cells prioritize newly arising or newly encountered attractants. We propose that this cellular memory, by promoting sequential chemotaxis to one attractant after another, is in fact responsible for the integration of competitive orienting signals over time, and allows combinations of chemoattractants to guide leukocytes in a step-by-step fashion to their destinations within tissues.
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29

Artemenko, Yulia, Lucas Axiotakis, Jane Borleis, Pablo A. Iglesias, and Peter N. Devreotes. "Chemical and mechanical stimuli act on common signal transduction and cytoskeletal networks." Proceedings of the National Academy of Sciences 113, no. 47 (November 7, 2016): E7500—E7509. http://dx.doi.org/10.1073/pnas.1608767113.

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Signal transduction pathways activated by chemoattractants have been extensively studied, but little is known about the events mediating responses to mechanical stimuli. We discovered that acute mechanical perturbation of cells triggered transient activation of all tested components of the chemotactic signal transduction network, as well as actin polymerization. Similarly to chemoattractants, the shear flow-induced signal transduction events displayed features of excitability, including the ability to mount a full response irrespective of the length of the stimulation and a refractory period that is shared with that generated by chemoattractants. Loss of G protein subunits, inhibition of multiple signal transduction events, or disruption of calcium signaling attenuated the response to acute mechanical stimulation. Unlike the response to chemoattractants, an intact actin cytoskeleton was essential for reacting to mechanical perturbation. These results taken together suggest that chemotactic and mechanical stimuli trigger activation of a common signal transduction network that integrates external cues to regulate cytoskeletal activity and drive cell migration.
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30

Hyduk, Sharon J., Jason R. Chan,, Stewart T. Duffy, Mian Chen, Mark D. Peterson, Thomas K. Waddell, Genevieve C. Digby, Katalin Szaszi, Andras Kapus, and Myron I. Cybulsky. "Phospholipase C, calcium, and calmodulin are critical for α4β1 integrin affinity up-regulation and monocyte arrest triggered by chemoattractants." Blood 109, no. 1 (September 7, 2006): 176–84. http://dx.doi.org/10.1182/blood-2006-01-029199.

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Abstract During inflammation, monocytes roll on activated endothelium and arrest after stimulation by proteoglycan-bound chemokines and other chemoattractants. We investigated signaling pathways downstream of G protein–coupled receptors (GPCRs) that are relevant to α4β1 integrin affinity up-regulation using formyl peptide receptor-transfected U937 cells stimulated with fMLP or stromal-derived factor-1α and human peripheral blood monocytes stimulated with multiple chemokines or chemoattractants. The up-regulation of soluble LDV peptide or vascular cell adhesion molecule-1 (VCAM-1) binding by these stimuli was critically dependent on activation of phospholipase C (PLC), inositol 1,4,5-triphosphate receptors, increased intracellular calcium, influx of extracellular calcium, and calmodulin, suggesting that this signaling pathway is required for α4 integrins to assume a high-affinity conformation. In fact, a rise in intracellular calcium following treatment with thapsigargin or ionomycin was sufficient to induce binding of ligand. Blockade of p44/42 and p38 mitogen-activated protein (MAP) kinases, phosphoinositide 3-kinase, or protein kinase C (PKC) signaling did not inhibit chemoattractant-induced LDV or VCAM-1 binding. However, activation of PKC by phorbol ester up-regulated α4β1 affinity with kinetics distinct from those of GPCR signaling. A critical role for PLC and calmodulin was also established for leukocyte arrest and adhesion strengthening.
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31

Funamoto, Satoru, Kristina Milan, Ruedi Meili, and Richard A. Firtel. "Role of Phosphatidylinositol 3′ Kinase and a Downstream Pleckstrin Homology Domain–Containing Protein in Controlling Chemotaxis inDictyostelium." Journal of Cell Biology 153, no. 4 (May 14, 2001): 795–810. http://dx.doi.org/10.1083/jcb.153.4.795.

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We show that cells lacking two Dictyostelium class I phosphatidylinositol (PI) 3′ kinases (PI3K and pi3k1/2-null cells) or wild-type cells treated with the PI3K inhibitor LY294002 are unable to properly polarize, are very defective in the temporal, spatial, and quantitative regulation of chemoattractant-mediated filamentous (F)-actin polymerization, and chemotax very slowly. PI3K is thought to produce membrane lipid-binding sites for localization of PH domain–containing proteins. We demonstrate that in response to chemoattractants three PH domain–containing proteins do not localize to the leading edge in pi3k1/2-null cells, and the translocation is blocked in wild-type cells by LY294002. Cells lacking one of these proteins, phdA-null cells, exhibit defects in the level and kinetics of actin polymerization at the leading edge and have chemotaxis phenotypes that are distinct from those described previously for protein kinase B (PKB) (pkbA)-null cells. Phenotypes of PhdA-dominant interfering mutations suggest that PhdA is an adaptor protein that regulates F-actin localization in response to chemoattractants and links PI3K to the control of F-actin polymerization at the leading edge during pseudopod formation. We suggest that PKB and PhdA lie downstream from PI3K and control different downstream effector pathways that are essential for proper chemotaxis.
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32

Nuzzi, Paul A., Melissa A. Senetar, and Anna Huttenlocher. "Asymmetric Localization of Calpain 2 during Neutrophil Chemotaxis." Molecular Biology of the Cell 18, no. 3 (March 2007): 795–805. http://dx.doi.org/10.1091/mbc.e06-09-0876.

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Chemoattractants induce neutrophil polarization through localized polymerization of F-actin at the leading edge. The suppression of rear and lateral protrusions is required for efficient chemotaxis and involves the temporal and spatial segregation of signaling molecules. We have previously shown that the intracellular calcium-dependent protease calpain is required for cell migration and is involved in regulating neutrophil chemotaxis. Here, we show that primary neutrophils and neutrophil-like HL-60 cells express both calpain 1 and calpain 2 and that chemoattractants induce the asymmetric recruitment of calpain 2, but not calpain 1, to the leading edge of polarized neutrophils and differentiated HL-60 cells. Using time-lapse microscopy, we show that enrichment of calpain 2 at the leading edge occurs during early pseudopod formation and that its localization is sensitive to changes in the chemotactic gradient. We demonstrate that calpain 2 is recruited to lipid rafts and that cholesterol depletion perturbs calpain 2 localization, suggesting that its enrichment at the front requires proper membrane organization. Finally, we show that catalytic activity of calpain is required to limit pseudopod formation in the direction of chemoattractant and for efficient chemotaxis. Together, our findings identify calpain 2 as a novel component of the frontness signal that promotes polarization during chemotaxis.
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33

Francis, Sanjeev A., Xun Shen, Jeffrey B. Young, Prashant Kaul, and Daniel J. Lerner. "Rho GEF Lsc is required for normal polarization, migration, and adhesion of formyl-peptide–stimulated neutrophils." Blood 107, no. 4 (February 15, 2006): 1627–35. http://dx.doi.org/10.1182/blood-2005-03-1164.

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Neutrophil migration requires continuous reorganization of the cytoskeleton and cellular adhesion apparatus. Chemoattractants initiate intracellular signals that direct this reorganization. The signaling pathways that link chemoattractant receptors to the cytoskeleton and cellular adhesion apparatus are now being defined. Formyl-peptide chemoattractants released from bacteria stimulate G-protein–linked receptors on the surface of neutrophils and regulate the neutrophil cytoskeleton and adhesion apparatus through RhoA-dependent pathways. Lsc is a RhoA guanine nucleotide exchange factor that binds the heterotrimeric G-protein α-subunits, Gα12 and Gα13. We have disrupted the Lsc gene and demonstrated that formyl-peptide–stimulated Lsc knock-out (KO) neutrophils are unable to generate and sustain a single-dominant pseudopod and migrate with increased speed and reduced directionality. Unexpectedly, we also found that Lsc is required for normal β2- and β1-integrin–dependent neutrophil adhesion. Lsc-deficient mice have a peripheral leukocytosis and extramedullary hematopoiesis, demonstrating that Lsc is required for leukocyte homeostasis. Lsc-deficient neutrophils are recruited normally to sites of bacterial peritonitis and chemical dermatitis, indicating that other signaling pathways compensate for the Lsc deficiency in some forms of inflammation. These results demonstrate that Lsc links formyl-peptide receptors to RhoA signaling pathways that regulate polarization, migration, and adhesion in neutrophils and that Lsc is required for leukocyte homeostasis.
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34

Devine, Ken, and Peter Jones. "Investigations into the chemoattraction of the potato cyst nematodes Globodera rostochiensis and G. pallida towards fractionated potato root leachate." Nematology 5, no. 1 (2003): 65–75. http://dx.doi.org/10.1163/156854102765216704.

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AbstractThe behaviour of stimulated second stage juveniles (J2) (i.e., hatched in root leachate from potato cv. Cara) and unstimulated J2 (spontaneously hatched in water) of Globodera rostochiensis and G. pallida in response to fractionated and unfractionated potato root leachate (PRL) was investigated in attraction assays. In PRL, fractionated by combined ion-exchange-gel permeation chromatography on Sephadex G-10, three classes of semiochemicals with activity towards J2 were distinguished: i) chemoattractants; ii) chemostats, and iii) chemorepellents. The motility of PRL-hatched G. rostochiensis J2 in one fraction (12) at 10 days after their removal from the root leachate was significantly greater than that of water-hatched J2 apparently due to sensitisation of PRL-hatched J2. PRL-hatched J2 of G. pallida were attracted to different fractions than those of G. rostochiensis, whereas the water-hatched J2 from the two species were attracted to common fractions, indicating that sensitisation by exposure to PRL was species selective. The attraction of PRL-hatched PCN J2 to unfractionated PRL appeared to be dependent on the ratio of chemoattractant to chemorepellent semiochemicals in the leachate. For both species there was no detectable correlation between hatching activity and either attractiveness of root leachates from 12 potato genotypes or chemoattraction in PRL fractions, indicating that hatching factors were not active chemoattractants.
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35

Lampert, Thomas, Cheryl Nugent, John Weston, Nathanael Braun, and Heather Kuruvilla. "Nociceptin Signaling Involves a Calcium-Based Depolarization in Tetrahymena thermophila." International Journal of Peptides 2013 (April 29, 2013): 1–7. http://dx.doi.org/10.1155/2013/573716.

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Tetrahymena thermophila are free-living, ciliated eukaryotes. Their behavioral response to stimuli is well characterized and easily observable, since cells swim toward chemoattractants and avoid chemorepellents. Chemoattractant responses involve increased swim speed or a decreased change in swim direction, while chemorepellent signaling involves ciliary reversal, which causes the organism to jerk back and forth, swim in small circles, or spin in an attempt to get away from the repellent. Many food sources, such as proteins, are chemoattractants for these organisms, while a variety of compounds are repellents. Repellents in nature are thought to come from the secretions of predators or from ruptured organisms, which may serve as “danger” signals. Interestingly, several peptides involved in vertebrate pain signaling are chemorepellents in Tetrahymena, including substances P, ACTH, PACAP, VIP, and nociceptin. Here, we characterize the response of Tetrahymena thermophila to three different isoforms of nociceptin. We find that G-protein inhibitors and tyrosine kinase inhibitors do not affect nociceptin avoidance. However, the calcium chelator, EGTA, and the SERCA calcium ATPase inhibitor, thapsigargin, both inhibit nociceptin avoidance, implicating calcium in avoidance. This result is confirmed by electrophysiology studies which show that 50 M nociceptin-NH2 causes a sustained depolarization of approximately 40 mV, which is eliminated by the addition of extracellular EGTA.
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36

Cassimeris, L., H. McNeill, and S. H. Zigmond. "Chemoattractant-stimulated polymorphonuclear leukocytes contain two populations of actin filaments that differ in their spatial distributions and relative stabilities." Journal of Cell Biology 110, no. 4 (April 1, 1990): 1067–75. http://dx.doi.org/10.1083/jcb.110.4.1067.

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Chemoattractants stimulate actin polymerization in lamellipodia of polymorphonuclear leukocytes. We find that removal of chemoattractant results in rapid (within 10 s at 37 degrees C) and selective depolymerization of the F-actin located in lamellipodia. Addition of 10 microM cytochalasin B, in the presence of chemoattractant, also resulted in rapid and selective depolymerization of lamellar F-actin. The elevated F-actin level induced by chemoattractant rapidly returns to the level present in unstimulated cells after (a) a 10-fold decrease in chemoattractant concentration; (b) the addition of 10 microM cytochalasin B; or (c) cooling to 4 degrees C. The F-actin levels of unstimulated cells are only slightly affected by these treatments. Based on the similar effects of cytochalasin addition and chemoattractant dilution, it is likely that both treatments result in actin depolymerization from the pointed ends of filaments. Based on our results we propose that chemoattractant-stimulated polymorphonuclear leukocytes contain two distinct populations of actin filaments. The actin filaments within the lamellipodia are highly labile and in the continued presence of chemoattractant these filaments are rapidly turning over, continually polymerizing at their plus (barbed) ends, and depolymerizing at their minus ends. In contrast, the cortical F-actin filaments of both stimulated and unstimulated cells are differentially stable.
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37

Formaggio, F., M. Pantano, M. Crisma, C. Toniolo, W. H. J. Boesten, H. E. Schoemaker, J. Kamphuis, and E. L. Becker. "Backbone modified formyl-methionyl tripeptide chemoattractants." Bioorganic & Medicinal Chemistry Letters 3, no. 5 (May 1993): 953–56. http://dx.doi.org/10.1016/s0960-894x(00)80699-x.

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38

Davies, Alun M. "Neural Development: Chemoattractants for navigating axons." Current Biology 4, no. 12 (December 1994): 1142–45. http://dx.doi.org/10.1016/s0960-9822(00)00258-x.

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39

Romagnani, S. "Cytokines and chemoattractants in allergic inflammation." Molecular Immunology 38, no. 12-13 (May 2002): 881–85. http://dx.doi.org/10.1016/s0161-5890(02)00013-5.

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40

VERTUANI, G., S. SPISANI, M. BOGGIAN, S. TRANIELLO, and A. SCATTURIN. "Conformational studies of synthetic tripeptide chemoattractants." International Journal of Peptide and Protein Research 29, no. 4 (January 12, 2009): 525–32. http://dx.doi.org/10.1111/j.1399-3011.1987.tb02280.x.

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41

Carlson, Robert H. "‘Chemoattractants’ Guide Metastases to Microenvironment Niches." Oncology Times 28, no. 22 (November 2006): 51–54. http://dx.doi.org/10.1097/01.cot.0000290047.04264.ca.

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42

Graves, Dana. "Monocyte chemoattractants produced by malignant cells." Journal of Pathology 161, no. 3 (July 1990): 187–88. http://dx.doi.org/10.1002/path.1711610302.

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43

Lymbery, Rowan A., W. Jason Kennington, and Jonathan P. Evans. "Egg chemoattractants moderate intraspecific sperm competition." Evolution Letters 1, no. 6 (November 28, 2017): 317–27. http://dx.doi.org/10.1002/evl3.34.

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44

Oppenheim, Joost J., Hui Fang Dong, Paul Plotz, Rachel R. Caspi, Michelle Dykstra, Susan Pierce, Roland Martin, et al. "Autoantigens act as tissue-specific chemoattractants." Journal of Leukocyte Biology 77, no. 6 (June 2005): 854–61. http://dx.doi.org/10.1189/jlb.1004623.

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45

Camp, Richard D. R. "Polypeptide Neutrophil Chemoattractants in the Skin." Dermatology 179, no. 1 (1989): 20–24. http://dx.doi.org/10.1159/000248443.

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46

Janco, RL, and PJ Morris. "Regulation of monocyte procoagulant by chemoattractants." Blood 65, no. 3 (March 1, 1985): 545–52. http://dx.doi.org/10.1182/blood.v65.3.545.545.

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Abstract Various n-formylated peptides function as receptor-specific chemoattractants for both granulocytes and monocytes. Because these agents are important tools in the study of leukocyte function in vitro, we chose to examine their effects on leukocyte procoagulant activity. The synthetic chemotactic peptide N-formyl-methionyl-leucyl phenylalanine (FMLP) induces a fourfold increase in procoagulant activity (PCA) in cultured human monocytes at an optimal dose of 5 X 10(-9) mol/L, whereas higher doses inhibit PCA response. Although nonadherent lymphocytes are not absolutely required for PCA expression, their presence significantly amplifies monocyte PCA. Irradiation of nonadherent lymphocytes before mixing them with FMLP and adherent cells abolishes their ability to amplify PCA. Kinetic studies demonstrate an increase in optimal dose FMLP-stimulated PCA over time whereas high- dose inhibition of PCA generation occurs at various incubation times. Cell viability is unaffected by inhibitory concentrations of FMLP. Supernates from high-dose FMLP-stimulated cells fail to inhibit later expression of PCA by cells exposed to endotoxin. The cellular procoagulant remains cell-bound and exhibits characteristics of thromboplastin (tissue factor), including inhibition by concanavalin A and phospholipase C as well as the ability to shorten the clotting times of factor VIII but not factor VII-deficient substrate plasmas. These results suggest a complex system of lymphoid cell regulation of procoagulant generation by monocytes exposed to various chemotactic peptides in vitro.
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47

Janco, RL, and PJ Morris. "Regulation of monocyte procoagulant by chemoattractants." Blood 65, no. 3 (March 1, 1985): 545–52. http://dx.doi.org/10.1182/blood.v65.3.545.bloodjournal653545.

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Various n-formylated peptides function as receptor-specific chemoattractants for both granulocytes and monocytes. Because these agents are important tools in the study of leukocyte function in vitro, we chose to examine their effects on leukocyte procoagulant activity. The synthetic chemotactic peptide N-formyl-methionyl-leucyl phenylalanine (FMLP) induces a fourfold increase in procoagulant activity (PCA) in cultured human monocytes at an optimal dose of 5 X 10(-9) mol/L, whereas higher doses inhibit PCA response. Although nonadherent lymphocytes are not absolutely required for PCA expression, their presence significantly amplifies monocyte PCA. Irradiation of nonadherent lymphocytes before mixing them with FMLP and adherent cells abolishes their ability to amplify PCA. Kinetic studies demonstrate an increase in optimal dose FMLP-stimulated PCA over time whereas high- dose inhibition of PCA generation occurs at various incubation times. Cell viability is unaffected by inhibitory concentrations of FMLP. Supernates from high-dose FMLP-stimulated cells fail to inhibit later expression of PCA by cells exposed to endotoxin. The cellular procoagulant remains cell-bound and exhibits characteristics of thromboplastin (tissue factor), including inhibition by concanavalin A and phospholipase C as well as the ability to shorten the clotting times of factor VIII but not factor VII-deficient substrate plasmas. These results suggest a complex system of lymphoid cell regulation of procoagulant generation by monocytes exposed to various chemotactic peptides in vitro.
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48

Gloer, James B., Jerrold Meinwald, Djamshid Shirazian, James E. Childs, and Everett L. Schiller. "Extraction of intersexual chemoattractants fromSchistosoma mansoni." Journal of Chemical Ecology 12, no. 8 (August 1986): 1725–28. http://dx.doi.org/10.1007/bf01022377.

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49

Kim, Chang H., Louis M. Pelus, John R. White, and Hal E. Broxmeyer. "Differential Chemotactic Behavior of Developing T Cells in Response to Thymic Chemokines." Blood 91, no. 12 (June 15, 1998): 4434–43. http://dx.doi.org/10.1182/blood.v91.12.4434.

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Abstract:
Abstract Differentiation-dependent thymocyte migration in the thymus may be important for T lymphopoiesis and might be regulated by thymic chemoattractants. We examined modulation of chemotactic responsiveness of thymocyte subsets during their early to late stages of development in response to 2 thymus-expressed chemokines, SDF-1 and CKβ-11/MIP-3β/ELC. SDF-1 shows chemotactic preference for immature thymocytes (subsets of triple negative thymocytes and double positive [DP] subset) over mature single positive (SP) thymocytes. CKβ-11/MIP-3β/ELC shows low chemotactic activity on the immature thymocytes, but it strongly attracts mature SP thymocytes, effects opposite to that of SDF-1. SDF-1–dependent chemoattraction of immature thymocytes is not significantly desensitized by a negative concentration gradient of CKβ-11/MIP-3β/ELC, and chemoattraction of mature SP thymocytes to CKβ-11/MIP-3β/ELC is not antagonized by SDF-1, demonstrating that these two chemokines have different chemoattractant preferences for thymocyte subsets and would probably not inhibit each other's chemotaxis in the event of microenvironmental coexpression. The chemotactic responsiveness of thymocytes and mature T cells to the 2 chemokines is respectively enhanced after selection process and migration to the spleen. These studies demonstrate the presence of thymocyte chemoattractants with differential chemotactic preference for thymocytes, a possible mechanism for thymocyte migration in the thymus.
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50

Kim, Chang H., Louis M. Pelus, John R. White, and Hal E. Broxmeyer. "Differential Chemotactic Behavior of Developing T Cells in Response to Thymic Chemokines." Blood 91, no. 12 (June 15, 1998): 4434–43. http://dx.doi.org/10.1182/blood.v91.12.4434.412k45_4434_4443.

Full text
Abstract:
Differentiation-dependent thymocyte migration in the thymus may be important for T lymphopoiesis and might be regulated by thymic chemoattractants. We examined modulation of chemotactic responsiveness of thymocyte subsets during their early to late stages of development in response to 2 thymus-expressed chemokines, SDF-1 and CKβ-11/MIP-3β/ELC. SDF-1 shows chemotactic preference for immature thymocytes (subsets of triple negative thymocytes and double positive [DP] subset) over mature single positive (SP) thymocytes. CKβ-11/MIP-3β/ELC shows low chemotactic activity on the immature thymocytes, but it strongly attracts mature SP thymocytes, effects opposite to that of SDF-1. SDF-1–dependent chemoattraction of immature thymocytes is not significantly desensitized by a negative concentration gradient of CKβ-11/MIP-3β/ELC, and chemoattraction of mature SP thymocytes to CKβ-11/MIP-3β/ELC is not antagonized by SDF-1, demonstrating that these two chemokines have different chemoattractant preferences for thymocyte subsets and would probably not inhibit each other's chemotaxis in the event of microenvironmental coexpression. The chemotactic responsiveness of thymocytes and mature T cells to the 2 chemokines is respectively enhanced after selection process and migration to the spleen. These studies demonstrate the presence of thymocyte chemoattractants with differential chemotactic preference for thymocytes, a possible mechanism for thymocyte migration in the thymus.
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