DISTRIBUTION OF LABELED LYMPH NODE CELLS IN MICE DURING THE LYMPHOCYTOSIS INDUCED BY <i>BORDETELLA PERTUSSIS </i>

Taub, Robert N.; Rosett, Walter; Adler, Ava; Morse, Stephen I.

doi:10.1084/jem.136.6.1581

Cited by 41 publications

(22 citation statements)

References 10 publications

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“…These results are consistent with those observed for CBA/J mice, which also exhibit a marked leukocytosis despite being resistant to histamine sensitization (40).…”

Section: Resultssupporting

confidence: 82%

Analysis of the Role ofBphs/Hrh1in the Genetic Control of Responsiveness to Pertussis Toxin

et al. 2003

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In vivo intoxication with Bordetella pertussis toxin (PTX) elicits a variety of physiological responses including a marked leukocytosis, disruption of glucose regulation, adjuvant activity, alterations in vascular function, hypersensitivity to vasoactive agents, and death. We recently identified Bphs, the locus controlling PTX-induced hypersensitivity to the vasoactive amine histamine, as the histamine H 1 receptor (Hrh1). In this study Bphs congenic mice and mice with a disrupted Hrh1 gene were used to examine the role of Bphs/Hrh1 in the genetic control of susceptibility to a number of phenotypes elicited following in vivo intoxication. We report that the contribution of Bphs/Hrh1 to the overall genetic control of responsiveness to PTX is restricted to susceptibility to histamine hypersensitivity and enhancement of antigen-specific delayed-type hypersensitivity responses. Furthermore, the genetic contribution of Bphs/Hrh1 to vasoactive amine sensitization is specific for histamine, since hypersensitivity to serotonin was unaffected by Bphs/Hrh1. Bphs/Hrh1 also did not significantly influence susceptibility to the lethal effects, the leukocytosis response, disruption of glucose regulation, and histamineindependent increases in vascular permeability associated with in vivo intoxication. Nevertheless, significant interstrain differences in susceptibility to the lethal effects of PTX and leukocytosis response were observed. These results indicate that the phenotypic variation in responsiveness to PTX reflects the genetic control of distinct intermediate phenotypes rather than allelic variation in genes controlling overall susceptibility to intoxication.Pertussis toxin (PTX) is a major virulence factor of Bordetella pertussis, the causative agent of whooping cough (9). The holotoxin is a hexameric protein that conforms to the A/B model of bacterial exotoxins (31). The A subunit is an ADPribosyltransferase which affects signal transduction by ribosylation of the ␣ subunit of trimeric Gi proteins while the B oligomer binds cell surface receptors on a variety of mammalian cells (19,31). PTX, when administered in vivo, elicits a large number of physiological responses including disruption of glucose regulation, leukocytosis, adjuvant activity, increased vascular permeability associated with alteration of blood-tissue barrier functions, sensitization to vasoactive agents, and death (12,24,27,29,44).Inbred strains of mice differ in susceptibility to vasoactive amine challenge following PTX sensitization in that genetically susceptible strains die from hypotensive and hypovolemic shock whereas resistant strains do not (29,43). Bphs, the gene controlling susceptibility to PTX-induced hypersensitivity to histamine, was previously mapped to the central region of mouse chromosome 6 (39) and recently identified as being the histamine H 1 receptor (Hrh1) (25). As the first step in positionally cloning Bphs, we generated a panel of interval-specific recombinant congenic lines by using marker-assisted selection to introgress the ...

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“…These results are consistent with those observed for CBA/J mice, which also exhibit a marked leukocytosis despite being resistant to histamine sensitization (40).…”

Section: Resultssupporting

confidence: 82%

Analysis of the Role ofBphs/Hrh1in the Genetic Control of Responsiveness to Pertussis Toxin

et al. 2003

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“…He found that PBL isolated from pertussis-treated mice migrated to tissues and lymph nodes at much lower levels than PBL isolated from control mice, and concluded that the inhibition of lymphocyte emigration from the circulation in pertussis-treated mice is due to an effect on the lymphocytes themselves and not on the tissues (Morse and Barron 1970). In a follow-up study using a similar approach, he found that labeled lymphocytes had reduced homing to lymphoid tissue whether the lymphocytes or the recipient mice were treated with pertussis lymphocytosis-promoting factor (LPF) (Taub et al 1972). He also found that LPF could bind to erythrocytes and lymphocytes and then spontaneously elute from these cells to affect other cells, and proposed this as a possible explanation for the inhibitory effect when LPF was injected into recipient mice (Taub et al 1972;Adler and Morse 1973).…”

Section: Studies Of Stephen Morsementioning

confidence: 86%

“…In a follow-up study using a similar approach, he found that labeled lymphocytes had reduced homing to lymphoid tissue whether the lymphocytes or the recipient mice were treated with pertussis lymphocytosis-promoting factor (LPF) (Taub et al 1972). He also found that LPF could bind to erythrocytes and lymphocytes and then spontaneously elute from these cells to affect other cells, and proposed this as a possible explanation for the inhibitory effect when LPF was injected into recipient mice (Taub et al 1972;Adler and Morse 1973). Using histopathology analysis, he found early massive depletion of lymphocytes from the spleen, and to a lesser extent from the thymus, in LPF-treated mice and subsequent depletion of lymphocytes from lymph nodes (Athanassiades and Morse 1973).…”

Section: Studies Of Stephen Morsementioning

confidence: 99%

Pertussis leukocytosis: mechanisms, clinical relevance and treatment

Carbonetti

2016

Pathogens and Disease

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One sentence summary: Pertussis infection in young infants is characterized by high white blood cell counts (leukocytosis) and this minireview covers the causes, clinical findings and possible treatments for pertussis leukocytosis. Editor: Patrik Bavoil ABSTRACTThe significant and sometimes dramatic rise in the number of circulating white blood cells (leukocytosis) in infants suffering from pertussis (whooping cough) has been recognized for over a century. Although pertussis is a disease that afflicts people of all ages, it can be particularly severe in young infants, and these are the individuals in whom leukocytosis is most pronounced. Very high levels of leukocytosis are associated with poor outcome in infants hospitalized with pertussis and modern treatments are often aimed at reducing the number of leukocytes. Pertussis leukocytosis is caused by pertussis toxin, a soluble protein toxin released by Bordetella pertussis during infection, but the exact mechanisms by which this occurs are still unclear. In this minireview, I discuss the history of clinical and experimental findings on pertussis leukocytosis, possible contributing mechanisms causing this condition and treatments aimed at reducing leukocytosis in hospitalized infants. Since recent studies have detailed significant associations between specific levels of pertussis leukocytosis and fatal outcome, this is a timely review that may stimulate new thinking on how to understand and combat this problem.

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“…We speculated that the enzymatic activity detected in plasma was likely released from cellular elements, that is, RBCs, that serve as depots of Ptx toxin 6 and could explain its protracted effect on cells. This turned out to be true (data not shown).…”

Section: Other Ptx-elicited Effectsmentioning

confidence: 99%

“…In vivo, Ptx causes lymphocytosis by inhibiting lymphocyte migration from blood to tissues, or across lymph node endothelium. [5][6][7][8] In mature leukocytes, chemotactic receptors and their ligands signal through G proteins, and such signaling is essential for their adhesion and directed migration to inflammatory sites. This G protein-dependent effect is suppressed by Ptx.…”

Section: Introductionmentioning

confidence: 99%

The role of G-protein signaling in hematopoietic stem/progenitor cell mobilization

Papayannopoulou

Priestley

Bönig

et al. 2003

Blood

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The directed migration of mature leukocytes to inflammatory sites and the lymphocyte trafficking in vivo are dependent on G protein-coupled receptors and delivered through pertussis toxin (Ptx)-sensitive G i -protein signaling. In the present study, we explored the in vivo role of G-protein signaling on the redistribution or mobilization of hematopoietic stem/progenitor cells (HPCs). A single injection of Ptx in mice elicits a long-lasting leukocytosis and a progressive increase in circulating colonyforming unit-culture (CFU-C) and colonyforming unit spleen (CFU-S). We found that the prolonged effect is sustained by a continuous slow release of Ptx bound to red blood cells or other cells and is potentially

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DISTRIBUTION OF LABELED LYMPH NODE CELLS IN MICE DURING THE LYMPHOCYTOSIS INDUCED BY BORDETELLA PERTUSSIS

Cited by 41 publications

References 10 publications

Analysis of the Role ofBphs/Hrh1in the Genetic Control of Responsiveness to Pertussis Toxin

Analysis of the Role ofBphs/Hrh1in the Genetic Control of Responsiveness to Pertussis Toxin

Pertussis leukocytosis: mechanisms, clinical relevance and treatment

The role of G-protein signaling in hematopoietic stem/progenitor cell mobilization

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