Defect of neutrophil motility in a child with recurrent bacterial infections and disseminated cytomegalovirus infection

Soriano, Rosalinda B.; South, Mary Ann; Goldman, Armond S.; Smith, C. Wayne

doi:10.1016/s0022-3476(73)80528-1

Cited by 40 publications

(7 citation statements)

References 16 publications

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“…A similar conclusion can also be achieved for the two patients (patients 4 and 5) who were longitudinally followed up and in whom it was found that chemotaxis was disturbed when they became infected. It has previously been shown that neutrophil chemotaxis is decreased during the course of recurrent infections, such as lower respiratory tract infections 16 , 17 . It is known that pulmonary infections in CF are associated with chronic colonization by bacterial pathogens and episodes of acute debilitating exacerbations usually due to bacteria 1 , 4 .…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand in the acutely infected CF patients, though random migration values are not significantly different from the other two groups, the chemotaxis index values are different significantly, indicating the possible role of infection itself on neutrophil chemotaxis. It has been previously shown that neutrophil chemotaxis is decreased during the course of recurrent infections, such as lower respiratory tract infections (16,17). It is known that pulmonary infections in CF are associated with chronic colonisation by bacterial pathogens and episodes of acute debilitating exacerbations usually due to bacteria (1,4).…”

Section: Clinically Stablementioning

confidence: 99%

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Neutrophil chemotaxis in acutely infected and clinically stable cystic fibrosis patients*

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Section: Clinically Stablementioning

confidence: 99%

Neutrophil chemotaxis in acutely infected and clinically stable cystic fibrosis patients*

et al. 1999

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“…The exact nature of the inhibitor(s) and its role in in vivo leucotaxis is at present unclear; but it could contribute at least in part to the enhanced susceptibility of sickle cell children to infection. Children with defective neutrophil motility are known to suffer from recurrent infections (Ward & Schlegel, 1969;Soriano et al, 1973). Acquired defects in leucotaxis due to the presence of inhibitors of neutrophil motility have been known to occur in other disease conditions (Gewurtz et al, 1967;Demeo & Anderson, 1972).…”

Section: Discussionmentioning

confidence: 99%

Inhibitor of in Vitro Neutrophil Migration in Sera of Children with Homozygous Sickle Cell Gene during Pain Crisis

Akenzua¹,

Amiengheme²

1981

Br J Haematol

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There is conflicting evidence for a causal relationship between infection and haematological crisis of sickle cell disease. To find out whether changes in leucotaxis occur during pain crisis, in-vitro neutrophil migration was determined in 38 children with Hb SS during steady state and during pain crisis. Migrations of neutrophils of sickle cell patients was 29 +/ 12 microns in steady state and 27.5 +/- 10.5 microns during pain crisis. These rates were comparable to migration of neutrophils of control children with normal haemoglobin of 34 +/- 9.6 microns. However, with addition of autologous serum to the cell suspension, neutrophil migration of patients in pain crisis was significantly retarded (16 +/- 13 microns) as compared to those in steady state (26 +/- 10.2 microns) and control children (28.7 +/- 10 microns). Sera of children in pain crisis also inhibited migration of neutrophils of healthy adults with normal Hb. Pooled normal plasma reversed inhibitory action of pain crisis serum on autologous and homologous neutrophil migration; but pain crisis plasma did not. Chemotactic effect of sera of Hb SS children in steady state or pain crisis and control children on neutrophils of eight adults with normal Hb were similar and comparable to that of pooled normal serum. Thus, children with sickle cell disease develop chemotactic inhibitor(s) in their circulation during pain crisis. They may lead to defective leucotaxis and enhanced susceptibility to infection.

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“…Recent clinical studies of children with recurrent infections (Ward & Schlegel 1969, Smith et al 1972, Clark et al 1973, Soriano et al 1973 have indicated that these individuals lack a plasma antagonist to a heat stable serum inhibitor of leukotaxis. Our results support this contention and suggest that the impaired antagonist-inhibitor system is transferable through plasma.…”

Section: Discussionmentioning

confidence: 99%

The influence of plasma and serum on the chemotactic response to plaque

Mary

Folke

1974

J of Periodontal Research

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The chemotactic response of human PMNL cells to: 1) normal plasma or serum, 2) heat inactivated plasma or serum, 3) autologous plaque mixed with saline, 4) autologous plaque mixed with a complement source (plasma or serum), and 5) autologous plaque mixed with heat inactivated plasma or serum was examined using the Boyden chamber technique. The results indicated serum to be more chemotactic than plasma but that the chemotactic properties of both were heat labile. The addition of autologous plasma to plaque enhanced the chemotactic response in some subjects and inhibited the response in others. Similarly, heat inactivated plasma mixed with autologous plaque suspension strongly inhibited the chemotactic response in 30 % of the subjects tested. The mechanism of this inhibition is unknown but cross matching experiments between individuals indicated that this effect was transferable by plasma.

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Defect of neutrophil motility in a child with recurrent bacterial infections and disseminated cytomegalovirus infection

Cited by 40 publications

References 16 publications

Neutrophil chemotaxis in acutely infected and clinically stable cystic fibrosis patients*

Neutrophil chemotaxis in acutely infected and clinically stable cystic fibrosis patients*

Inhibitor of in Vitro Neutrophil Migration in Sera of Children with Homozygous Sickle Cell Gene during Pain Crisis

The influence of plasma and serum on the chemotactic response to plaque

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