Chemotactic Receptor of Cord Blood Granulocytes to the Synthesized Chemotactic Peptide N-Formyl-Methionyl-Leucyl-Phenylalanine

Nunoi, Hiroyuki; Endo, Fumio; Chikazawa, Shoji; Namikawa, T; Matsuda, Ichiro

doi:10.1203/00006450-198301000-00011

Cited by 14 publications

(10 citation statements)

References 12 publications

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“…The whole blood chemotaxis assay used in this study approximates in vivo conditions more closely than separated cell assays, however, it is less useful for determination of the relative effects of serum and cellular factors on PMN chemotaxis. Previous studies in healthy neonates have identified both humoral (6,8,(21)(22)(23) and cellular (3)(4)(5)(24)(25)(26) abnormalities which could explain decreased PMN chemotaxis in neonates compared with adults. Serum defects have included decreased levels of complement (8,(21)(22) and the presence of a chemotactic factor inactivator (8,23).…”

Section: Discussionmentioning

confidence: 99%

“…Serum defects have included decreased levels of complement (8,(21)(22) and the presence of a chemotactic factor inactivator (8,23). Cellular defects have included decreased membrane receptors for chemoattractants (24), impaired microtubule assembly (25), decreased adherence (3-9, and decreased membrane deformability (26). Decreased PMN chemotaxis in the stressed neonates might have been due to further impairment in any one or more of these defects or might have resulted from other defects such as the presence of a cell directed inhibitor or activated complement fragments.…”

Section: Discussionmentioning

confidence: 99%

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Polymorphonuclear Leukocyte Adherence and Chemotaxis in Stressed and Healthy Neonates

et al. 1986

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ABSTRACT. Defects in polymorphonuclear neutrophil (PMN) adherence and chemotaxis in neonates are thought to be an important cause of their increased susceptibility to overwhelming bacterial infection. Few studies of these functions have been carried out in stressed neonates who are at even greater risk of infection. PMN adherence and chemotaxis were examined in 33 stressed neonates with acute lower respiratory illness, 13 healthy neonates, and 43 healthy adults using whole blood PMN adherence and chemotaxis assays. PMN chemotaxis was significantly decreased in stressed neonates (locomotion index of 38.4 + 9.7 pm) compared with that of healthy neonates (48.9 + 12.8 pm, p < 0.01) or adults (61.6 9 11.9 pm,p < 0.001).PMN chemotaxis was studied during illness and recovery in 13 of the 33 stressed neonates and showed significant improvement during recovery (41.6 2 9.9 and 53.2 + 11.9 pm, respectively, p = 0.012). PMN adherence was de- Bacterial infections are a major cause of morbidity and mortality in newborn infants primarily because of immaturity of their host defense mechanisms (1, 2). Neutrophils (PMNs) are the major cellular elements which defend against bacterial invasion. They respond to infection by adhering to vascular endothehum, moving toward the site of infection along a chemotactic gradient (chemotaxis) and killing ingested bacteria. The functional capacity of neonatal PMNs have been carefully studied and although results are not entirely consistent, PMN adherence (3-5) and chemotaxis (6-8) appear to be depressed in healthy neonates compared with that of adults while phagocytosis and microbial killing (9-12) are intact. In studies of neonates with underlying illness or stress, PMN phagocytosis has been found to be normal ( I 1-1 5) while microbial killing has been found to Received Junc 17. 1985: accepted November 26, 1985 be decreased ( 11-1 3, 15, 16). There have been few studies of PMN adherence and chemotaxis in stressed neonates (17). Since further impairment in these functions could help explain the increased susceptibility of stressed neonates to overwhelming bacterial infection, we prospectively studied PMN adherence and chemotaxis in healthy newborn infants and those with respiratory distress syndrome, pneumonia, and other cardiorespiratory illnesses. MATERIALS AND METHODSSubjects. Blood was obtained from 33 stressed neonates with a median chronological age of 3 days (range 1-88 days) and median gestational age of 36 wk (range 25-43 wk), 13 healthy neonates with a median chronological age of 6 days (range 3-88 days) and median gestational age of 36 wk (range 27-42 wk) and 43 healthy adults.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Polymorphonuclear Leukocyte Adherence and Chemotaxis in Stressed and Healthy Neonates

et al. 1986

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“…f. Met-Le~-[~HlPhe (specific activity, 46.4 Ci/mol) was purchased from New England Nuclear Corp., purified on Dowex 50 W X 2 with 0.01 N HCl, stored at 4"C, and used after neutralizing with 0.1 N NaOH as described (17). The 0.05 pCi of labeled peptide M) was incubated with 20 p1 of either the patient's or control's serum at 37°C for 2 h. After incubation the medium was deproteinized with acetone and lyophilized.…”

Section: Methodsmentioning

confidence: 99%

Hyperimmunoglobulin-E-Associated Recurrent Infection Syndrome Accompanied by Chemotactic Inhibition of Polymorphonuclear Leukocytes and Monocytes

et al. 1984

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“…In the human neonate, factors suggested to be responsible for the defect include deficiency of membrane receptors, cytoskeletal abnormalities, and membrane rigidity (2)(3)(4)(5)17). We have previously shown that chemotaxis of neutrophils obtained from human cord blood is comparable to adult values and "increased" in comparison to chemotaxis of neutrophils from same infant 48-72 h after birth (18).…”

Section: Neutrophil Chemotaxis Withmentioning

confidence: 99%

“…Defects in phagocyte chemotaxis may be due to membrane defects, reduced number of receptors for the chemotactic agent, or to cytoskeletal abnormalities. The chemotactic defect of human neonatal phagocyte originally described by Miller (1) may be due to deficiencies in any or all these components (2)(3)(4)(5). Ontogeny of some phagocytic functions, but not chemotaxis, has been evaluated in fetal and neonatal animal models (6,7).…”

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confidence: 99%

Ontogeny of Neutrophil Chemotaxis in Fetal Lambs

et al. 1986

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ABSTRAfl. Ontogeny of neutrophil chemotactic response using endotoxin activated adult sheep plasma as a source of complement derived chemotactic factor was examined in fetal lambs of gestational age 120-150 days. (Gestational period in sheep is approximately 150 days.) Neutrophils from fetal lambs of gestational age 120-130 days failed to respond to this chemotactic factor whereas neutrophils from fetal lambs above 131 days of gestational age responded at levels comparable to adult values. Examination of neutrophil chemotaxis in older fetuses using a different chemotactic factor derived from mitogen stimulated adult mononuclear cells revealed a selective failure of fetal neutrophils to respond to lymphocyte-derived chemotactic factor in the presence of a normal response to complement derived chemotactic factor. Among prematurely delivered twin fetuses alterations in comparison with the first twin or age-matched controls in peripheral neutrophi1 count (increase) and in chemotaxis (increase or decrease) were noted in second of twins delivered r 20 min after the first lamb, suggesting an extreme sensitivity of neutrophil functions to a variety of influences, similar to that seen in humans. Directed migration or chemotaxis of phagocytes induced by various chemotactic agents is an essential component of inflammatory response. Defects in chemotaxis are associated, as a clinical consequence, with an increased susceptibility to infections. Defects in phagocyte chemotaxis may be due to membrane defects, reduced number of receptors for the chemotactic agent, or to cytoskeletal abnormalities. The chemotactic defect of human neonatal phagocyte originally described by Miller (1) may be due to deficiencies in any or all these components (2-5). Ontogeny of some phagocytic functions, but not chemotaxis, has been evaluated in fetal and neonatal animal models (6, 7). The ovine fetus has been shown by us and other investigators to be an appropriate animal model to study the ontogeny of various biological phenomena (8,9). In this report, we describe the developmental sequence of neutrophil chemotaxis in fetal lambs, utilizing EAP as a source of complement-derived chemotactic factor. Results from simultaneous evaluation of neutrophil chemotactic responses to EAP and another chemotactic factor derived from mitogen-stimulated adult ovine mononuclear leukocyte (N-LDCF) in a limited number of fetuses are presented. In addition, neutrophil counts and chemotaxis in normal fetal lambs and their twins have been compared to document alterations that may be due to "stress" of delayed delivery. MATERIALS AND METHODSSample collection. Normal adult sheep were used as controls.Heparinized (10 U/ml) blood was collected from the external jugular vein. Lambs of gestational age 120-1 50 days and postnatal age 1-6 days were compared with adults. The gestational age was determined by time-dated breeding. The fetal lambs were normal and were being delivered prematurely for other studies. The fetuses were exposed by hysterotomy under maternal spinal anes...

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Chemotactic Receptor of Cord Blood Granulocytes to the Synthesized Chemotactic Peptide N-Formyl-Methionyl-Leucyl-Phenylalanine

Cited by 14 publications

References 12 publications

Polymorphonuclear Leukocyte Adherence and Chemotaxis in Stressed and Healthy Neonates

Polymorphonuclear Leukocyte Adherence and Chemotaxis in Stressed and Healthy Neonates

Hyperimmunoglobulin-E-Associated Recurrent Infection Syndrome Accompanied by Chemotactic Inhibition of Polymorphonuclear Leukocytes and Monocytes

Ontogeny of Neutrophil Chemotaxis in Fetal Lambs

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