Human polymorphonuclear-leukocyte inhibition of incorporation of chitin precursors into mycelia of Coccidioides immitis

J. N. Galgiani, C. M. Payne, J. F. Jones

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Human polymorphonuclear leukocytes (PMNLs), when added to arthroconidial suspensions of Coccidioides immitis, markedly inhibit fungal incorporation of the cell-wall precursor N-acetylglucosamine. This effect does not require serum but is facilitated by a heat-labile serum component(s), probably by promoting PMNL atachment to the arthroconidia. Inhibition is entirely reversible within 24 hr. In parallel with this finding, PMNLs exhibited virtually no killing of arthroconidia and (as determined by electron microscopy) did not produce damage to the fungal ultrastructure. PMNLs from a patient with chronic granulomatous disease suppressed fungal incorporation of N-acetyl-glucosamine by only 0%-22% under various conditions, as compared with 54%-85% suppression by PMNLs from normal donors. Our studies demonstrate that PMNLs can influence the metabolism of C immitis and raise the possibility that their presence in coccidioidal histopathology may be an important immediate host defense in limiting progression early after infection.

Original languageEnglish (US)
Pages (from-to)404-412
Number of pages9
JournalJournal of Infectious Diseases
Volume149
Issue number3
StatePublished - 1984

Fingerprint

Coccidioides
Chitin
Mycelium
Neutrophils
Chronic Granulomatous Disease
Acetylglucosamine
Glucosamine
Serum
Cell Wall
Suspensions
Electron Microscopy
Hot Temperature
Tissue Donors
Infection

ASJC Scopus subject areas

  • Immunology
  • Public Health, Environmental and Occupational Health

Cite this

Human polymorphonuclear-leukocyte inhibition of incorporation of chitin precursors into mycelia of Coccidioides immitis. / Galgiani, J. N.; Payne, C. M.; Jones, J. F.

In: Journal of Infectious Diseases, Vol. 149, No. 3, 1984, p. 404-412.

Research output: Contribution to journalArticle

@article{4fffc8dcf3634d35a9bb5d94cc6daa20,
title = "Human polymorphonuclear-leukocyte inhibition of incorporation of chitin precursors into mycelia of Coccidioides immitis",
abstract = "Human polymorphonuclear leukocytes (PMNLs), when added to arthroconidial suspensions of Coccidioides immitis, markedly inhibit fungal incorporation of the cell-wall precursor N-acetylglucosamine. This effect does not require serum but is facilitated by a heat-labile serum component(s), probably by promoting PMNL atachment to the arthroconidia. Inhibition is entirely reversible within 24 hr. In parallel with this finding, PMNLs exhibited virtually no killing of arthroconidia and (as determined by electron microscopy) did not produce damage to the fungal ultrastructure. PMNLs from a patient with chronic granulomatous disease suppressed fungal incorporation of N-acetyl-glucosamine by only 0{\%}-22{\%} under various conditions, as compared with 54{\%}-85{\%} suppression by PMNLs from normal donors. Our studies demonstrate that PMNLs can influence the metabolism of C immitis and raise the possibility that their presence in coccidioidal histopathology may be an important immediate host defense in limiting progression early after infection.",
author = "Galgiani, {J. N.} and Payne, {C. M.} and Jones, {J. F.}",
year = "1984",
language = "English (US)",
volume = "149",
pages = "404--412",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "3",

}

TY - JOUR

T1 - Human polymorphonuclear-leukocyte inhibition of incorporation of chitin precursors into mycelia of Coccidioides immitis

AU - Galgiani, J. N.

AU - Payne, C. M.

AU - Jones, J. F.

PY - 1984

Y1 - 1984

N2 - Human polymorphonuclear leukocytes (PMNLs), when added to arthroconidial suspensions of Coccidioides immitis, markedly inhibit fungal incorporation of the cell-wall precursor N-acetylglucosamine. This effect does not require serum but is facilitated by a heat-labile serum component(s), probably by promoting PMNL atachment to the arthroconidia. Inhibition is entirely reversible within 24 hr. In parallel with this finding, PMNLs exhibited virtually no killing of arthroconidia and (as determined by electron microscopy) did not produce damage to the fungal ultrastructure. PMNLs from a patient with chronic granulomatous disease suppressed fungal incorporation of N-acetyl-glucosamine by only 0%-22% under various conditions, as compared with 54%-85% suppression by PMNLs from normal donors. Our studies demonstrate that PMNLs can influence the metabolism of C immitis and raise the possibility that their presence in coccidioidal histopathology may be an important immediate host defense in limiting progression early after infection.

AB - Human polymorphonuclear leukocytes (PMNLs), when added to arthroconidial suspensions of Coccidioides immitis, markedly inhibit fungal incorporation of the cell-wall precursor N-acetylglucosamine. This effect does not require serum but is facilitated by a heat-labile serum component(s), probably by promoting PMNL atachment to the arthroconidia. Inhibition is entirely reversible within 24 hr. In parallel with this finding, PMNLs exhibited virtually no killing of arthroconidia and (as determined by electron microscopy) did not produce damage to the fungal ultrastructure. PMNLs from a patient with chronic granulomatous disease suppressed fungal incorporation of N-acetyl-glucosamine by only 0%-22% under various conditions, as compared with 54%-85% suppression by PMNLs from normal donors. Our studies demonstrate that PMNLs can influence the metabolism of C immitis and raise the possibility that their presence in coccidioidal histopathology may be an important immediate host defense in limiting progression early after infection.

UR - http://www.scopus.com/inward/record.url?scp=0021321111&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021321111&partnerID=8YFLogxK

M3 - Article

C2 - 6715897

AN - SCOPUS:0021321111

VL - 149

SP - 404

EP - 412

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 3

ER -