Influence of sputum IgA and elastase on tracheal cell bacterial adherence

M. S. Niederman, W. W. Merrill, L. M. Polomski, Herbert Reynolds, J. B. Gee

Research output: Contribution to journalArticle

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Abstract

Bacterial adherence is an important pathogenetic mechanism for airway colonization, but the influence of airway proteins on this phenomenon is largely unknown. We measured tracheal cell bacterial binding in 13 subjects with chronic tracheostomy and related these results to measurements of sputum IgA, elastase activity, and total protein from the same subjects. Tracheal cell adherence was related directly to sputum elastase activity (r = 0.61, p = 0.02); and elastase activity, primarily a serine protease, was higher in subjects colonized by Pseudomonas aeruginosa than in those without this finding (p = 0.02). Sputum levels of IgA/mg protein were related inversely to tracheal cell adherence (r = -0.64, p = 0.02). Sputum IgA concentrations, in turn, were affected by host nutritional status and airway elastase activity. Evidence that elastase can degrade sputum IgA was provided by an inverse relationship observed between these 2 proteins (r = -0.56, p = 0.04) and by in vitro mixing experiments showing fragmentation of IgA by purified neutrophil elastase. In addition, sucrose density gradient separation indicated IgA fragmentation to have occurred in vivo. These data suggest that, once adherence leads to airway colonization, the resulting inflammatory response may foster microbial growth by an elastase-dependent IgA cleavage and hence enhanced tracheal cell adherence.

Original languageEnglish (US)
Pages (from-to)255-260
Number of pages6
JournalAmerican Review of Respiratory Disease
Volume133
Issue number2
StatePublished - Jun 11 1986

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Pancreatic Elastase
Sputum
Immunoglobulin A
Proteins
Leukocyte Elastase
Tracheostomy
Serine Proteases
Nutritional Status
Pseudomonas aeruginosa
Sucrose
Growth

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

Niederman, M. S., Merrill, W. W., Polomski, L. M., Reynolds, H., & Gee, J. B. (1986). Influence of sputum IgA and elastase on tracheal cell bacterial adherence. American Review of Respiratory Disease, 133(2), 255-260.
Niederman, M. S. ; Merrill, W. W. ; Polomski, L. M. ; Reynolds, Herbert ; Gee, J. B. / Influence of sputum IgA and elastase on tracheal cell bacterial adherence. In: American Review of Respiratory Disease. 1986 ; Vol. 133, No. 2. pp. 255-260.
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Niederman, MS, Merrill, WW, Polomski, LM, Reynolds, H & Gee, JB 1986, 'Influence of sputum IgA and elastase on tracheal cell bacterial adherence', American Review of Respiratory Disease, vol. 133, no. 2, pp. 255-260.

Influence of sputum IgA and elastase on tracheal cell bacterial adherence. / Niederman, M. S.; Merrill, W. W.; Polomski, L. M.; Reynolds, Herbert; Gee, J. B.

In: American Review of Respiratory Disease, Vol. 133, No. 2, 11.06.1986, p. 255-260.

Research output: Contribution to journalArticle

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N2 - Bacterial adherence is an important pathogenetic mechanism for airway colonization, but the influence of airway proteins on this phenomenon is largely unknown. We measured tracheal cell bacterial binding in 13 subjects with chronic tracheostomy and related these results to measurements of sputum IgA, elastase activity, and total protein from the same subjects. Tracheal cell adherence was related directly to sputum elastase activity (r = 0.61, p = 0.02); and elastase activity, primarily a serine protease, was higher in subjects colonized by Pseudomonas aeruginosa than in those without this finding (p = 0.02). Sputum levels of IgA/mg protein were related inversely to tracheal cell adherence (r = -0.64, p = 0.02). Sputum IgA concentrations, in turn, were affected by host nutritional status and airway elastase activity. Evidence that elastase can degrade sputum IgA was provided by an inverse relationship observed between these 2 proteins (r = -0.56, p = 0.04) and by in vitro mixing experiments showing fragmentation of IgA by purified neutrophil elastase. In addition, sucrose density gradient separation indicated IgA fragmentation to have occurred in vivo. These data suggest that, once adherence leads to airway colonization, the resulting inflammatory response may foster microbial growth by an elastase-dependent IgA cleavage and hence enhanced tracheal cell adherence.

AB - Bacterial adherence is an important pathogenetic mechanism for airway colonization, but the influence of airway proteins on this phenomenon is largely unknown. We measured tracheal cell bacterial binding in 13 subjects with chronic tracheostomy and related these results to measurements of sputum IgA, elastase activity, and total protein from the same subjects. Tracheal cell adherence was related directly to sputum elastase activity (r = 0.61, p = 0.02); and elastase activity, primarily a serine protease, was higher in subjects colonized by Pseudomonas aeruginosa than in those without this finding (p = 0.02). Sputum levels of IgA/mg protein were related inversely to tracheal cell adherence (r = -0.64, p = 0.02). Sputum IgA concentrations, in turn, were affected by host nutritional status and airway elastase activity. Evidence that elastase can degrade sputum IgA was provided by an inverse relationship observed between these 2 proteins (r = -0.56, p = 0.04) and by in vitro mixing experiments showing fragmentation of IgA by purified neutrophil elastase. In addition, sucrose density gradient separation indicated IgA fragmentation to have occurred in vivo. These data suggest that, once adherence leads to airway colonization, the resulting inflammatory response may foster microbial growth by an elastase-dependent IgA cleavage and hence enhanced tracheal cell adherence.

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Niederman MS, Merrill WW, Polomski LM, Reynolds H, Gee JB. Influence of sputum IgA and elastase on tracheal cell bacterial adherence. American Review of Respiratory Disease. 1986 Jun 11;133(2):255-260.