Literature DB >> 1452351

Ovine pulmonary surfactant induces killing of Pasteurella haemolytica, Escherichia coli, and Klebsiella pneumoniae by normal serum.

K A Brogden1.   

Abstract

Pulmonary surfactant has been shown to play an increasingly important role in bacterial clearance at the alveolar surface in the lung. This study describes a bactericidal mechanism in which ovine pulmonary surfactant induces killing of Pasteurella haemolytica by normal serum. To demonstrate killing, six bacterial species were incubated first with pulmonary surfactant for 60 min at 37 degrees C and then with serum for an additional 60 min at 37 degrees C. P. haemolytica type A1 strains 82-25 and L101, a P. haemolytica type 2 strain, Escherichia coli, and Klebsiella pneumoniae were susceptible and Pasteurella multocida, Serratia marcescens, and Pseudomonas aeruginosa were not susceptible to killing by ovine pulmonary surfactant and normal serum. No bacteria incubated with bovine pulmonary surfactant were killed by normal serum. Although the species origin of pulmonary surfactant was selective, the species origin of serum was not. P. haemolytica incubated with ovine pulmonary surfactant was killed by fetal calf serum, gnotobiotic calf serum, pooled normal sheep serum, pooled normal rabbit serum, and pooled guinea pig serum. Ultrastructurally, killed P. haemolytica suspensions contained dead cells and cells distorted with vacuoles between the cytoplasmic membrane and the cytoplasm. The mechanism of killing did not correlate with concentrations of complement or lysozyme or titers of residual antibody in either the pulmonary surfactant or the serum, and killing was reduced by preincubation of surfactant with P. haemolytica lipopolysaccharide. Preliminary characterization of both surfactant and serum implicate a low-molecular-weight proteinaceous component in the surfactant and serum albumin in the serum. This mechanism may help clear certain gram-negative bacteria from the lungs of sheep as a part of the pulmonary innate defense system.

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Year:  1992        PMID: 1452351      PMCID: PMC258295          DOI: 10.1128/iai.60.12.5182-5189.1992

Source DB:  PubMed          Journal:  Infect Immun        ISSN: 0019-9567            Impact factor:   3.441


  33 in total

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  7 in total

1.  Increased anionic peptide distribution and intensity during progression and resolution of bacterial pneumonia.

Authors:  Amanda J Fales-Williams; Jack M Gallup; Rafael Ramírez-Romero; Kim A Brogden; Mark R Ackermann
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2.  Congeners of SMAP29 kill ovine pathogens and induce ultrastructural damage in bacterial cells.

Authors:  V C Kalfa; H P Jia; R A Kunkle; P B McCray; B F Tack; K A Brogden
Journal:  Antimicrob Agents Chemother       Date:  2001-11       Impact factor: 5.191

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Authors:  K Brogden; C Clarke
Journal:  Infect Immun       Date:  1997-03       Impact factor: 3.441

4.  Small, anionic, and charge-neutralizing propeptide fragments of zymogens are antimicrobial.

Authors:  K A Brogden; M Ackermann; K M Huttner
Journal:  Antimicrob Agents Chemother       Date:  1997-07       Impact factor: 5.191

5.  Isolation of an ovine pulmonary surfactant-associated anionic peptide bactericidal for Pasteurella haemolytica.

Authors:  K A Brogden; A J De Lucca; J Bland; S Elliott
Journal:  Proc Natl Acad Sci U S A       Date:  1996-01-09       Impact factor: 11.205

6.  Binding between lipopolysaccharide and cecropin A.

Authors:  A J De Lucca; T J Jacks; K A Brogden
Journal:  Mol Cell Biochem       Date:  1995-10-18       Impact factor: 3.396

7.  Zn-Enhanced Asp-Rich Antimicrobial Peptides: N-Terminal Coordination by Zn(II) and Cu(II), Which Distinguishes Cu(II) Binding to Different Peptides.

Authors:  Adriana Miller; Agnieszka Matera-Witkiewicz; Aleksandra Mikołajczyk; Joanna Wątły; Dean Wilcox; Danuta Witkowska; Magdalena Rowińska-Żyrek
Journal:  Int J Mol Sci       Date:  2021-06-28       Impact factor: 6.208

  7 in total

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