This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bufler, P. Articles by Griese, M. Search for Related Content PubMed PubMed Citation Articles by Bufler, P. Articles by Griese, M.

Surfactant Protein A and D Differently Regulate the Immune Response to Nonmucoid Pseudomonas aeruginosa and Its Lipopolysaccharide

Dr. von Haunersches Kinderspital, University of Munich, Munich, Germany; Department of Pathology, Washington University, School of Medicine, St. Louis, Missouri; and Max von Pettenkofer Institut, University of Munich, Munich, Germany

Address correspondence to: Matthias Griese, Dr. von Haunersches Kinderspital, University of Munich, Pettenkoferstrasse 8a, D-80336 Munich, Germany. E-mail: griese{at}pk-i.med.uni-muenchen.de

We investigated the role of the surfactant proteins (SPs) A and D in the pulmonary immune defense of nonmucoid strains of Pseudomonas aeruginosa, the most etiologic agents of nosocomial Pseudomonas pneumonia. We first examined the interactions of recombinant human SP-D dodecamers and purified natural or recombinant human SP-A with two smooth, and two rough, clinical isolates of nonmucoid P. aeruginosa. SP-D bound to all four isolates, but agglutinated only one rough and one smooth strain. SP-D functioned as an opsonin to enhance the uptake of all four strains by the human monocytic cell line Mono Mac 6 (MM6). SP-D also enhanced tumor necrosis factor- secretion by MM6 cells in response to purified lipopolysaccharide (LPS) isolated from the rough, but not the smooth, strains. Although SP-A bound to all four strains, it did not cause bacterial aggregation or enhance uptake. It showed small but statistically significant inhibitory effects on the cytokine response of MM6 cells to one strain of smooth organisms, but did not significantly alter the response to purified LPS. This study in combination with previously published data strongly suggests that SP-D may play important roles in the local innate pulmonary defense against nonmucoid P. aeruginosa of diverse LPS phenotypes, and preferentially augments the cellular response to rough P. aeruginosa endotoxin.

Abbreviations: colony-forming units, cfu • ethylenediamine tetraacetic acid, EDTA • fetal calf serum, FCS • fluorescein isothiocyanate, FITC • lipopolysaccharide, LPS • Mono Mac 6, MM6 • phosphate-buffered saline, PBS • surfactant protein, SP • Tris-buffered saline, TBS • tumor necrosis factor, TNF

This article has been cited by other articles:

				H. Sahly, Y. Keisari, E. Crouch, N. Sharon, and I. Ofek Recognition of Bacterial Surface Polysaccharides by Lectins of the Innate Immune System and Its Contribution to Defense against Infection: the Case of Pulmonary Pathogens Infect. Immun., April 1, 2008; 76(4): 1322 - 1332. [Full Text] [PDF]

				E. Giannoni, T. Sawa, L. Allen, J. Wiener-Kronish, and S. Hawgood Surfactant Proteins A and D Enhance Pulmonary Clearance of Pseudomonas aeruginosa Am. J. Respir. Cell Mol. Biol., June 1, 2006; 34(6): 704 - 710. [Abstract] [Full Text] [PDF]

				J. Casey, J. Kaplan, E. N. Atochina-Vasserman, A. J. Gow, H. Kadire, Y. Tomer, J. H. Fisher, S. Hawgood, R. C. Savani, and M. F. Beers Alveolar Surfactant Protein D Content Modulates Bleomycin-induced Lung Injury Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 869 - 877. [Abstract] [Full Text] [PDF]

				R. Chaby, I. Garcia-Verdugo, Q. Espinassous, and L. A. Augusto Interactions between LPS and lung surfactant proteins Innate Immunity, June 1, 2005; 11(3): 181 - 185. [Abstract] [PDF]

				R. T. Sadikot, T. S. Blackwell, J. W. Christman, and A. S. Prince Pathogen-Host Interactions in Pseudomonas aeruginosa Pneumonia Am. J. Respir. Crit. Care Med., June 1, 2005; 171(11): 1209 - 1223. [Abstract] [Full Text] [PDF]

				M. Ni, D. J. Evans, S. Hawgood, E. M. Anders, R. A. Sack, and S. M. J. Fleiszig Surfactant Protein D Is Present in Human Tear Fluid and the Cornea and Inhibits Epithelial Cell Invasion by Pseudomonas aeruginosa Infect. Immun., April 1, 2005; 73(4): 2147 - 2156. [Abstract] [Full Text] [PDF]

				L. M. Schaeffer, F. X. McCormack, H. Wu, and A. A. Weiss Interactions of Pulmonary Collectins with Bordetella bronchiseptica and Bordetella pertussis Lipopolysaccharide Elucidate the Structural Basis of Their Antimicrobial Activities Infect. Immun., December 1, 2004; 72(12): 7124 - 7130. [Abstract] [Full Text] [PDF]

				M. Griese, R. Essl, R. Schmidt, E. Rietschel, F. Ratjen, M. Ballmann, K. Paul, and for the BEAT Study Group Pulmonary Surfactant, Lung Function, and Endobronchial Inflammation in Cystic Fibrosis Am. J. Respir. Crit. Care Med., November 1, 2004; 170(9): 1000 - 1005. [Abstract] [Full Text] [PDF]

				T. O. Hirche, E. C. Crouch, M. Espinola, T. J. Brokelman, R. P. Mecham, N. DeSilva, J. Cooley, E. Remold-O'Donnell, and A. Belaaouaj Neutrophil Serine Proteinases Inactivate Surfactant Protein D by Cleaving within a Conserved Subregion of the Carbohydrate Recognition Domain J. Biol. Chem., June 25, 2004; 279(26): 27688 - 27698. [Abstract] [Full Text] [PDF]

				J. K. van de Wetering, F. E. J. Coenjaerts, A. B. Vaandrager, L. M. G. van Golde, and J. J. Batenburg Aggregation of Cryptococcus neoformans by Surfactant Protein D Is Inhibited by Its Capsular Component Glucuronoxylomannan Infect. Immun., January 1, 2004; 72(1): 145 - 153. [Abstract] [Full Text] [PDF]