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Sialyl Lewis(x) hybridized complement receptor type 1 moderates acid aspiration injury.
Am J Physiol Lung Cell Mol Physiol. 2001 Dec; 281(6):L1494-9.AJ

Abstract

The potentially enhanced anti-inflammatory effects of the sialyl Lewis(x) (sLe(x))-decorated version of soluble complement receptor type 1 (sCR1) in moderating acid aspiration injury are examined. HCl was instilled in tracheostomy tubes placed in mice, and extravasation of (125)I-labeled albumin in bronchoalveolar lavage (BAL) fluid was used to calculate the vascular permeability index (PI). Neutrophil counts in BAL fluid and immunohistochemistry were performed. PI was moderated by 82% after treatment with sCR1sLe(x) compared with 54% in sCR1-untreated mice (P < 0.05). Respective reductions in PI in mice treated 0.5 and 1 h after acid aspiration with sCR1sLe(x) of 70 and 57% were greater than the decreases in PI of 45 and 38% observed in respective sCR1-treated groups (P < 0.05). BAL fluid neutrophil counts in sCR1sLe(x)-treated mice were significantly less than those in sCR1-treated animals, which were similar to those in untreated mice. Immunohistochemistry stained for sCR1 only on the pulmonary vascular endothelium of sCR1sLe(x)- but not sCR1-treated mice. In conclusion, sCR1sLe(x) moderates permeability by antagonizing complement activation and neutrophil adhesion. Delayed complement and neutrophil antagonism significantly reduces injury.

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Authors+Show Affiliations

Kyriakides C
Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Wang Y
No affiliation info available
Austen WG
No affiliation info available
Favuzza J
No affiliation info available
Kobzik L
No affiliation info available
Moore FD
No affiliation info available
Hechtman HB
No affiliation info available

MeSH

AnimalsCell AdhesionComplement ActivationComplement Inactivator ProteinsEndothelium, VascularHydrochloric AcidImmunohistochemistryLungMaleMiceMice, Inbred C57BLNeutrophilsOligosaccharidesPneumonia, AspirationReceptors, ComplementRecombinant ProteinsSelectinsSialyl Lewis X Antigen

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11704546

Citation

Kyriakides, C, et al. "Sialyl Lewis(x) Hybridized Complement Receptor Type 1 Moderates Acid Aspiration Injury." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 281, no. 6, 2001, pp. L1494-9.
Kyriakides C, Wang Y, Austen WG, et al. Sialyl Lewis(x) hybridized complement receptor type 1 moderates acid aspiration injury. Am J Physiol Lung Cell Mol Physiol. 2001;281(6):L1494-9.
Kyriakides, C., Wang, Y., Austen, W. G., Favuzza, J., Kobzik, L., Moore, F. D., & Hechtman, H. B. (2001). Sialyl Lewis(x) hybridized complement receptor type 1 moderates acid aspiration injury. American Journal of Physiology. Lung Cellular and Molecular Physiology, 281(6), L1494-9.
Kyriakides C, et al. Sialyl Lewis(x) Hybridized Complement Receptor Type 1 Moderates Acid Aspiration Injury. Am J Physiol Lung Cell Mol Physiol. 2001;281(6):L1494-9. PubMed PMID: 11704546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sialyl Lewis(x) hybridized complement receptor type 1 moderates acid aspiration injury. AU - Kyriakides,C, AU - Wang,Y, AU - Austen,W G,Jr AU - Favuzza,J, AU - Kobzik,L, AU - Moore,F D,Jr AU - Hechtman,H B, PY - 2001/11/13/pubmed PY - 2002/1/18/medline PY - 2001/11/13/entrez SP - L1494 EP - 9 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am J Physiol Lung Cell Mol Physiol VL - 281 IS - 6 N2 - The potentially enhanced anti-inflammatory effects of the sialyl Lewis(x) (sLe(x))-decorated version of soluble complement receptor type 1 (sCR1) in moderating acid aspiration injury are examined. HCl was instilled in tracheostomy tubes placed in mice, and extravasation of (125)I-labeled albumin in bronchoalveolar lavage (BAL) fluid was used to calculate the vascular permeability index (PI). Neutrophil counts in BAL fluid and immunohistochemistry were performed. PI was moderated by 82% after treatment with sCR1sLe(x) compared with 54% in sCR1-untreated mice (P < 0.05). Respective reductions in PI in mice treated 0.5 and 1 h after acid aspiration with sCR1sLe(x) of 70 and 57% were greater than the decreases in PI of 45 and 38% observed in respective sCR1-treated groups (P < 0.05). BAL fluid neutrophil counts in sCR1sLe(x)-treated mice were significantly less than those in sCR1-treated animals, which were similar to those in untreated mice. Immunohistochemistry stained for sCR1 only on the pulmonary vascular endothelium of sCR1sLe(x)- but not sCR1-treated mice. In conclusion, sCR1sLe(x) moderates permeability by antagonizing complement activation and neutrophil adhesion. Delayed complement and neutrophil antagonism significantly reduces injury. SN - 1040-0605 UR - https://www.unboundmedicine.com/medline/citation/11704546/Sialyl_Lewis_x__hybridized_complement_receptor_type_1_moderates_acid_aspiration_injury_ L2 - https://journals.physiology.org/doi/10.1152/ajplung.2001.281.6.L1494?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -