HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

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

Generation by Bacterial Proteinases of Leukotactic Factors from Human Serum, and Human C3 and C5¹

From the Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06032

Abstract

Proteinases derived from Serratia marcescens and group A, -hemolytic Streptococcus are each able to generate, by cleavage, leukotactic fragments from human C3 and C5. In whole human serum, the Serratia enzyme produces a C3-related leukotactic factor, while the streptococcal proteinase produces a C5-related factor. The finding that proteinases derived from bacteria are able to generate complement-dependent leukotactic factors suggests that this may be one mechanism by which bacteria incite and maintain inflammatory reactions in tissues.

Footnotes

¹ This is publication 34 from the Department of Pathology, The University of Connecticut Health Center, Farmington, Connecticut 06032; supported by Grants AI-06091, AI-08251 and T01 AI-00438 from the National Institute of Allergy and Infectious Diseases. Portions of this paper were presented at the Complement Workshop, Baltimore, Maryland, January 1971 (J. Immunol., 107: 317 (Abs.), 1971; the annual meeting of the American Association of Immunologists, Chicago, Ill., April 1971 (Fed. Proc., 30: 355 (Abs.) 1971; and the First International Congress of Immunology, Washington, D. C., August 1971 (Progress in Immunology, Edited by B. D. Amos, p. 584–587). Academic Press, Inc. New York, 1971.

² Work performed in partial fulfillment of the requirements for the M.D. degree, School of Medicine, University of Connecticut; portions of these studies were conducted during a summer fellowship supported by National Institute of Allergy and Infectious Diseases Training Grant T01 AI-00438.

³ Work performed in partial fulfillment of the requirements for the Ph.D. degree, Graduate School, University of Connecticut; portions of these studies were conducted during a predoctoral fellowship supported by a National Institute of Allergy and Infectious Diseases Training Grant T01 AI-00438.