Modulation of neutrophil function by lysozyme. Potential negative feedback system of inflammation

L. I. Gordon, S. D. Douglas, N. E. Kay, O. Yamada, E. F. Osserman, H. S. Jacob

Research output: Contribution to journalArticlepeer-review

98 Scopus citations


Host responses to infectious organisms should be modulated so that tissue-damaging products of inflammatory cells do not produce excessive destruction of normal tissue. Lysozyme, which is continuously secreted by monocytes, which, in turn, migrate relatively late to inflammatory areas, was found to significantly dampen several responses of neutrophils to inflammatory stimulants. Thus, human lysozyme obtained and purified from the urine of patients with monocytic leukemia (but not its structurally similar and comparably cationic analogue, eggwhite lysozyme) depresses chemotaxis of normal neutrophils to activated complement, bacterial supernate, and N-formylmethionylphenylalanine. In addition, human (but not eggwhite) lysozyme depresses oxidative metabolism (hexose monophosphate shunt activity) and superoxide generation of neutrophils. The specificity of the suppressive effects was indicated by inhibition studies with rabbit anti-human lysozyme antibody, and with the trisaccharide of N-acetylglucosamine, a specific inhibitor of lysozyme. The results suggest that lysozyme, a product of inflammatory cells themselves, may function in a negative feedback system to modulate the inflammatory response.

Original languageEnglish (US)
Pages (from-to)226-232
Number of pages7
JournalUnknown Journal
Issue number1
StatePublished - 1979

ASJC Scopus subject areas

  • General Medicine


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