# BIOCHEMICAL BASIS OF PHAGOCYTOSIS

> **NIH NIH R01** · HARVARD MEDICAL SCHOOL · 1991 · $153,295

## Abstract

The long term objectives of this program are to define, at
molecular and cellular levels, interactions between bacteria and
mammalian cells.  The focus is on: (1) Biochemical changes
phagocytic leukocytes undergo when they ingest a bacterium (or
are otherwise stimulated) - insofar as these changes are part of
the leukocyte's anti-bacterial armamentarium; (ii) The effect on
the host organism's cells of substances released as a result of
phagocytic killing and dismantling of the bacterium.  In the
first context, release of active oxygen radicals by phagocytic
leukocytes is the main focus, and is in the mainstream of studies
of control of infection.  In the second context the focus is on
the effect on mammalian cells of muramyl peptides (components of
the bacterial cell wall) that are released from engulfed bacteria
(and also by enzyme action on dead bacteria of the gut).  The
latter substances are known to stimulate the host immune system.
They also are fever-inducing.  Finally, they are somnogenic
(i.e., promote slow-wave sleep).  The last mentioned
consideration is neglected in the mainstream of investigations of
infection.  Experiments to achieve the goals outlined consist in
isolating appropriate mammalian cells, and in the first context,
stimulating them in a variety of ways while following release of
superoxide and monitoring other cellular, especially membrane,
functions.  In the second category, the questions have developed
into considerations of the mechanism(s) by which muramyl peptides
induce physiological changes in mammalian cells - i.e., the
matter has progressed from the "whole-animal" effect (e.g., slow-
wave sleep induction) to the cellular level - in particular,
studies of specific cellular binding sites (receptors?) for
muramyl peptides and sequels of binding.  A key matter is that
muramyl peptides (immunostimulants) and serotonin (a neuro-
transmitter) compete for the same cellular binding sites, and
induce several responses in common.  In addition, B-lymphocytes
of narcoleptics (who have a derangement of normal sleep) do not
bind muramyl peptides in contradistinction to cells of normals.
Since narcolepsy is characterized by a specific immune situation
(expression of histocompatibility antigen DR2, DQwl) this
constitutes a further link between the immune and neurological
systems.  These matters are health-related in that they deal with
the host's antimicrobial mechanisms, and with secondary effects
of bacterial death, i.e., neuro-immune interactions due to
bacterial breakdown products.

## Key facts

- **NIH application ID:** 3124130
- **Project number:** 5R01AI003260-32
- **Recipient organization:** HARVARD MEDICAL SCHOOL
- **SAM.gov UEI:** JDLVAVGYJQ21
- **Principal Investigator:** MANFRED L KARNOVSKY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $153,295
- **Award type:** 5
- **Project period:** 1978-01-01 → 1992-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124130

## Citation

> US National Institutes of Health, RePORTER application 3124130, BIOCHEMICAL BASIS OF PHAGOCYTOSIS (5R01AI003260-32). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124130. Licensed CC0.

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