Modulation of macrophage Ia expression by lipopolysaccharide: Stem cell requirements, accessory lymphocyte involvement, and IA-inducing factor production
The mechanism of induction of murine macrophage Ia expression by lipopolysaccharide (LPS) was studied. Intraperitoneal injection of 1 microgram of LPS resulted in a 3- to 10-fold increase in the number of IA-positive peritoneal macrophages (flow cytometry and immunofluorescence) and a 6-to 16-fold increase by radioimmunoassay. The isolated lipid A moiety of LPS was a potent inducer of macrophage Ia expression. Ia induction required a functional myelopoietic system as indicated by the finding that the response to LPS was eliminated in irradiated (900 rads) mice and reinstated by reconstitution with bone marrow cells. Comparison of LPS-induced Ia expression in normal and LPS-primed mice revealed a faster secondary response to LPS. The memory response could be adoptively transferred to normal mice with nonadherent spleen cells prepared 60 days after LPS injection. Spleen cells prepared 5 days after LPS injection caused Ia induction in LPS-nonresponder mice; such induction was not observed in irradiated (900 rads) recipients. The cell responsible for this phenomenon was identified as a Thy-1+, immunoglobulin-negative nonadherent cell. The biosynthesis and expression of Ia were not increased by direct exposure of macrophages to LPS in vitro. Small amounts of LPS inhibited Ia induction by gamma interferon. LPS showed positive regulatory effects on Ia expression by delaying the loss of Ia expression on cultured macrophages and by stimulating the production of Ia-inducing factors. Supernatants from cultured spleen cells stimulated with LPS in vitro contained antiviral and Ia-inducing activity that was acid labile, indicating that the active factor is gamma interferon. We conclude that induction of Ia expression by LPS in vivo is a bone-marrow-dependent, radiation-sensitive process which involves the stimulation of a gamma interferon-producing accessory lymphocyte and a delay in Ia turnover.
- Research Organization:
- Emory Univ. School of Medicine, Atlanta, GA (USA)
- OSTI ID:
- 5874006
- Journal Information:
- Infect. Immun.; (United States), Vol. 57:7
- Country of Publication:
- United States
- Language:
- English
Similar Records
Ia-restricted B-B cell interaction. I. The MHC haplotype of bone marrow cells present during B cell ontogeny dictates the self-recognition specificity of B cells in the polyclonal B cell activation by a B cell differentiation factor, B151-TRF2
Tumor necrosis factor induced stimulation of granulopoiesis and radioprotection
Related Subjects
59 BASIC BIOLOGICAL SCIENCES
IMMUNOGLOBULINS
BIOSYNTHESIS
LIPOPOLYSACCHARIDES
BIOLOGICAL FUNCTIONS
BONE MARROW CELLS
CELL CULTURES
CELL FLOW SYSTEMS
INTERFERON
INTRAPERITONEAL INJECTION
LYMPHOCYTES
LYMPHOKINES
MACROPHAGES
MICE
RADIATION CHIMERAS
RADIOIMMUNOASSAY
SPLEEN CELLS
STEM CELLS
ANIMAL CELLS
ANIMALS
BIOASSAY
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BODY FLUIDS
CARBOHYDRATES
CHIMERAS
CONNECTIVE TISSUE CELLS
FUNCTIONS
GLOBULINS
GROWTH FACTORS
IMMUNOASSAY
IMMUNOLOGY
INJECTION
INTAKE
ISOTOPE APPLICATIONS
LEUKOCYTES
LIPIDS
MAMMALS
MATERIALS
MITOGENS
MOSAICISM
ORGANIC COMPOUNDS
PHAGOCYTES
POLYSACCHARIDES
PROTEINS
RADIOASSAY
RADIOIMMUNOLOGY
RODENTS
SACCHARIDES
SOMATIC CELLS
SYNTHESIS
TRACER TECHNIQUES
VERTEBRATES
560152* - Radiation Effects on Animals- Animals
550201 - Biochemistry- Tracer Techniques