Role of cell surface receptors in the regulation of intracellular killing of bacteria by murine peritoneal exudate neutrophils

P. H. Hart, L. K. Spencer, A. Nikoloutsopoulos, A. F. Lopez, M. A. Vadas, P. J. McDonald, J. J. Finlay-Jones

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Abstract

The role of the Fc and third component of complement (C3) receptors on mouse neutrophils in the control of killing of Proteus mirabilis, opsonized in normal mouse serum (NMS) or heated immune mouse serum (HIMS), was studied. The events following incubation of neutrophils with P. mirabilis and the events associated with bacterial killing were assayed. The respiratory burst was quantified by chemiluminescence (CL). Levels of leukocyte-associated bacteria were determined after a 20-min ingestion period as a measure of phagocytosis. Bacterial killing was measured while ingestion was allowed to continue or as a discrete process when extracellular, noningested bacteria had been removed and neutrophils with intracellular bacteria were incubated in the presence of serum. Modification of these responses in the presence of three monoclonal antibodies (MAb), NIMP-R10 and M1/70, which bind to different epitopes of the mouse C3 receptor, and 2.4G2, which binds to the mouse Fc receptor, was investigated. MAb to the C3, but not to the Fc, receptors reduced CL, ingestion, and intracellular killing of NMS-opsonized P. mirabilis. MAb to the Fc receptor diminished CL to and reduced the rate of ingestion of HIMS-opsonized bacteria. The two MAb to the C3 receptor each produced a similar inhibition of ingestion and intracellular killing of HIMS-opsonized bacteria, but they only partially blocked CL. A range of MAb preparations reactive with other murine antigens did not inhibit these events, either with NMS- or HIMS-opsonized P. mirabilis. The results suggest that C3 receptors on mouse neutrophils played a predominant role in regulation of the killing of P. mirabilis. Similar results were found for Staphylococcus aureus. C3 receptors were necessary for maximal expression of all functions culminating in bacterial kill. That MAb to the C3 receptor inhibited phagocytosis of HIMS-opsonized bacteria in similar fashion to the effect of MAb to the Fc receptor and in contrast to the lack of effect of control MAb may reflect steric hindrance of the Fc receptor by MAb binding to the C3 receptor, or it may reflect that the receptors are linked in murine neutrophils as they are in human neutrophils.

Original languageEnglish
Pages (from-to)245-251
Number of pages7
JournalInfection and Immunity
Volume52
Issue number1
Publication statusPublished - 25 Jun 1986
Externally publishedYes

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Cell Surface Receptors
Exudates and Transudates
Neutrophils
Bacteria
Monoclonal Antibodies
Proteus mirabilis
Fc Receptors
Immune Sera
Luminescence
Eating
Serum
Complement Receptors
Complement C3
Respiratory Burst
Phagocytosis
Staphylococcus aureus
Epitopes
Leukocytes
Antigens

Cite this

Hart, P. H., Spencer, L. K., Nikoloutsopoulos, A., Lopez, A. F., Vadas, M. A., McDonald, P. J., & Finlay-Jones, J. J. (1986). Role of cell surface receptors in the regulation of intracellular killing of bacteria by murine peritoneal exudate neutrophils. Infection and Immunity, 52(1), 245-251.
Hart, P. H. ; Spencer, L. K. ; Nikoloutsopoulos, A. ; Lopez, A. F. ; Vadas, M. A. ; McDonald, P. J. ; Finlay-Jones, J. J. / Role of cell surface receptors in the regulation of intracellular killing of bacteria by murine peritoneal exudate neutrophils. In: Infection and Immunity. 1986 ; Vol. 52, No. 1. pp. 245-251.
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abstract = "The role of the Fc and third component of complement (C3) receptors on mouse neutrophils in the control of killing of Proteus mirabilis, opsonized in normal mouse serum (NMS) or heated immune mouse serum (HIMS), was studied. The events following incubation of neutrophils with P. mirabilis and the events associated with bacterial killing were assayed. The respiratory burst was quantified by chemiluminescence (CL). Levels of leukocyte-associated bacteria were determined after a 20-min ingestion period as a measure of phagocytosis. Bacterial killing was measured while ingestion was allowed to continue or as a discrete process when extracellular, noningested bacteria had been removed and neutrophils with intracellular bacteria were incubated in the presence of serum. Modification of these responses in the presence of three monoclonal antibodies (MAb), NIMP-R10 and M1/70, which bind to different epitopes of the mouse C3 receptor, and 2.4G2, which binds to the mouse Fc receptor, was investigated. MAb to the C3, but not to the Fc, receptors reduced CL, ingestion, and intracellular killing of NMS-opsonized P. mirabilis. MAb to the Fc receptor diminished CL to and reduced the rate of ingestion of HIMS-opsonized bacteria. The two MAb to the C3 receptor each produced a similar inhibition of ingestion and intracellular killing of HIMS-opsonized bacteria, but they only partially blocked CL. A range of MAb preparations reactive with other murine antigens did not inhibit these events, either with NMS- or HIMS-opsonized P. mirabilis. The results suggest that C3 receptors on mouse neutrophils played a predominant role in regulation of the killing of P. mirabilis. Similar results were found for Staphylococcus aureus. C3 receptors were necessary for maximal expression of all functions culminating in bacterial kill. That MAb to the C3 receptor inhibited phagocytosis of HIMS-opsonized bacteria in similar fashion to the effect of MAb to the Fc receptor and in contrast to the lack of effect of control MAb may reflect steric hindrance of the Fc receptor by MAb binding to the C3 receptor, or it may reflect that the receptors are linked in murine neutrophils as they are in human neutrophils.",
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Hart, PH, Spencer, LK, Nikoloutsopoulos, A, Lopez, AF, Vadas, MA, McDonald, PJ & Finlay-Jones, JJ 1986, 'Role of cell surface receptors in the regulation of intracellular killing of bacteria by murine peritoneal exudate neutrophils' Infection and Immunity, vol. 52, no. 1, pp. 245-251.

Role of cell surface receptors in the regulation of intracellular killing of bacteria by murine peritoneal exudate neutrophils. / Hart, P. H.; Spencer, L. K.; Nikoloutsopoulos, A.; Lopez, A. F.; Vadas, M. A.; McDonald, P. J.; Finlay-Jones, J. J.

In: Infection and Immunity, Vol. 52, No. 1, 25.06.1986, p. 245-251.

Research output: Contribution to journalArticle

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AU - Hart, P. H.

AU - Spencer, L. K.

AU - Nikoloutsopoulos, A.

AU - Lopez, A. F.

AU - Vadas, M. A.

AU - McDonald, P. J.

AU - Finlay-Jones, J. J.

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N2 - The role of the Fc and third component of complement (C3) receptors on mouse neutrophils in the control of killing of Proteus mirabilis, opsonized in normal mouse serum (NMS) or heated immune mouse serum (HIMS), was studied. The events following incubation of neutrophils with P. mirabilis and the events associated with bacterial killing were assayed. The respiratory burst was quantified by chemiluminescence (CL). Levels of leukocyte-associated bacteria were determined after a 20-min ingestion period as a measure of phagocytosis. Bacterial killing was measured while ingestion was allowed to continue or as a discrete process when extracellular, noningested bacteria had been removed and neutrophils with intracellular bacteria were incubated in the presence of serum. Modification of these responses in the presence of three monoclonal antibodies (MAb), NIMP-R10 and M1/70, which bind to different epitopes of the mouse C3 receptor, and 2.4G2, which binds to the mouse Fc receptor, was investigated. MAb to the C3, but not to the Fc, receptors reduced CL, ingestion, and intracellular killing of NMS-opsonized P. mirabilis. MAb to the Fc receptor diminished CL to and reduced the rate of ingestion of HIMS-opsonized bacteria. The two MAb to the C3 receptor each produced a similar inhibition of ingestion and intracellular killing of HIMS-opsonized bacteria, but they only partially blocked CL. A range of MAb preparations reactive with other murine antigens did not inhibit these events, either with NMS- or HIMS-opsonized P. mirabilis. The results suggest that C3 receptors on mouse neutrophils played a predominant role in regulation of the killing of P. mirabilis. Similar results were found for Staphylococcus aureus. C3 receptors were necessary for maximal expression of all functions culminating in bacterial kill. That MAb to the C3 receptor inhibited phagocytosis of HIMS-opsonized bacteria in similar fashion to the effect of MAb to the Fc receptor and in contrast to the lack of effect of control MAb may reflect steric hindrance of the Fc receptor by MAb binding to the C3 receptor, or it may reflect that the receptors are linked in murine neutrophils as they are in human neutrophils.

AB - The role of the Fc and third component of complement (C3) receptors on mouse neutrophils in the control of killing of Proteus mirabilis, opsonized in normal mouse serum (NMS) or heated immune mouse serum (HIMS), was studied. The events following incubation of neutrophils with P. mirabilis and the events associated with bacterial killing were assayed. The respiratory burst was quantified by chemiluminescence (CL). Levels of leukocyte-associated bacteria were determined after a 20-min ingestion period as a measure of phagocytosis. Bacterial killing was measured while ingestion was allowed to continue or as a discrete process when extracellular, noningested bacteria had been removed and neutrophils with intracellular bacteria were incubated in the presence of serum. Modification of these responses in the presence of three monoclonal antibodies (MAb), NIMP-R10 and M1/70, which bind to different epitopes of the mouse C3 receptor, and 2.4G2, which binds to the mouse Fc receptor, was investigated. MAb to the C3, but not to the Fc, receptors reduced CL, ingestion, and intracellular killing of NMS-opsonized P. mirabilis. MAb to the Fc receptor diminished CL to and reduced the rate of ingestion of HIMS-opsonized bacteria. The two MAb to the C3 receptor each produced a similar inhibition of ingestion and intracellular killing of HIMS-opsonized bacteria, but they only partially blocked CL. A range of MAb preparations reactive with other murine antigens did not inhibit these events, either with NMS- or HIMS-opsonized P. mirabilis. The results suggest that C3 receptors on mouse neutrophils played a predominant role in regulation of the killing of P. mirabilis. Similar results were found for Staphylococcus aureus. C3 receptors were necessary for maximal expression of all functions culminating in bacterial kill. That MAb to the C3 receptor inhibited phagocytosis of HIMS-opsonized bacteria in similar fashion to the effect of MAb to the Fc receptor and in contrast to the lack of effect of control MAb may reflect steric hindrance of the Fc receptor by MAb binding to the C3 receptor, or it may reflect that the receptors are linked in murine neutrophils as they are in human neutrophils.

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