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British Journal of Experimental Pathology logoLink to British Journal of Experimental Pathology
. 1983 Jun;64(3):268–276.

Opsonization and phagocytosis of Haemophilus influenzae type B organisms by mouse polymorphonuclear leucocytes and antiribosomal serum.

M A Katz, M Solotorovsky, M Lynn
PMCID: PMC2040660  PMID: 6603862

Abstract

Sera from rabbits immunized with ribosomes passively protect mice challenged with Haemophilus influenzae type b. The protective antibody interacted with organisms in the blood and possibly at the sites of dissemination, but not at the site of inoculation. Macrophages did not phagocytize oposonized bacteria in our system. However, immune serum enhanced phagocytosis and intracellular killing by polymorphonuclear leucocytes (PMN) by reducing viable counts by 77 to 93% and 35 to 50%, respectively. There was a strong correlation between opsonizing activity and passive protection in immune and normal serum. Inactivation of complement significantly reduced the opsonizing activity of the immune serum. A significant portion of the protection associated with the immune serum is localized in the IgM fraction. Immune serum, depleted of IgG, enhanced phagocytosis to a degree similar to intact immune serum. However, immune serum depleted of IgM, opsonized bacteria to the same degree as normal serum. Therefore, the immune component of serum responsible for protection and opsonization appears to be localized in the IgM fraction. These data indicate that protection induced by antiribosomal antibodies results from an interaction with the cell surface of H. influenzae organisms, leading to increased phagocytosis by PMN.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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