Differences in the Rate of Intracellular Killing of Catalase‐Negative and Catalase‐Positive Listeria monocytogenes by Normal and Interferon‐Gamma‐Activated Macrophages

Abstract

Intracellular killing of catalase-positive bacteria by murine resident macrophages requires the presence of extracellular serum, whereas killing of catalase-negative bacteria can occur in the absence of serum. To find out whether the intracellular killing of bacteria by rIFN-gamma-activated macrophages also requires serum stimulation, we investigated the handling of ingested catalase-negative and -positive Listeria monocytogenes by peritoneal macrophages of normal Swiss mice and mice injected i.p. with 1 x 10(4) U rIFN-gamma 18 h earlier. In the absence of extracellular serum, rIFN-gamma-activated macrophages killed ingested catalase-negative Listeria more efficiently (P < 0.01) than normal resident macrophages. Maximal killing of catalase-negative bacteria by rIFN-gamma-activated macrophages required an extracellular serum concentration of only 1.0 to 2.5% compared with the 10% needed by normal macrophages. No differences were observed in the rates of intracellular killing of catalase-positive Listeria by rIFN-gamma-activated and normal resident macrophages: both populations of macrophages required 10% extracellular serum for maximal killing of these bacteria, and killing was minimal in the absence of serum. The rIFN-gamma-activated macrophages displayed enhanced O2-consumption after stimulation with phorbol myristate acetate and heat-killed Listeria compared with macrophages from normal mice. These findings indicate that, under suboptimal stimulation by extracellular serum, rIFN-gamma enhances the intracellular killing of catalase-negative Listeria which lack endogenous catalase acting as a scavenger of reactive oxygen intermediates. The mechanism underlying the enhancement is probably the amplification of the respiratory burst by IFN-gamma.

Crucial Role of Interferon Consensus Sequence Binding Protein, but neither of Interferon Regulatory Factor 1 nor of Nitric Oxide Synthesis for Protection Against Murine Listeriosis

“…The effector mechansim responsible for listericidal properties of macrophages is widely studied and still not clearly defined. ROI (14)(15)(16)(17)(18)(19) as well as RNI (20)(21)(22)(23) have been proposed to be of major importance. Therefore NO production (measured as nitrite accumulation in culture medium) and respiratory burst upon PMA stimulation (H 2 O 2 production measured by chemiluminescence) were tested in PEM cultures stimulated with LPS and/or IFN-␥ as described in Materials and Methods.…”

“…However, the involved signaling pathways are not known, and the effector mechanisms used by macrophages for killing of Listeria are still debated. The role of reactive oxygen intermediates (ROI) 1 (14)(15)(16)(17)(18)(19) as well as reactive nitrogen intermediates (RNI) (20)(21)(22)(23) has been analyzed repeatedly; these experiments revealed variations between different experimental setups and analyzed species.…”

Efficient In Vivo Presentation ofListeria monocytogenes- Derived CD4 and CD8 T Cell Epitopes in the Absence of IFN-γ

“…Mice with a targeted disruption of the genes coding for IFN-␥ (GKO) 3 (3) or the IFN-␥ receptor (RKO) (4) die after infection with a relatively low dose of L. monocytogenes. Generally, it is believed that the most important function of IFN-␥ during L. monocytogenes infection is the stimulation of the killing of bacteria in infected macrophages (5)(6)(7). For the T cell-dependent antilisterial immunity, IFN-␥ is not essential (3).…”

Multi-omics analyses reveal bacteria and catalase associated with keloid disease

“… 11 Some previous studies have found that some types of bacteria produce CAT, while others do not. 12 , 13 In this study, we used multiomics to systemically explore specific typies of bacteria involved in keloid disease and used CDX model to study how CAT regulate the growth of keloid.…”