Interferon‐gamma and resistance to bacterial infections

Czarniecki, Christine W.; Sonnenfeld, Gerald

doi:10.1111/j.1699-0463.1993.tb00073.x

Cited by 25 publications

(6 citation statements)

References 107 publications

(64 reference statements)

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“…G. bethesdensis -stimulated normal monocytes pre-treated with IFN-γ produced significantly more superoxide, as measured by chemiluminescence, compared to monocytes not receiving IFN-γ (data not shown), suggesting a link between induced superoxide and enhanced antibacterial activity after IFN-γ treatment. These data confirm that IFN-γ treatment is important for the maintenance of in vitro monocyte bactericidal activity and may augment phagocytic killing in vivo (29, 30). …”

Section: Resultssupporting

confidence: 71%

Persistence of the Bacterial Pathogen Granulibacter bethesdensis in Chronic Granulomatous Disease Monocytes and Macrophages Lacking a Functional NADPH Oxidase

Chu

Song

Zarember

et al. 2013

The Journal of Immunology

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Granulibacter bethesdensis is a Gram-negative pathogen in patients with Chronic Granulomatous Disease (CGD), a deficiency in the phagocyte NADPH oxidase. Repeated isolation of genetically identical strains from the same patient over years, and prolonged waxing and waning seropositivity in some subjects, raises the possibility of long-term persistence. G. bethesdensis resists killing by serum, CGD polymorphonuclear leukocytes (PMN), and antimicrobial peptides, indicating resistance to non-oxidative killing mechanisms. While G. bethesdensis extends the survival of PMN, persistent intracellular bacterial survival might rely on longer-lived macrophages and their precursor monocytes. Therefore, we examined phagocytic killing by primary human monocytes and monocyte-derived macrophages (MDM). Cells from both normal and CGD subjects internalized G. bethesdensis similarly. G. bethesdensis stimulated superoxide production in normal monocytes, but to a lesser degree than in normal PMN. Normal but not CGD monocytes and MDM killed G. bethesdensis and required in vitro treatment with interferon-γ (IFN-γ) to maintain this killing effect. Although in vitro IFN-γ did not enhance G. bethesdensis killing in CGD monocytes, it restricted growth in proportion to CGD PMN residual superoxide production, providing a potential method to identify patients responsive to IFN-γ therapy. In IFN-γ-treated CGD MDM, G. bethesdensis persisted for the duration of the study (7 days) without decreasing viability of the host cells. These results indicate that G. bethesdensis is highly resistant to oxygen-independent microbicides of myeloid cells, requires an intact NADPH oxidase for clearance, and can persist long-term in CGD mononuclear phagocytes, likely relating to the persistence of this microorganism in infected CGD patients.

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Section: Resultssupporting

confidence: 71%

Persistence of the Bacterial Pathogen Granulibacter bethesdensis in Chronic Granulomatous Disease Monocytes and Macrophages Lacking a Functional NADPH Oxidase

Chu

Song

Zarember

et al. 2013

The Journal of Immunology

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“…It suggested that TGF-β1 was suppressed at the initial phase of mammary infection . IFN-γ is a cytokine that is very important for innate and adaptive immunity against infection of virus and intracellular bacteria [ 23 ]. The mRNA expression of IFN-γ decreased slightly at 6 and 12 h pi, but increased dramatically at 48 h pi and then declined gradually at 72 and 96 h pi (Fig.…”

Section: Resultsmentioning

confidence: 99%

Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model

Wang

et al. 2015

Acta Vet Scand

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BackgroundStaphylococcus aureus causes subclinical mastitis as well as persistent and chronic infections in cattle. Bovine mastitis induced by S. aureus is often refractory to antibiotic treatment. Local innate immune defenses play an important role in eliminating the invading bacteria. TLR2 and NOD2 are important pathogen recognition receptors, but their functions have not been investigated in the context of early stages of mastitis. The present study examined TLR2, NOD2, and related cytokines in mammary glands infection induced by S. aureus at early stages in a rat mastitis model.FindingsAll inoculated mammary glands developed mastitis. Acute changes were induced in mammary tissues infected with S. aureus at early stages and then chronic infections persisted until the end of the experiment. TLR2 and NOD2 mRNA expression increased significantly after inoculation with S. aureus. The expression levels of cytokine mRNAs, including TNF-α, IL-1β, IL-6, IL-10, and CXCL1, also increased. TGF-β1 expression was suppressed at early phase and IFN-γ mRNA expression increased significantly at a later stage.ConclusionsMammary innate immune responses were activated after S. aureus inoculation. TLR2, NOD2, and inflammatory cytokines (TNF-α, IL-1β, IL-6, CXCL1, IL-10, TGF-β1, and IFN-γ) are involved in the response to mastitis induced by S. aureus.Electronic supplementary materialThe online version of this article (doi:10.1186/s13028-015-0116-0) contains supplementary material, which is available to authorized users.

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“…In the case of meningitic infections, consideration of IFNg is often focused on its protective role, associated primarily with modulating bacterial clearance (Czarniecki and Sonnenfeld 1993;Rottenberg and others 2000;Shtrichman and Samuel 2001;Siddiqui and others 2005;Sasaki and others 2006). In our previous (Mitchell and others 2012;Too and others 2014) and present findings, however, we demonstrate that IFNg and its downstream effects may, in part, drive the pathogenesis of PM.…”

Section: Introductionmentioning

confidence: 99%

Interferon-γ-Induced Nitric Oxide Synthase-2 Contributes to Blood/Brain Barrier Dysfunction and Acute Mortality in ExperimentalStreptococcus pneumoniaeMeningitis

Yau

Mitchell

Too

et al. 2016

Journal of Interferon & Cytokine Research

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The proinflammatory cytokine interferon-gamma (IFNγ) recently was shown to play a crucial role in experimental pneumococcal meningitis (PM) pathogenesis, and we aimed in this study to investigate IFNγ-driven nitric oxide synthase-2 (NOS2)-mediated pathogenesis of murine PM. We demonstrate that costimulation of toll-like receptors and IFNγ receptors was synergistic for NOS2 expression in cultured murine microglia. Using an experimental PM model, wild-type mice treated with anti-IFNγ antibody, as well as IFNγ and NOS2 gene knockout (GKO) mice, were inoculated intracerebroventricularly with 10(3) colony-forming units of Streptococcus pneumoniae (WU2 strain). Mice were monitored daily during a 200-h disease course to assess survival rate and blood-brain barrier (BBB) permeability measured at 48 h. IFNγ deficiency was protective in PM, with an approximate 3-fold increase in survival rates in both antibody-treated and IFNγ GKO mice compared to controls (P < 0.01). At 48 h postinoculation, brain NOS2 mRNA expression was significantly increased in an IFNγ-dependent manner. Mortality was significantly delayed in NOS2 GKO mice compared to controls (P < 0.01), and BBB dysfunction was reduced by 54% in IFNγ GKO mice and abolished in NOS2 GKO. These data suggest that IFNγ-dependent expression of NOS2 in the brain contributes to BBB breakdown and early mortality in murine PM.

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Interferon‐gamma and resistance to bacterial infections

Cited by 25 publications

References 107 publications

Persistence of the Bacterial Pathogen Granulibacter bethesdensis in Chronic Granulomatous Disease Monocytes and Macrophages Lacking a Functional NADPH Oxidase

Persistence of the Bacterial Pathogen Granulibacter bethesdensis in Chronic Granulomatous Disease Monocytes and Macrophages Lacking a Functional NADPH Oxidase

Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model

Interferon-γ-Induced Nitric Oxide Synthase-2 Contributes to Blood/Brain Barrier Dysfunction and Acute Mortality in ExperimentalStreptococcus pneumoniaeMeningitis

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