scholarly journals Poxvirus-Encoded Gamma Interferon Binding Protein Dampens the Host Immune Response to Infection

2007 ◽  
Vol 81 (7) ◽  
pp. 3346-3353 ◽  
Author(s):  
Isaac G. Sakala ◽  
Geeta Chaudhri ◽  
R. Mark Buller ◽  
Anthony A. Nuara ◽  
Hongdong Bai ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Replication ◽  
Deletion Mutant ◽  
Binding Protein ◽  
Small Animal ◽  
Host Immune Response ◽  
Gamma Interferon ◽  
Mutant Virus ◽  
Ifn Γ

ABSTRACT Ectromelia virus (ECTV), a natural mouse pathogen and the causative agent of mousepox, is closely related to variola virus (VARV), which causes smallpox in humans. Mousepox is an excellent surrogate small-animal model for smallpox. Both ECTV and VARV encode a multitude of host response modifiers that target components of the immune system and that are thought to contribute to the high mortality rates associated with infection. Like VARV, ECTV encodes a protein homologous to the ectodomain of the host gamma interferon (IFN-γ) receptor 1. We generated an IFN-γ binding protein (IFN-γbp) deletion mutant of ECTV to study the role of viral IFN-γbp (vIFN-γbp) in host-virus interaction and also to elucidate the contribution of this molecule to the outcome of infection. Our data show that the absence of vIFN-γbp does not affect virus replication per se but does have a profound effect on virus replication and pathogenesis in mice. BALB/c mice, which are normally susceptible to infection with ECTV, were able to control replication of the mutant virus and survive infection. Absence of vIFN-γbp from ECTV allowed the generation of an effective host immune response that was otherwise diminished by this viral protein. Mice infected with a vIFN-γbp deletion mutant virus, designated ECTV-IFN-γbpΔ, produced increased levels of IFN-γ and generated robust cell-mediated and antibody responses. Using several strains of mice that exhibit differential degrees of resistance to mousepox, we show that recovery or death from ECTV infection is determined by a balance between the host's ability to produce IFN-γ and the virus' ability to dampen its effects.

scholarly journals Differential Cytokine Pattern in the Spleens and Livers of BALB/c Mice Infected with Penicillium marneffei: Protective Role of Gamma Interferon

2003 ◽  
Vol 71 (1) ◽  
pp. 465-473 ◽  
Author(s):  
Francesca Sisto ◽  
Annarita Miluzio ◽  
Orazio Leopardi ◽  
Maurizio Mirra ◽  
Johan R. Boelaert ◽  
...  
Keyword(s):  
Immune Response ◽  
Gamma Interferon ◽  
Penicillium Marneffei ◽  
Yeast Cells ◽  
Interleukin 12 ◽  
Type 2 Cytokines ◽  
Ifn Γ

ABSTRACT Penicillium marneffei is an intracellular opportunistic fungus causing invasive mycosis in AIDS patients. T cells and macrophages are important for protection in vivo. However, the role of T-cell cytokines in the immune response against P. marneffei is still unknown. We studied by semiquantitative reverse transcription-PCR and biological assays the patterns of expression of Th1 and Th2 cytokines in the organs of wild-type (wt) and gamma interferon (IFN-γ) knockout (GKO) mice infected intravenously with P. marneffei conidia. At 3 × 105 conidia/mouse, a self-limiting infection developed in wt BALB/c mice, whereas all GKO mice died at day 18 postinoculation. Splenic and hepatic granulomas were present in wt mice, whereas disorganized masses of macrophages and yeast cells were detected in GKO mice. The infection resolved faster in the spleens than in the livers of wt mice and was associated with the local expression of type 1 cytokines (high levels of interleukin-12 [IL-12] and IFN-γ) but not type 2 cytokines (low levels of IL-4 and IL-10). Conversely, both type 1 and type 2 cytokines were detected in the livers of wt animals. Disregulation of the cytokine profile was seen in the spleens but not in the livers of GKO mice. The inducible nitric oxide synthase mRNA level was low and the TNF-α level was high in both spleens and livers of GKO mice compared to wt mice. These data suggest that the polarization of a protective type 1 immune response against P. marneffei is regulated at the level of individual organs and that the absence of IFN-γ is crucial for the activation of fungicidal macrophages and the development of granulomas.

scholarly journals CD8 T Cells in Old Mice Contribute to the Innate Immune Response to Mycobacterium tuberculosis via Interleukin-12p70-Dependent and Antigen-Independent Production of Gamma Interferon

2009 ◽  
Vol 77 (8) ◽  
pp. 3355-3363 ◽  
Author(s):  
Bridget Vesosky ◽  
Erin K. Rottinghaus ◽  
Craig Davis ◽  
Joanne Turner
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Cd8 T Cells ◽  
The Elderly ◽  
Gamma Interferon ◽  
Ifn Γ ◽  
Aerosol Infection ◽  
Old Mice

ABSTRACT Elderly individuals have increased morbidity and mortality associated with infectious diseases due in part to the progressive age-associated decline in immune function. Despite this, the old mouse model of Mycobacterium tuberculosis infection has revealed a CD8- and gamma interferon (IFN-γ)-dependent early resistance to infection. In this study, we investigated the mechanism by which CD8 T cells from old mice contributed to the early immune response to M. tuberculosis. Following a low-dose aerosol infection with M. tuberculosis, CD8 T cells were identified as being a dominant source of IFN-γ expression in the lungs of old mice early after infection, before the typical onset of antigen-specific immunity. In addition, M. tuberculosis-induced IFN-γ production by CD8 T cells isolated from naïve old mice was major histocompatibility complex class I independent but was dependent on interleukin-12p70, confirming an innate role of CD8 T cells during M. tuberculosis infection. Moreover, the ability of CD8 T cells from old mice to produce increased innate IFN-γ levels in response to M. tuberculosis infection was defined as a unique function of CD8 T cells from old mice and not the aged lung environment. Finally, we have identified increased expression of SET as being one possible mechanism by which CD8 T cells from old mice produce enhanced levels of IFN-γ. Additional characterizations of the signaling events that lead to enhanced innate IFN-γ production by CD8 T cells in old mice may lead to novel strategies to further enhance or perpetuate beneficial immune responses in the elderly.

scholarly journals Resistance to Acute Babesiosis Is Associated with Interleukin-12- and Gamma Interferon-Mediated Responses and Requires Macrophages and Natural Killer Cells

2003 ◽  
Vol 71 (4) ◽  
pp. 2002-2008 ◽  
Author(s):  
Irma Aguilar-Delfin ◽  
Peter J. Wettstein ◽  
David H. Persing
Keyword(s):  
Nk Cells ◽  
Gamma Interferon ◽  
Interleukin 12 ◽  
No Production ◽  
Cytokine Responses ◽  
Early Production ◽  
Ifn Γ ◽  
Crucial Part

ABSTRACT We examined the role of the cytokines gamma interferon (IFN-γ) and interleukin-12 (IL-12) in the model of acute babesiosis with the WA1 Babesia. Mice genetically deficient in IFN-γ-mediated responses (IFNGR2KO mice) and IL-12-mediated responses (Stat4KO mice) were infected with the WA1 Babesia, and observations were made on the course of infection and cytokine responses. Levels of IFN-γ and IL-12 in serum increased 24 h after parasite inoculation. The augmented susceptibility observed in IFNGR2KO and Stat-4KO mice suggests that the early IL-12- and IFN-γ-mediated responses are involved in protection against acute babesiosis. Resistance appears to correlate with an increase in nitric oxide (NO) production. In order to assess the contribution of different cell subsets to resistance against the parasite, we also studied mice lacking B cells, CD4+ T cells, NK cells, and macrophages. Mice genetically deficient in B lymphocytes or CD4+ T lymphocytes were able to mount protective responses comparable to those of immunosufficient mice. In contrast, in vivo depletion of macrophages or NK cells resulted in elevated susceptibility to the infection. Our observations suggest that a crucial part of the response that protects from the pathogenic Babesia WA1 is mediated by macrophages and NK cells, probably through early production of IL-12 and IFN-γ, and induction of macrophage-derived effector molecules like NO.

The possible role of the frontal and sub-parietal gland systems of the pentastomidReighardia sternae(Diesing, 1864) in the evasion of the host immune response

Parasitology ◽  
1979 ◽  
Vol 78 (1) ◽  
pp. 53-66 ◽  
Author(s):  
J. Riley ◽  
J. L. James ◽  
A. A. Banaja
Keyword(s):  
Immune Response ◽  
Alternative Explanation ◽  
Surface Membrane ◽  
Membrane System ◽  
Host Immune Response ◽  
Entire Surface ◽  
Strong Immune Response ◽  
Concomitant Immunity ◽  
Host Parasite

SUMMARYThe frontal and sub-parietal glands of the pentastomidReighardia sternaeelaborate lamellate secretion which is poured on to the cuticle. The entire surface of the cuticle, including the mouth, hook pits and reproductive apertures, is coated with secretion. Electron microscope studies indicate that the glands are continuously active, which implies a turnover of surface membranes. The postulated function of these membranes is to protect certain vital areas of the host–parasite interface, notably the pores of ion-transporting cells, from the host immune response. The available evidence suggests that pentastomids do evoke a strong immune response but since most are long-lived they must circumvent it. We believe the surface membrane system to be instrumental in this. Studies on another pentastomid,Porocephalus crotaliin rats have shown that an immune response stimulated by a primary infection will kill subsequent infections and that the surface membranes are strongly immunogenic. Obvious parallels between this situation and that of schistosome infections in mammals are discussed. An alternative explanation of concomitant immunity is proposed.

scholarly journals Immunity and its role in periodontal diseases

2017 ◽  
Vol 63 (1) ◽  
pp. 24-27
Author(s):  
Irina Dumitrache ◽  
Keyword(s):  
Immune Response ◽  
Chronic Disease ◽  
Periodontal Disease ◽  
Clinical Efficacy ◽  
Periodontal Diseases ◽  
Adult Population ◽  
Host Immune Response ◽  
Immunomodulatory Therapy ◽  
Common Chronic Disease

Periodontal disease is one of the most common chronic disease, with a prevalence between 5% and 30% in adult population aged 25-75. In the pathogenesis of periodontal disease, the host immune response has a great importance and in the last years it has been underlined the role of immunomodulatory therapy in the management of periodontal disease. Septilin is a herbal immunomodulatory with clinical efficacy proven in the periodontal disease.

scholarly journals Role of Host Immune Response and Viral Load in the Differential Outcome of Pandemic H1N1 (2009) Influenza Virus Infection in Indian Patients

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13099 ◽  
Author(s):  
Vidya A. Arankalle ◽  
Kavita S. Lole ◽  
Ravi P. Arya ◽  
Anuradha S. Tripathy ◽  
Ashwini Y. Ramdasi ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Viral Load ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Host Immune Response ◽  
Pandemic H1n1 ◽  
Differential Outcome ◽  
Pandemic H1n1 2009

Role of DNA repair in host immune response and inflammation

2015 ◽  
Vol 763 ◽  
pp. 246-257 ◽  
Author(s):  
Fabrícia Lima Fontes ◽  
Daniele Maria Lopes Pinheiro ◽  
Ana Helena Sales de Oliveira ◽  
Rayssa Karla de Medeiros Oliveira ◽  
Tirzah Braz Petta Lajus ◽  
...  
Keyword(s):  
Immune Response ◽  
Dna Repair ◽  
Host Immune Response

scholarly journals Review on the Role of Host Immune Response in Protection and Immunopathogenesis during Cutaneous Leishmaniasis Infection

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Teshager Dubie ◽  
Yasin Mohammed
Keyword(s):  
Immune Response ◽  
Cutaneous Leishmaniasis ◽  
Proinflammatory Cytokines ◽  
Parasitic Infection ◽  
Host Immune Response ◽  
Immune Defense ◽  
Host Cells ◽  
Infected Host ◽  
Major Public Health Problem

Cutaneous leishmaniasis (CL) is a major public health problem worldwide and spreads to human via the bite of sand flies during blood meal. Following its inoculation, the promastigotes are immediately taken up by phagocytic cells and these leishmania-infected host cells produce proinflammatory cytokines that activate other immune cells and these infected host cells produce more cytokines and reactive nitrogen and oxygen species for efficient control of leishmania infection. Many experimental studies showed that resistance to infection with leishmania paraites is associated with the production of proinflammatory cytokines and activation of CD4+ Th1 response. On the other hand, vulnerability to this parasitic infection is correlated to production of T helper 2 cytokines that facilitate persistence of parasites and disease progression. In addition, some studies have also indicated that CD8+ T cells play a vital role in immune defense through cytokine production and their cytotoxic activity and excessive production of proinflammatory mediators promote amplified recruitment of cells. This could be correlated with excessive inflammatory reaction and ultimately resulted in tissue destruction and development of immunopathogenesis. Thus, there are contradictions regarding the role of immune responses in protection and immunopathogenesis of CL disease. Therefore, the aim of this paper was to review the role of host immune response in protection and its contribution to disease severity for CL infection. In order to obtain more meaningful data regarding the nature of immune response to leishmania, further in-depth studies focused on immune modulation should be conducted to develop better therapeutic strategies.

scholarly journals Role of Gamma Interferon in Helicobacter pylori Induction of Inflammatory Mediators during Murine Infection

2002 ◽  
Vol 70 (6) ◽  
pp. 3295-3299 ◽  
Author(s):  
Marygorret Obonyo ◽  
Donald G. Guiney ◽  
Julia Harwood ◽  
Joshua Fierer ◽  
Sheri P. Cole
Keyword(s):  
Helicobacter Pylori ◽  
Gene Knockout ◽  
Gamma Interferon ◽  
Epithelial Cell Line ◽  
Inos Mrna ◽  
Inflammatory Protein ◽  
Ifn Γ ◽  
H Pylori ◽  
Oxide Synthase

ABSTRACT Gamma interferon (IFN-γ) has been proposed to play an important role in Helicobacter-related gastritis. Using the IFN-γ gene knockout (IFN-γ−/−) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible nitric oxide synthase (iNOS) mRNA only in wild-type mice. MIP-2 and iNOS mRNA were also induced by H. pylori in GSM06 cells. Induction of cyclooxygenase 2 mRNA through IFN-γ was demonstrated in GSM06 cells. These data indicate that IFN-γ mediates the induction of MIP-2 and iNOS mRNA expression by H. pylori in mice.

scholarly journals Role of Endogenous Interleukin-12 in Immune Response to Staphylococcal Enterotoxin B in Mice

2001 ◽  
Vol 69 (9) ◽  
pp. 5949-5952 ◽  
Author(s):  
Fanny N. Lauw ◽  
Sandrine Florquin ◽  
Peter Speelman ◽  
Sander J. H. van Deventer ◽  
Tom van der Poll
Keyword(s):  
Immune Response ◽  
Gamma Interferon ◽  
Staphylococcal Enterotoxin ◽  
Interleukin 12 ◽  
Staphylococcal Enterotoxin B ◽  
Induced Responses ◽  
Independent Mechanism ◽  
Enterotoxin B

ABSTRACT In the present study, the roles of interleukin 12 (IL-12) and IL-18 and their possible interaction during superantigen-induced responses were studied by injection of staphylococcal enterotoxin B (SEB) into mice. These data suggest that the role of IL-12 in SEB-induced responses is limited to sustaining gamma interferon release by an IL-18-independent mechanism.

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