Differential Regulation of the Interleukin-12 Receptor during the Innate Immune Response to Leishmania major

ABSTRACT Previous studies have shown the central role of interleukin 12 (IL-12) in the development of resistance to Leishmania major infection in C3H mice. We now show that during the innate immune response the lymph node cells of L. major-infected C3H mice upregulate the IL-12 receptor on CD4+, CD8+, and B220+ cells. An increase in the ability of the lymph node cells to bind IL-12 correlates with 9.3- and 4.6-fold increases in the mRNA expression levels of the IL-12Rβ1 and -β2 subunits, respectively. In contrast, BALB/c mice, which are susceptible to L. major infection, have no increase in the ability of the lymph node cells to bind IL-12 and correspondingly smaller increases in the mRNA expression levels of the IL-12Rβ1 and -β2 subunits of 2- and 1.5-fold, respectively. Neutralizing IL-4 and the administration of exogenous IL-12 upregulate IL-12R expression in BALB/c mice, while the neutralization of IL-12 in C3H mice blocks increased IL-12 receptor expression. These experiments reveal an important role for the regulation of the IL-12 receptor during the innate immune response after infection of mice with a pathogen.

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CpG Oligodeoxynucleotides Increase the Susceptibility of Normal Mice to Infection by Candida albicans

Infection and Immunity ◽

10.1128/iai.73.9.6154-6156.2005 ◽

2005 ◽

Vol 73 (9) ◽

pp. 6154-6156 ◽

Cited By ~ 12

Author(s):

Shuichi Ito ◽

Joao Pedras-Vasconcelos ◽

Dennis M. Klinman

Keyword(s):

Immune Response ◽

Candida Albicans ◽

Innate Immune Response ◽

Host Resistance ◽

Cytokine Production ◽

Innate Immune ◽

Interleukin 12 ◽

Cpg Oligodeoxynucleotides ◽

Cpg Motifs ◽

Resistance To Infection

ABSTRACT Synthetic oligodeoxynucleotides containing CpG motifs trigger an innate immune response that typically increases host resistance to infection. Yet CpG treatment reduces the resistance of normal mice to Candida albicans infection. This effect is mediated by CpG-induced interleukin-12, indicating that CpG-dependent cytokine production may have adverse consequences for the host.

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The role of the innate immune response in Th1 cell development following Leishmania major infection

Journal of Leukocyte Biology ◽

10.1002/jlb.57.4.515 ◽

1995 ◽

Vol 57 (4) ◽

pp. 515-522 ◽

Cited By ~ 85

Author(s):

Tanya Scharton-Kersten ◽

Phillip Scott

Keyword(s):

Immune Response ◽

Innate Immune Response ◽

Leishmania Major ◽

Cell Development ◽

Innate Immune ◽

Th1 Cell ◽

Major Infection

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Effects of Sodium Octanoate on Innate Immune Response of Mammary Epithelial Cells duringStaphylococcus aureusInternalization

BioMed Research International ◽

10.1155/2013/927643 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

Nayeli Alva-Murillo ◽

Alejandra Ochoa-Zarzosa ◽

Joel E. López-Meza

Keyword(s):

Immune Response ◽

Epithelial Cells ◽

Mrna Expression ◽

Innate Immune Response ◽

Mammary Epithelial Cells ◽

Short Chain Fatty Acids ◽

Mammary Epithelial ◽

Innate Immune ◽

Sodium Octanoate ◽

Bovine Mammary Epithelial Cells

Bovine mammary epithelial cells (bMECs) are capable of initiating an innate immune response to invading bacteria. Short chain fatty acids can reduceStaphylococcus aureusinternalization into bMEC, but it has not been evaluated if octanoic acid (sodium octanoate, NaO), a medium chain fatty acid (MCFA), has similar effects. In this study we determined the effect of NaO onS. aureusinternalization into bMEC and on the modulation of innate immune elements. NaO (0.25–2 mM) did not affectS. aureusgrowth and bMEC viability, but it differentially modulated bacterial internalization into bMEC, which was induced at 0.25–0.5 mM (~60%) but inhibited at 1-2 mM (~40%). Also, bMEC showed a basal expression of all the innate immune genes evaluated, which were induced byS. aureus. NaO induced BNBD4, LAP, and BNBD10 mRNA expression, but BNBD5 and TNF-αwere inhibited. Additionally, the pretreatment of bMEC with NaO inhibited the mRNA expression induction generated by bacteria which coincides with the increase in internalization; only TAP and BNDB10 showed an increase in their expression; it coincides with the greatest effect on the reduction of bacterial internalization. In conclusion, NaO exerts a dual effect onS. aureusinternalization in bMEC and modulates elements of innate immune response.

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Influence of host and parasite factors on the innate immune response and Th2 stability following infection with Leishmania major

Microbes and Infection ◽

10.1016/s1286-4579(99)80016-1 ◽

1999 ◽

Vol 1 (1) ◽

pp. 65-71 ◽

Cited By ~ 6

Author(s):

Brian Hondowicz ◽

Phillip Scott

Keyword(s):

Immune Response ◽

Innate Immune Response ◽

Leishmania Major ◽

Innate Immune ◽

Parasite Factors

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Role of the Yersinia pestis Ail Protein in Preventing a Protective Polymorphonuclear Leukocyte Response during Bubonic Plague

Infection and Immunity ◽

10.1128/iai.05307-11 ◽

2011 ◽

Vol 79 (12) ◽

pp. 4984-4989 ◽

Cited By ~ 34

Author(s):

B. Joseph Hinnebusch ◽

Clayton O. Jarrett ◽

Julie A. Callison ◽

Donald Gardner ◽

Susan K. Buchanan ◽

...

Keyword(s):

Immune Response ◽

Lymph Node ◽

Yersinia Pestis ◽

Innate Immune Response ◽

Innate Immune ◽

Fundamental Aspect ◽

Mouse Serum ◽

Bubonic Plague ◽

Content Type ◽

Systemic Spread

ABSTRACTThe ability ofYersinia pestisto forestall the mammalian innate immune response is a fundamental aspect of plague pathogenesis. In this study, we examined the effect of Ail, a 17-kDa outer membrane protein that protectsY. pestisagainst complement-mediated lysis, on bubonic plague pathogenesis in mice and rats. TheY. pestis ailmutant was attenuated for virulence in both rodent models. The attenuation was greater in rats than in mice, which correlates with the ability of normal rat serum, but not mouse serum, to killail-negativeY. pestis in vitro. Intradermal infection with theailmutant resulted in an atypical, subacute form of bubonic plague associated with extensive recruitment of polymorphonuclear leukocytes (PMN or neutrophils) to the site of infection in the draining lymph node and the formation of large purulent abscesses that contained the bacteria. Systemic spread and mortality were greatly attenuated, however, and a productive adaptive immune response was generated after high-dose challenge, as evidenced by high serum antibody levels againstY. pestisF1 antigen. TheY. pestisAil protein is an important bubonic plague virulence factor that inhibits the innate immune response, in particular the recruitment of a protective PMN response to the infected lymph node.

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Langerhans Cells Orchestrate the Protective Antiviral Innate Immune Response in the Lymph Node

Cell Reports ◽

10.1016/j.celrep.2019.10.118 ◽

2019 ◽

Vol 29 (10) ◽

pp. 3047-3059.e3 ◽

Cited By ~ 3

Author(s):

Eric Wong ◽

Brian Montoya ◽

Colby Stotesbury ◽

Maria Ferez ◽

Ren-Huan Xu ◽

...

Keyword(s):

Immune Response ◽

Lymph Node ◽

Innate Immune Response ◽

Langerhans Cells ◽

Innate Immune

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Oral Immune Activation by Disgust and Disease-Related Pictures

Journal of Psychophysiology ◽

10.1027/0269-8803/a000143 ◽

2015 ◽

Vol 29 (3) ◽

pp. 119-129 ◽

Cited By ~ 4

Author(s):

Richard J. Stevenson ◽

Deborah Hodgson ◽

Megan J. Oaten ◽

Luba Sominsky ◽

Mehmet Mahmut ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Innate Immune Response ◽

Negative Control ◽

Innate Immune ◽

Innate Immune Responses ◽

Immune Markers ◽

Before And After ◽

Secondary Analyses ◽

Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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