RhoGTPases and inflammasomes: Guardians of effector-triggered immunity

Pathogens have evolved smart strategies to invade hosts and hijack their immune responses. One such strategy is the targeting of the host RhoGTPases by toxins or virulence factors to hijack the cytoskeleton dynamic and immune processes. In response to this microbial attack, the host has evolved an elegant strategy to monitor the function of virulence factors and toxins by sensing the abnormal activity of RhoGTPases. This innate immune strategy of sensing bacterial effector targeting RhoGTPase appears to be a bona fide example of effector-triggered immunity (ETI). Here, we review recently discovered mechanisms by which the host can sense the activity of these toxins through NOD and NOD-like receptors (NLRs).

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The Role of Porphyromonas gingivalis Virulence Factors in Periodontitis Immunopathogenesis

Dentika Dental Journal ◽

10.32734/dentika.v23i1.3421 ◽

2020 ◽

Vol 23 (1) ◽

pp. 6-12

Author(s):

Tienneke Riana Septiwidyati ◽

Endang Winiati Bachtiar

Keyword(s):

Immune Responses ◽

Porphyromonas Gingivalis ◽

Virulence Factors ◽

Defense Mechanisms ◽

Tooth Loss ◽

Innate Immune ◽

Not Given ◽

Innate Immune Responses ◽

Oral Bacterium

Porphyromonas gingivalis is an anaerobic Gram-negative oral bacterium involved in the pathogenesis of periodontitis. Periodontitis is an infection that is characterized by damage to the supporting tissues of the teeth so that it can cause tooth loss if not given treatment. P. gingivalis locally can invade periodontal tissue and avoid host defense mechanisms. This bacterium has virulence factors which can cause deregulation of innate immune responses and inflammation in the host. The role of P. gingivalis virulence factors such as capsules, fimbriae, lipopolysaccharides, and gingipain in the pathogenesis of periodontitis will be discussed in this paper.

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Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome

Toxins ◽

10.3390/toxins13010068 ◽

2021 ◽

Vol 13 (1) ◽

pp. 68

Author(s):

Lianci Peng ◽

Jiali Jiang ◽

Tingting Chen ◽

Dongyi Xu ◽

Fengqing Hou ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Virulence Factors ◽

Toxic Shock Syndrome ◽

Opportunistic Pathogen ◽

Peritoneal Macrophages ◽

Innate Immune ◽

Toxic Shock ◽

Pyrin Domain ◽

Toxic Shock Syndrome Toxin

Staphylococcus aureus is a Gram-positive opportunistic pathogen which causes infections in a variety of vertebrates. Virulence factors are the main pathogenesis of S. aureus as a pathogen, which induce the host’s innate and adaptive immune responses. Toxic shock syndrome toxin 1 (TSST-1) is one of the most important virulence factors of S. aureus. However, the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) in TSST-1-induced innate immune response is still unclear. Here, purified recombinant TSST-1 (rTSST-1) was prepared and used to stimulate mouse peritoneal macrophages. The results showed that under the action of adenosine-triphosphate (ATP), rTSST-1 significantly induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) production in mouse macrophages and the production was dose-dependent. In addition, rTSST-1+ATP-stimulated cytokine production in macrophage depends on the activation of toll like receptor 4 (TLR4), but not TLR2 on the cells. Furthermore, the macrophages of NLRP3−/− mice stimulated with rTSST-1+ATP showed significantly low levels of IL-1β production compared to that of wild-type mice. These results demonstrated that TSST-1 can induce the expression of inflammatory cytokines in macrophages via the activation of the TLR4 and NLRP3 signaling pathways. Our study provides new information about the mechanism of the TSST-1-inducing host’s innate immune responses.

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Receptors in the induction of the plant innate immunity

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-07-20-0173-cr ◽

2021 ◽

Author(s):

Tian-Ying Yu ◽

Meng-Kun Sun ◽

Li-Kun Liang

Keyword(s):

Immune Responses ◽

Innate Immune System ◽

Effector Proteins ◽

Innate Immune ◽

Leucine Rich Repeat ◽

Nucleotide Binding Domain ◽

Effector Triggered Immunity ◽

Growth Development ◽

Immune Pathway ◽

Molecular Patterns

Plants adjust amplitude and duration of immune responses via different strategies to maintain growth, development and resistance to pathogens. Pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) and effector-triggered immunity (ETI) play vital roles. PRRs (pattern recognition receptors), comprising a large number of receptor-like protein kinases (RLKs) and receptor-like proteins (RLPs), recognize related ligands and trigger immunity. PTI is the first layer of the innate immune system, and it recognizes PAMPs at plasma membrane to prevent infection. However, pathogens exploit effector proteins to bypass or directly inhibit the PTI immune pathway. Consistently, plants have evolved intracellular nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins to detect pathogenic effectors and trigger a hypersensitive response to activate ETI. PTI and ETI work together to protect plants from infection of virus and other pathogens. Diverse receptors and the corresponding ligands, especially several pairs of well-studied receptors and ligands in PTI immunity, are reviewed to illustrate the dynamic process of PTI response here.

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Pneumolysin, PspA, and PspC Contribute to Pneumococcal Evasion of Early Innate Immune Responses during Bacteremia in Mice

Infection and Immunity ◽

10.1128/iai.01727-06 ◽

2007 ◽

Vol 75 (4) ◽

pp. 2067-2070 ◽

Cited By ~ 38

Author(s):

Lisa R. Quin ◽

Quincy C. Moore ◽

Larry S. McDaniel

Keyword(s):

Immune Responses ◽

Virulence Factors ◽

Innate Immune ◽

Blood Clearance ◽

Innate Immune Responses

ABSTRACTThe pneumococcal virulence factors include capsule, PspA, PspC, and Ply. Cytometric analysis demonstrated that the greatest levels of C3 deposition were on a ΔplyPspA−PspC−mutant. Also, Ply, PspA, and PspC expression resulted in C3 degradation in vitro and in vivo. Finally, blood clearance assays demonstrated that there was enhanced clearance of ΔplyPspA−PspC−pneumococci compared to the clearance of nonencapsulated pneumococci.

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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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