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The hosts' susceptibility to infection depends on several factors. The integrity of the skin and mucous membranes helps protect the body against microbial attacks. When the skin is altered, the chance of infection, limb loss, and even death increases.
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Chronic Pancreatitis I: Introduction01:24

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Related Experiment Video

Updated: Mar 5, 2026

Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing
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Microbiota, Immune Subversion, and Chronic Inflammation.

Carolyn D Kramer1, Caroline Attardo Genco1

  • 1Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine , Boston, MA , USA.

Frontiers in Immunology
|March 29, 2017
PubMed
Summary
This summary is machine-generated.

Certain bacteria, like Porphyromonas gingivalis, evade the innate immune system by altering lipid A structures, which can lead to chronic inflammation and atherosclerosis. Understanding this mechanism is key to managing inflammatory diseases.

Keywords:
atherosclerosisimmune dysregulationimmune subversioninflammationinnate immunitymicrobiotatoll-like receptors

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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
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Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Host-adapted pathogens can evade innate immunity, causing low-grade inflammation and chronic inflammatory disorders.
  • Microbiota play a significant role in chronic inflammatory diseases.
  • Toll-like receptors (TLRs) are crucial in immune signaling, but some microbes can subvert their protective functions.

Purpose of the Study:

  • To review the role of microbiota in chronic inflammatory diseases.
  • To discuss how specific microorganisms, particularly Porphyromonas gingivalis, evade TLR signaling.
  • To highlight the impact of microbial lipid A structures on TLR4 signaling and systemic immunopathology.

Main Methods:

  • Review of recent studies on microbiota and chronic inflammation.
  • Analysis of Porphyromonas gingivalis's lipid A structures and their effect on TLR4 signaling.
  • Experimental use of P. gingivalis mutant strains with distinct lipid A moieties.
  • Comparison of disease susceptibility in TLR4-deficient mice versus wild-type mice after P. gingivalis infection.

Main Results:

  • P. gingivalis can express underacylated or modified lipid A, altering TLR4 signaling.
  • Antagonist lipid A expression in P. gingivalis correlated with systemic inflammation and immunopathology.
  • Agonist lipid A expression resulted in modest systemic inflammation.
  • TLR4-deficient mice were more susceptible to vascular inflammation after P. gingivalis infection.

Conclusions:

  • P. gingivalis dysregulates innate and adaptive immune responses, leading to systemic inflammation and immunopathology.
  • Microbial modulation of lipid A structures is a key mechanism for immune evasion.
  • Anti-TLR4 interventions require careful consideration due to the dual role of TLR signaling in host defense and pathology.