{"id":24204,"date":"2025-05-19T15:11:39","date_gmt":"2025-05-19T13:11:39","guid":{"rendered":"https:\/\/www.biolife-publisher.it\/iji\/?p=24204"},"modified":"2025-05-19T15:11:39","modified_gmt":"2025-05-19T13:11:39","slug":"mechanisms-with-which-microbes-bind-and-activate-toll-like-receptors-and-the-nf-kb-signaling-pathway","status":"publish","type":"post","link":"https:\/\/www.biolife-publisher.it\/iji\/mechanisms-with-which-microbes-bind-and-activate-toll-like-receptors-and-the-nf-kb-signaling-pathway\/","title":{"rendered":"MECHANISMS WITH WHICH MICROBES BIND AND ACTIVATE TOLL-LIKE RECEPTORS AND THE NF-KB SIGNALING PATHWAY"},"content":{"rendered":"

Ambrosini G. Mechanisms with which microbes bind and activate toll-like receptors and the Nf-kB signaling pathway. International Journal of Infection.<\/em> 2023;7(1):15-17.<\/p>\n

\n

G. Ambrosini*<\/sup><\/p>\n

Experimental Cancer Research, \u00c9cole Polytechnique F\u00e9d\u00e9rale de Lausanne, Lausanne, Switzerland.<\/p>\n

*Correspondence to:<\/em>
\nGiovanna Ambrosini,
\nExperimental Cancer Research,
\n\u00c9cole Polytechnique F\u00e9d\u00e9rale de Lausanne,
\n1015, Lausanne, Switzerland.
\ne-mail: ambrosini.studiomedico@gmail.com<\/a><\/p>\n\n\n\n
Received: 30 November, 2022
\nAccepted: 17 February, 2023<\/p>\n

\"adobe-pdf-download-icon\"<\/a><\/td>\n

ISSN 1972-6945 [online]
\nCopyright 2023 \u00a9 by Biolife-publisher
\nThis publication and\/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: all authors report no conflicts of interest relevant to this article.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

KEYWORDS:<\/strong> Microbe, toll-like receptor, NF-kB, signal pathway, immune response, pattern recognition receptor<\/em><\/p>\n

 <\/p>\n

INTRODUCTION<\/strong><\/p>\n

 <\/p>\n

The interaction between microbes and the immune system takes place by complex biochemical processes. Microbial proteins are ligands for the toll-like receptor (TLR) of host cells. The binding of microbes to the TLR allows microorganisms such as viruses or bacteria to enter the host cell through the process of phagocytosis. Inside the cell, the microorganism modifies the host cell mechanisms to proliferate and evade the immune system.<\/p>\n

The TLR is localized on the host cell membrane and when microorganisms bind to it, immune responses become activated. Innate immunity is guided by pattern recognition receptors (PRRs), which recognize and bind to conserved molecular structures of microorganisms that are known as pathogen-associated molecular patterns (PAMPs). Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-\u03baB) is a family of transcription factor protein complexes that control the transcription of DNA, cytokine production, and cell survival. Activation of the TLR leads to phosphorylation and subsequent degradation of I\u03baB, which releases NF-\u03baB and induces the production of pro-inflammatory cytokines such as TNF, IL-1\u03b2, and IL-6 (Fig.1).<\/p>\n

 <\/p>\n

\"\"<\/p>\n

Fig. 1.<\/strong> Sequence of activation that begins with the toll-like receptor (TLR) to result in the release of cytokines and chemokines.<\/em><\/p>\n

 <\/p>\n

DISCUSSION<\/strong><\/p>\n

 <\/p>\n

Microbes can infect host cells through complex biochemical processes that involve interactions between the microorganism and the immune system (1). The binding of the microbe to the TLR expressed by the host cell leads to activation of the NF-kB signaling pathway, which controls the expression of genes involved in inflammation, the immune response, cell proliferation, and survival (2).<\/p>\n

Microbes, such as bacteria, viruses, and fungi, enter host cells through various mechanisms such as endocytosis or direct penetration of the cell membrane (phagocytosis) carried out mainly by macrophages, dendritic cells, and neutrophilic granulocytes. The bond between the host cell and the microorganism is facilitated by surface microbial proteins (2). Once inside the cell, microorganisms can influence the machinery of the host cell to facilitate their survival and replication. These processes include microbial resistance, switching of cellular processes, and evasion of immune responses (3).<\/p>\n

The TLR is a cell membrane protein that is capable of binding microorganisms. To date, eleven mammalian TLRs have been identified, each of which perform a specific function. For example, TLR4 recognizes lipopolysaccharide (LPS), which is a product of Gram-negative bacteria. The interaction between microbes and host cells that occurs through the activation of the TLR leads to a biochemical cascade with the production of pro-inflammatory cytokines.<\/p>\n

PAMPs include microbial molecular structures such as proteins from Gram-positive bacteria and LPS from Gram-negative bacteria. The endogenous ligands, or host-derived damage-associated molecular patterns (DAMPs), are usually produced as a result of injury and non-physiological cell death. DAMPs include extracellular matrix components, plasma membrane constituents, nuclear and cytosolic proteins, and elements of damaged fragmented organelles such as mitochondrial DNA.<\/p>\n

TLRs are\u00a0an important family of receptors that constitute the first line of defence system against microbes (4). Once the TLR has recognized the microbial agent or some of its products (such as LPS, for example) it transmits the information to both the innate and adaptive immune system. Immune cells, along with many other types of cells, possess TLRs that can activate specific intracellular signaling cascades related to immune responses. These reactions lead to the generation of immune molecules such as cytokines and chemokines that can be inflammatory (5). TLR-dependent signaling pathways are increased during innate immune responses by a variety of negative regulators (6). Overactivation of TLRs can ultimately lead to disruption of immune homeostasis and thus, increases the risk for inflammatory diseases and autoimmune disorders (7).<\/p>\n

NF-\u03baB is a transcription factor that controls the expression of genes involved in inflammation, immune responses, cell proliferation, and cell survival. Activation of the TLR leads to the phosphorylation and subsequent degradation of I\u03baB that results in the release of NF-\u03baB (8). Free NF-\u03baB translocates to the nucleus, where it binds to specific DNA sequences to regulate gene transcription (9).<\/p>\n

Activation of NF-\u03baB results in the production of pro-inflammatory cytokines including TNF, IL-1\u03b2, and IL-6, which are essential for initiating and sustaining inflammatory responses (10). These cytokines help recruit and activate various immune cells at the site of infection, but when the cytokines are overexpressed, they induce inflammation which can be serious enough to lead to the patient’s death (11).<\/p>\n

Infection by microorganisms activates the expression of antimicrobial peptides and other defence molecules which are upregulated (12). This enhances the ability of the host to directly kill pathogens and limit their spread. NF-\u03baB also plays a role in the maturation and function of antigen-presenting cells, bridging the innate and adaptive immune responses (13). This aids in the activation of T cells and the development of a specific immune response against the pathogen.<\/p>\n

 <\/p>\n

CONCLUSIONS<\/strong><\/p>\n

 <\/p>\n

The interaction between microbes and host cells triggers a cascade of biochemical events mediated by several molecules including TLRs and the NF-\u03baB pathway. TLRs recognize specific microbial components, leading to the activation of NF-\u03baB, which then induces the expression of genes involved in inflammation, immune defenses, and cellular survival. This coordinated response is critical for controlling infections and ensuring an effective immune response. For this reason, antagonists or inhibitors targeting the TLR signaling pathways have emerged as novel therapeutics to treat inflammation in infectious diseases.<\/p>\n

 <\/p>\n

Conflict of interest <\/em><\/p>\n

The author declares that they have no conflict of interest.<\/p>\n

 <\/p>\n

REFERENCES<\/strong><\/p>\n

    \n
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  8. Lee Y, Kim H, Kim S, Kim KH, Chung JH. Activation of toll\u2010like receptors 2, 3 or 5 induces matrix metalloproteinase\u20101 and \u20109 expression with the involvement of MAPKs and NF\u2010\u03baB in human epidermal keratinocytes. Experimental Dermatology<\/em>. 2010;19(8). doi:https:\/\/doi.org\/10.1111\/j.1600-0625.2009.00963.x<\/li>\n
  9. Karin M, Ben-Neriah Y. Phosphorylation Meets Ubiquitination: The Control of NF-\u03baB Activity. Annual Review of Immunology<\/em>. 2000;18(1):621-663. doi:https:\/\/doi.org\/10.1146\/annurev.immunol.18.1.621<\/li>\n
  10. Yun SW, Kim JK, Han MJ, Kim DH. Lacticaseibacillus paracasei<\/em> NK112 mitigates Escherichia coli<\/em>-induced depression and cognitive impairment in mice by regulating IL-6 expression and gut microbiota. Beneficial Microbes<\/em>. 2021;12(6):541-551. doi:https:\/\/doi.org\/10.3920\/bm2020.0109<\/li>\n
  11. L\u00f3pez\u2010Haber C, Netting DJ, Hutchins Z, Ma X, Hamilton KE, Mantegazza AR. The phagosomal solute transporter SLC15A4 promotes inflammasome activity via mTORC1 signaling and autophagy restraint in dendritic cells. The EMBO Journal<\/em>. 2022;41(20). doi:https:\/\/doi.org\/10.15252\/embj.2022111161<\/li>\n
  12. Sonenshine DE, Macaluso KR. Microbial Invasion vs. Tick Immune Regulation. Frontiers in Cellular and Infection Microbiology<\/em>. 2017;7. doi:https:\/\/doi.org\/10.3389\/fcimb.2017.00390<\/li>\n
  13. Ghislat G, Cheema AS, Baudoin E, et al. NF-\u03baB\u2013dependent IRF1 activation programs cDC1 dendritic cells to drive antitumor immunity. Science Immunology<\/em>. 2021;6(61). doi:https:\/\/doi.org\/10.1126\/sciimmunol.abg3570<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

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