• Journal of Microbiology and Biotechnology
• /
• 제33권3호
• /
• pp.288-298
• /
• 2023

Host defense peptides are expressed in various immune cells, including phagocytic cells and epithelial cells. These peptides selectively alter innate immune pathways in response to infections by pathogens, such as bacteria, fungi, and viruses, and modify the subsequent adaptive immune environment. Consequently, they play a wide range of roles in both innate and adaptive immune responses. These peptides are of increasing importance due to their broad-spectrum antimicrobial activity and their functions as mediators linking innate and adaptive immune responses. This review focuses on the pleiotropic biological functions and related mechanisms of action of human host defense peptides and discusses their potential clinical applications.

• 한국식품영양학회지
• /
• 제21권3호
• /
• pp.275-282
• /
• 2008

Hot-water($100^{\circ}C$) and cold-water($4^{\circ}C$) extracts of Taraxacum officinale root were assessed for the effects of innate and adaptive immune responses in mice. Hot water extracts(TO-100) and cold water extracts(TO-4) did not affect the viability of macrophages at concentrations below to 18 mg/ml and 8 mg/ml, respectively. The thioglycollate-induced macrophages cultured with TO-100 and TO-4 produced a significantly higher quantity of various cytokines, such as IL-6 and IL-12, than those treated with medium. This shows that the extracts potently stimulated the innate immune response. When mice were subcutaneously immunized(sc) with OVA+FIA(Freund's incomplete adjuvant)-emulsified TO-100, TO-100 did not affect the production of IgE, but enhanced the production of IgG1, IgG2a and IgG2b. The culture supernatant obtained from the splenocytes of mice treated with OVA+FIA-emulsified TO-100 also evidenced elevated levels of both OVA-specific Th1-type(IFN-$\gamma$) and Th2-type cytokines(IL-4, IL-6 and IL-10). These results suggested that TO-100 can modulate the immune responses to allergens in mice.

• IMMUNE NETWORK
• /
• 제11권5호
• /
• pp.245-252
• /
• 2011

Antimicrobial peptides/proteins are ancient and naturally-occurring antibiotics in innate immune responses in a variety of organisms. Additionally, these peptides have been recognized as important signaling molecules in regulation of both innate and adaptive immunity. During mycobacterial infection, antimicrobial peptides including cathelicidin, defensin, and hepcidin have antimicrobial activities against mycobacteria, making them promising candidates for future drug development. Additionally, antimicrobial peptides act as immunomodulators in infectious and inflammatory conditions. Multiple crucial functions of cathelicidins in antimycobacterial immune defense have been characterized not only in terms of direct killing of mycobacteria but also as innate immune regulators, i.e., in secretion of cytokines and chemokines, and mediating autophagy activation. Defensin families are also important during mycobacterial infection and contribute to antimycobacterial defense and inhibition of mycobacterial growth both in vitro and in vivo. Hepcidin, although its role in mycobacterial infection has not yet been characterized, exerts antimycobacterial effects in activated macrophages. The present review focuses on recent efforts to elucidate the roles of host defense peptides in innate immunity to mycobacteria.

• Toxicological Research
• /
• 제23권2호
• /
• pp.97-105
• /
• 2007

Toll-like receptors (TLRs) playa crucial role in initiating and regulating innate and adaptive immune responses by detecting invading microbial pathogens. TLRs can also respond to non-microbial molecules derived from damaged tissue. Accumulating evidence suggests that deregulation of TLRs results in the dysfunction of immune system and ultimately increases the risk of many immune and inflammatory diseases including infectious diseases, allergy, and autoimmune diseases. Therefore, understanding how the immune system is controlled by TLRs will provide new insight to find the way to prevent or treat infectious diseases and immune disorders.

• 생명과학회지
• /
• 제18권6호
• /
• pp.891-896
• /
• 2008

The function of mast cells as effector cells in allergy has been extensively studied. Mast cells activated through high affinity IgE-receptor ($Fc{\varepsilon}RI$) release diverse mediators, and lead to smooth muscle constriction, vasodilation, increase of vascular permeability, leukocyte recruitment and activation, mucus secretion, and tissue proliferation and remodeling. However, various other immunological and non-immunological signals can lead to the activation of mast cells. In resent years, mast cells have been identified to be involved in a complex range of immune functions. Mast cells can be important as key players in the regulation of innate as well as adapted immune responses, and may influence the development of allergy, autoimmune disorder and peripheral tolerance. This review summarizes the recent advances in the understanding of effector functions of mast cells in immune responses.

• Genomics & Informatics
• /
• 제10권3호
• /
• pp.153-166
• /
• 2012

A variety of ligands differ in their capacity to bind the receptor, elicit gene expression, and modulate physiological responses. Such receptors include Toll-like receptors (TLRs), which recognize various patterns of pathogens and lead to primary innate immune activation against invaders, and G-protein coupled receptors (GPCRs), whose interaction with their cognate ligands activates heterotrimeric G proteins and regulates specific downstream effectors, including immuno-stimulating molecules. Once TLRs are activated, they lead to the expression of hundreds of genes together and bridge the arm of innate and adaptive immune responses. We characterized the gene expression profile of Toll-like receptor 4 (TLR4) in RAW 264.7 cells when it bound with its ligand, 2-keto-3-deoxyoctonate (KDO), the active part of lipopolysaccharide. In addition, to determine the network communications among the TLR, Janus kinase (JAK)/signal transducer and activator of transcription (STAT), and GPCR, we tested RAW 264.7 cells with KDO, interferon-${\beta}$, or cAMP analog 8-Br. The ligands were also administered as a pair of double and triple combinations.

• Toxicological Research
• /
• 제25권4호
• /
• pp.159-173
• /
• 2009

Nuclear factor erythroid derived 2-related factor-2 (Nrf2) is a master transcription regulator of antioxidant and cytoprotective proteins that mediate cellular defense against oxidative and inflammatory stresses. Disruption of cellular stress response by Nrf2 deficiency causes enhanced susceptibility to infection and related inflammatory diseases as a consequence of exacerbated immune-mediated hypersensitivity and autoimmunity. The cellular defense capacity potentiated by Nrf2 activation appears to balance the population of $CD4^+$ and $CD8^+$ of lymph node cells for proper innate immune responses. Nrf2 can negatively regulate the activation of pro-inflammatory signaling molecules such as p38 MAPK, NF-${\kappa}B$, and AP-1. Nrf2 subsequently functions to inhibit the production of pro-inflammatory mediators including cytokines, chemokines, cell adhesion molecules, matrix metalloproteinases, COX-2 and iNOS. Although not clearly elucidated, the antioxidative function of genes targeted by Nrf2 may cooperatively regulate the innate immune response and also repress the expression of pro-inflammatory mediators.

• Clinical and Experimental Pediatrics
• /
• 제48권11호
• /
• pp.1153-1161
• /
• 2005

As known by other name(natural immunity), the innate immune system comprises all those mechanisms for dealing with infection that are constitutive or built in, changing little with age or with experience of infection. Though in some ways less sophisticated than adaptive immunity, innate immunity should not belittled, since it has evidently protected thousands of species of invertebrates sufficiently to survive for up to 2 billion years. In the innate immune system, molecules of both cellular and humoral types are involved, corresponding to the need to recognize and dispose of different types of pathogen, to promote inflammatory responses and to interact to the adaptive immune system. A major features of innate immunity are the presence of the normal gut flora, complements, macrophages, dendritic cells, natural killer cells and many cytokines that can block the establishment of infection. Both phagocytic cells and complement system have tremendous potential for damaging host cells, but fortunately they are normally only triggered by foreign materials, and usually most of their destructive effects are focussed on the surface of these or in the safe environment of the phagolysosome. This article addreses the comprehensive mechanisms of the major components of the innate immune system to prevent the infection.

• BMB Reports
• /
• 제41권2호
• /
• pp.93-101
• /
• 2008

The major cell wall components of bacteria are lipopolysaccharide, peptidoglycan, and teichoic acid. These molecules are known to trigger strong innate immune responses in the host. The molecular mechanisms by which the host recognizes the peptidoglycan of Gram-positive bacteria and amplifies this peptidoglycan recognition signals to mount an immune response remain largely unclear. Recent, elegant genetic and biochemical studies are revealing details of the molecular recognition mechanism and the signalling pathways triggered by bacterial peptidoglycan. Here we review recent progress in elucidating the molecular details of peptidoglycan recognition and its signalling pathways in insects. We also attempt to evaluate the importance of this issue for understanding innate immunity.

• IMMUNE NETWORK
• /
• 제10권6호
• /
• pp.181-187
• /
• 2010

Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.