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Results for “Immunity, Innate”

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PubMed2006

Pathogen recognition and signalling in the Drosophila innate immune response.

Genetic analysis of the innate immune response in Drosophila has provided important insights into the mechanism of microbial sensing and the subsequent host signalling events. The two major players following immune challenge are the Toll and Immune deficiency (IMD) pathways, which are essential for fruit flies to survive infection. These pathways are homologous to the mammalian Toll-like receptor and tumour necrosis factor pathways, respectively. Moreover, microbial pattern-recognition receptors upstream of Toll and IMD, such as the peptidoglycan recognition proteins, have been isolated and studied at the structural and functional level. In the present, we will review recent data pertaining to the genetic, genomic, RNAi and infection studies that have added new complexities to the system.

Animals↗

PubMed2000

The role of CpG motifs in innate immunity.

Pattern recognition receptors of the innate immune system are able to distinguish certain prokaryotic DNAs from vertebrate DNAs by detecting unmethylated CpG dinucleotides in particular base contexts ('CpG motifs'). Recent studies have begun to define the molecular mechanisms of actions of CpG motifs and have demonstrated their stimulatory effects on leukocytes from humans and vertebrates other than mice. Oligodeoxynucleotides containing CpG motifs are highly effective Th1-like vaccine adjuvants through multiple routes of immunization and show promise as immunotherapeutic agents for cancer and allergic diseases.

Adjuvants, Immunologic↗

PubMed2005

Innate immunity and angiogenesis.

Activation of an innate immune response is among the first lines of defense after tissue injury. Restoring blood flow to the site of injured tissue is often a necessary prerequisite for mounting an initial immune response to pathogens and for subsequent initiation of a successful repair of wounded tissue. The multiple links among pathogen recognition and suppression, increased angiogenesis, and tissue repair are the topics of this review, which examines of the roles of antimicrobial peptides, mammalian toll-like receptors (TLRs), inflammatory cytokines, and putative "danger" signals, among other signaling pathways, in triggering, sustaining, and then terminating an angiogenic response.

Adenosine↗

PubMed2006

Self-harm caused by an insect's innate immunity.

It has been a long-held assumption that the innate immune system of insects causes self-harm when used to combat an immune insult. We show empirically that this assumption is correct. Invertebrate innate immunity relies heavily on effector systems which, on activation, produce cytotoxins that kill pathogens. Reliance on these robust, fast-acting, generic killing mechanisms ensures a potent and rapid response to pathogen invasion, but has the potential disadvantage of causing self-damage. We show that the innate immune response against an immune insult produces measurable phenotypic and functional damage to self-tissue in the beetle Tenebrio molitor. This type of self-harm (autoreactivity) and the life-history implications that arise from it are important to understand evolutionary phenomena such as the dynamics between hosts and parasites as well as the nature of immune system costs.

Animals↗

PubMed2006

Toll-like receptors and corneal innate immunity.

The ocular surface is constantly exposed to a wide array of microorganisms. The ability of the cornea to recognize pathogens as foreign and eliminate them is critical to retain its transparency, hence preservation of sight. In the eye, as in other parts of the body, the early response against invading pathogens is provided by innate immunity. Corneal innate immune system uses a series of pattern recognition receptors to detect the presence of pathogens thus allowing for rapid host defense responses to invading microbes. A key component of such receptors is the "Toll-like receptors" (TLRs), which have come to occupy the center stage in innate immunity against invading pathogens. An increasing number of studies have shown that TLRs are expressed by a variety of tissues and cells of the eye and play an important role in ocular defense against microbial infection. Here in this review we summarize the current knowledge about TLR expression in human eye with main emphasis on the cornea, and discuss the future directions of the field.

Animals↗

PubMed2006

Neural regulation of innate immunity: a coordinated nonspecific host response to pathogens.

The central nervous system (CNS) regulates innate immune responses through hormonal and neuronal routes. The neuroendocrine stress response and the sympathetic and parasympathetic nervous systems generally inhibit innate immune responses at systemic and regional levels, whereas the peripheral nervous system tends to amplify local innate immune responses. These systems work together to first activate and amplify local inflammatory responses that contain or eliminate invading pathogens, and subsequently to terminate inflammation and restore host homeostasis. Here, I review these regulatory mechanisms and discuss the evidence indicating that the CNS can be considered as integral to acute-phase inflammatory responses to pathogens as the innate immune system.

Animals↗

PubMed2001

Innate immunity and autoimmunity: from self-protection to self-destruction.

Innate immune responses provide the body with its first line of defense against infections. Signals generated by a subset of lymphocytes, including natural killer (NK) cells and natural killer T (NKT) cells, during the early host response might have an additional role in determining the nature of downstream adaptive immune responses. Here, Fu-Dong Shi, Hans-Gustaf Ljunggren and Nora Sarvetnick discuss the role of cellular and soluble components of innate immunity in the development of autoimmune diseases. Some putative pathways leading from innate immunity to autoimmunity are proposed.

Animals↗

PubMed2003

Innate immunity to herpes simplex virus type 2.

Herpes simplex virus type 2 (HSV-2) is responsible for most cases of genital herpes and also can cause fatal disseminated disease in perinatally infected newborns. Sexually transmitted infections initiate in the skin or mucosa and quickly spread into peripheral nerves to establish latency. Innate immunity, the first line of defense during both primary and recurrent infection, is essential during this period of acute infection to limit initial viral replication and to facilitate an appropriate adaptive immune response. The innate immune response consists of a complex multilayered system of mechanical and secreted defenses, immediate chemokine and IFN responses, and rapidly recruited cellular defenses. HSV has devised equally elaborate strategies to evade or interfere with innate immunity. This review summarizes our current understanding of the innate immune responses to HSV-2 and the mechanisms by which HSV-2 can overcome these barriers. Newly emerging links between products of innate responses and the development of adaptive immune responses are also discussed.

Animals↗

PubMed2001

The importance of the innate immune system in controlling HIV infection and disease.

The innate immune system is the first line of defense against invading pathogens and is particularly important in warding off bacterial and viral infections presenting at the mucosal cell surface. From this primitive immune response, the more sophisticated adaptive immune system was derived. Despite nearly two decades of research directed at inducing adaptive immune responses to HIV, no successful immunological therapy or vaccine has been developed. On the basis of recent observations, it is suggested that instead emphasis should now be placed on the alternative arm of the immune system, the innate immune response. Novel approaches should be developed to elicit this rapidly responding immune activity in HIV infection.

Animals↗

PubMed2000

The role of scavenger receptors in the innate immune system.

Akey aspect of the innate immune system is the ability to discriminate between self and infectious nonself. This is achieved through pattern recognition receptors which directly recognise molecular epitopes expressed by microbes. Scavenger receptors (SRs) have been studied primarily due to their ability to bind and internalise modified lipoproteins, suggesting an important role in foam cell formation and the pathogenesis of atherosclerosis. However, the ability of some SRs to function as pattern recognition receptors through their binding of a wide variety of pathogens indicates a potential role in host defence. This review will detail our current understanding of the function of SRs in innate immunity, and in the initiation of aquired immune responses.

Animals↗

PubMed2005

Mucosal innate immune response to intragastric infection by Salmonella enterica serovar Choleraesuis.

The innate immune response is critical to enteric disease resistance and the induction of mucosal adaptive immunity. In mucosae of the small intestine, Peyer's patches play a central role in immune surveillance and sampling of bacteria by specialized M cells. The innate immune response to Salmonella enterica serovar Choleraesuis, an enteric pathogen of swine, involves IL-1beta and IL-8 mRNA induction but not that of IL-6 and TNFalpha, in contrast to Salmonella serovar Typhimurium infection of murine small intestine. We investigated in vivo responses to Salmonella and potential effects of animal variation since the gut environment is highly dynamic and constantly changing physiologically. Salmonella serovar Choleraesuis induced an early proinflammatory cytokine response at 6h after infection, which was characterized by a 4-fold increase in production of CXCL2 mRNA by jejunal Peyer's patches (JPP), and a 12-fold increase in IL-1beta and 4-fold increase in IL-8 (CXCL8) mRNAs by distal ileal Peyer's patches (IPP). Levels of IL-1beta and IL-8 mRNA were positively correlated with numbers of mucosal neutrophils in the distal IPP. Salmonella DNA was also detected in ileal tissues, including Peyer's patches, absorptive epithelium and mesenteric lymph nodes, in 33-83% of infected animals, compared to the jejunal tissues, which were positive in 0-33% of infected pigs. Notwithstanding substantial animal-to-animal variation, IL-1beta was increased in both proximal and distal IPP, IL-8 was increased in the distal IPP, and calprotectin was associated with both by cluster analysis. These data indicate that IL-1beta and IL-8 expression in the IPP plays a key role early in the interaction between Salmonella serovar Choleraesuis and the small intestine.

Animals↗

PubMed2000

Molecular mechanisms of innate immunity.

All species require a rapid, systemic reply to pathogens in their environment. This response is known as the innate immune response and is characterized by de novo synthesis of mediators that directly or indirectly through phagocytosis remove and kill the pathogen. Innate immune responses have been preserved throughout evolution and have been studied in detail in organisms from the fruit fly Drosophila melanogaster to humans. In my laboratory, studies performed during the past 25 yr have focused on defining the molecular basis of innate immune responses to microbial pathogens. Specifically, we have used bacterial endotoxin (lipopolysaccharide) as a model stimulus to define how the innate immune system recognizes products of microbial pathogens and initiates responses to remove and/or kill such organisms. Such studies also serve as models to understand more fully the mechanisms underlying a serious human disease known as septic shock. This article discusses septic shock and its relationship to innate immunity.

Animals↗

PubMed2006

[Humoral and cellular responses in innate immunity].

The immune system is divided into innate and adaptive immunity. Either immunity consists of humoral and cellular responses, and immunity is maximized when both responses coordinately function. Adaptive immunity has been intensively studied, while it was only recently that we gained some understanding of innate immunity. In particular, cellular responses in innate immunity have been poorly understood compared with humoral responses. In addition, the mechanisms and roles of innate immune responses could be distinct between the organisms that possess both innate and adaptive immunity and those possessing only innate immunity. On the other hand, invading pathogenic microbes employ various strategies to inhibit the host immune system for their survival. I here summarize what needs to be known to gain a deeper understanding of the innate immune response. The readers are suggested to refer to the accompanying articles for more detailed description.

Animals↗

PubMed2005

Novel collectin/C1q receptor mediates mast cell activation and innate immunity.

Mast cells play a critical role in innate immunity, allergy, and autoimmune diseases. The receptor/ligand interactions that mediate mast cell activation are poorly defined. The alpha2beta1 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin, and several viruses, has been implicated in normal developmental, inflammatory, and oncogenic processes. We recently reported that alpha2 integrin subunit-deficient mice exhibited markedly diminished neutrophil and IL-6 responses during Listeria monocytogenes- and zymosan-induced peritonitis. Peritoneal mast cells require alpha2beta1 integrin expression for activation in response to pathogens, yet the ligand and molecular mechanisms by which the alpha2beta1 integrin induces activation and cytokine secretion remain unknown. We now report that the alpha2beta1 integrin is a novel receptor for multiple collectins and the C1q complement protein. We demonstrate that the alpha2beta1 integrin provides a costimulatory function required for mast cell activation and cytokine secretion. This finding suggests that the alpha2beta1 integrin is not only important for innate immunity but may serve as a critical target for the regulation of autoimmune/allergic disorders.

Animals↗

PubMed2006

Cytokine modulation of the innate immune response in feline immunodeficiency virus-infected cats.

BACKGROUND: In vitro data suggest that innate immune function in human immunodeficiency virus type 1-infected patients is compromised; however, in vivo studies are lacking. Feline immunodeficiency virus (FIV) infection in cats provides an excellent model to explore innate immune function in vivo. The innate response against Listeria monocytogenes is well understood, making it a useful immune probe. METHODS: Recombinant L. monocytogenes carrying eukaryotic expression plasmids for feline tumor necrosis factor (TNF)- alpha , interleukin (IL)-10, interferon (IFN)- gamma , and IL-15 were created to determine whether specific cytokines would modulate innate immune function. L. monocytogenes was delivered subcutaneously, and local lymph nodes were evaluated for size, cell subpopulations, and L. monocytogenes burden. Two months later, memory responses were evaluated by IFN- gamma enzyme-linked immunospot assay. RESULTS: FIV-positive cats had significantly less lymph-node enlargement and a greater L. monocytogenes burden than FIV-negative control cats. TNF- alpha improved listericidal activity in FIV-negative control cats but not in FIV-positive cats, whereas IL-10 modestly reduced function in FIV-negative control cats. IFN- gamma improved memory responses but not clearance of L. monocytogenes. IL-15 improved innate function in FIV-positive cats and increased the percentage of natural killer cells. CONCLUSIONS: Lentivirus infection impairs innate immune function in vivo, and IL-15 can significantly restore function. We hypothesize that altered dendritic-cell function and increased regulatory T cell activity may underlie the innate immune defect in HIV infection.

Animals↗

PubMed2006

Innate immunity, assessed by plasma NO measurements, is not suppressed during the incubation fast in eiders.

Immunity is hypothesized to share limited resources with other physiological functions and may mediate life history trade-offs, for example between reproduction and survival. However, vertebrate immune defense is a complex system that consists of three components. To date, no study has assessed all of these components for the same animal model and within a given situation. Previous studies have determined that the acquired immunity of common eiders (Somateria mollissima) is suppressed during incubation. The present paper aims to assess the innate immune response in fasting eiders in relation to their initial body condition. Innate immunity was assessed by measuring plasma nitric oxide (NO) levels, prior to and after injection of lipopolysaccharides (LPS), a method which is easily applicable to many wild animals. Body condition index and corticosterone levels were subsequently determined as indicators of body condition and stress level prior to LPS injection. The innate immune response in eiders did not vary significantly throughout the incubation period. The innate immune response of eiders did not vary significantly in relation to their initial body condition but decreased significantly when corticosterone levels increased. However, NO levels after LPS injection were significantly and positively related to initial body condition, while there was a significant negative relationship with plasma corticosterone levels. Our study suggests that female eiders preserve an effective innate immune response during incubation and this response might be partially determined by the initial body condition.

Animals↗

PubMed2005

Carp (Cyprinus carpio L.) innate immune factors are present before hatching.

Expression of the innate immune factors, complement factor 3 (C3), alpha2-macroglobulin (alpha2M), serum amyloid A (SAA) and a complement factor 1 r/s--mannose binding lectin associated serine protease-like molecule (C1/MASP2), was determined with Real Time Quantitative-PCR in carp (Cyprinus carpio L.) ontogeny around hatching. Furthermore, the expression of C3 mRNA and the presence of C3 protein were studied in carp embryos and larvae using In Situ Hybridisation, Western Blotting and Immunohistochemistry. C3, alpha2M, SAA and C1/MASP2 mRNA were produced by embryos from 12 h post-fertilisation, which is relatively long before hatching (2 days post-fertilisation (dpf)), indicating either involvement of these factors in development itself or more probably a preparation of the immune system for the post-hatching period. In addition, maternal mRNA of the aforementioned innate immune factors and maternal C3- and immunoglobulin protein was present in unfertilised eggs. Furthermore, C3 mRNA production was situated in the yolk syncytial layer in embryos from 24 h post-fertilisation to 5 dpf, followed by the liver in larvae, providing a new sequence of C3 production in teleost development.

Animals↗

PubMed2006

Polymorphisms in innate immunity genes and risk of non-Hodgkin lymphoma.

Genetic variation in innate immunity may alter host-pathogen defence mechanisms and promote aberrant immune responses and non-Hodgkin lymphoma (NHL). To test this hypothesis, we investigated polymorphisms in innate immune genes in a pooled analysis of two population-based case-control studies of NHL from the San Francisco Bay Area (308 cases, 684 controls) and UK (596 cases, 758 controls). The caspase recruitment domain-containing protein 1007fs homozygote variant was positively associated with NHL risk (odds ratios (OR) = 3.1, 95% confidence intervals (CI) 1.1-8.8), whereas the toll-like receptor 4 1063A>G variant allele was inversely associated with diffuse large cell lymphoma (OR = 0.67, 95% CI 0.45-0.99). These results suggest that variation in innate immune genes may alter NHL susceptibility.

Case-Control Studies↗