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Results for “Immunity, Innate”

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At least 451 records · Page 25Linked to original sources
PubMed2006

Energy restriction with different protein quantities and source: implications for innate immunity.

OBJECTIVE: Physical age, energy restriction (ER), and weight loss have been reported to suppress indices of innate immunity, which may increase the risk of illness. To evaluate these interactions, we recruited older, postmenopausal women (50 to 80 years) to fill one of the following 9-week ER (1250 kcal/d) groups: beef [n = 14; reported intakes 46% carbohydrate (CHO):24% protein (PRO):30% fat], chicken (n = 15; 51% CHO:25% PRO:24% fat), or CHO (n = 14; 59% CHO:17% PRO:24% fat), or a non-intervention control (n = 11). RESEARCH METHODS AND PROCEDURES: Fasting blood was collected before and after ER to determine leukocyte phenotype, neutrophil oxidative burst capacity, natural killer cell activity, stimulated interleukin-2 and interferon-gamma production, and blood zinc and iron concentrations. RESULTS: No significant effects of ER (8.6% weight loss) or PRO quantity and source were found for the majority of indices of innate immunity. Small but significant (p < 0.05) declines in interleukin-2 production were found in the chicken and CHO groups only; however, the clinical significance of this finding is not known. DISCUSSION: In the present study, 9 weeks of moderate ER did not suppress immunity in postmenopausal women. Also, contrary to our hypothesis, differential zinc and iron intakes did not significantly alter immunity.

Aged↗
PubMed2005

NK cells in innate immunity.

NK cells have an important role in innate immune responses, particularly in anti-viral immunity. Recent studies have revealed a molecular basis for NK cell recognition of virus-infected cells, implicating the activating KIR and Ly49 receptors and NKG2D in this process. Additionally, mutual cooperation between NK cells and dendritic cells suggests that these innate cells can shape the nature of an adaptive immune response. These findings, as well as advances in understanding NK cell development and homeostasis, indicate that NK cell biology is more sophisticated than previously appreciated.

Animals↗
PubMed2001

Regulation of antibacterial and antifungal innate immunity in fruitflies and humans.

Insects have been very successful in adapting to their environment, and the ability of the insect immune system to detect and elicit the appropriate response against various invading pathogens has helped in this success. Unlike the vertebrate immune system, which consists of both innate and adaptive components, insect immunity probably consists entirely of an innate immune response, as no evidence of an adaptive response has been found. The innate immune response is described as either a reaction against "lack of self," or the interaction between host germline-encoded receptors and molecules unique to a particular class of invading organisms. Once the invading organism is recognized, the host immune response can be activated via signaling pathways that lead to the appropriate reaction. This review endeavors to put forth how through genetic, molecular, and biochemical studies of the fruit fly Drosophila melanogaster, as well as other insects, it is now understood that aspects of the insect and vertebrate innate immune system are very similar.

Animals↗
PubMed2006

Early local and systemic innate immune responses in the teleost gilthead seabream after intraperitoneal injection of whole yeast cells.

The early cellular innate immune responses of the teleost gilthead seabream (Sparus aurata L.) against whole yeast cells were studied. Fish received a single intraperitoneal (i.p.) injection of Saccharomyces cerevisiae and leukocyte mobilization, degranulation, peroxidase content, respiratory burst, phagocytic and cytotoxic activities were assayed in both head-kidney leukocytes (HKLs) and peritoneal exudate leukocytes (PELs). The total number of PELs significantly increased from 4 h post-injection until the end of the experiment (3 days). Interestingly, flow cytometric analysis revealed variations in the proportion of cell-types in the PE. Thus, PE acidophilic granulocytes increased to a significant extent 4 h post-injection and were restored thereafter. Moreover, PE monocyte-macrophages started to increase from 24 h, the enhancement being statistically significant after 48 and 72 h. Degranulation was greater in PELs throughout the assay. The peroxidase content of the leukocytes was affected differently in HKLs and PELs. The respiratory burst activity was not affected in HKLs but significantly increased in PELs from 4 to 48 h post-injection with yeast cells. On the other hand, HKL phagocytosis had decreased 72 h post-injection with yeast cells while it increased after 4 and 24 h post-injection in the PELs. Conversely, the cytotoxic activity was significantly enhanced in HKLs from 24 to 72 h post-injection but slightly decreased in PELs. Finally, our data demonstrate that seabream injected with the yeast Saccharomyces cerevisiae show leukocyte mobilization and cellular innate immune response activation at the site of invasion and also in the head-kidney. The implications of the leukocyte-types and the immune responses observed, as well as analogies with other particulated antigens, will be discussed as possible models for investigating the effect of potential pathogens.

Animals↗
PubMed2006

Cutting edge: T cell Ig mucin-3 reduces inflammatory heart disease by increasing CTLA-4 during innate immunity.

Autoimmune diseases can be reduced or even prevented if proinflammatory immune responses are appropriately down-regulated. Receptors (such as CTLA-4), cytokines (such as TGF-beta), and specialized cells (such as CD4+CD25+ T regulatory cells) work together to keep immune responses in check. T cell Ig mucin (Tim) family proteins are key regulators of inflammation, providing an inhibitory signal that dampens proinflammatory responses and thereby reducing autoimmune and allergic responses. We show in this study that reducing Tim-3 signaling during the innate immune response to viral infection in BALB/c mice reduces CD80 costimulatory molecule expression on mast cells and macrophages and reduces innate CTLA-4 levels in CD4+ T cells, resulting in decreased T regulatory cell populations and increased inflammatory heart disease. These results indicate that regulation of inflammation in the heart begins during innate immunity and that Tim-3 signaling on cells of the innate immune system critically influences regulation of the adaptive immune response.

Acute Disease↗
PubMed2005

Lipopolysaccharide and lipoteichoic acid induce different innate immune responses in bovine mammary epithelial cells.

The objective of the present study was to characterize the innate immune responses induced by in vitro stimulation of bovine primary mammary epithelial cells (bMEC) using gram-negative lipopolysaccharide (LPS) and gram-positive lipoteichoic acid (LTA) bacterial cell wall components. Quantitative real-time PCR (qRT-PCR) was employed to examine the mRNA expression of a panel of 22 cytokines, chemokines, beta-defensins and components of the Toll-Like Receptor signaling pathway. Stimulation of bMEC with LPS for 24h elicited a marked increase in mRNA expression for IL-1beta, IL-8, TNFalpha, CXCL6 and beta-defensin while members of the Toll-Like Receptor pathway, although present, were largely unaffected. Surprisingly, stimulation of these cells with LTA for 24 h did not significantly alter the expression of these genes. A time course of the expression of IL-1beta, IL-8, TNFalpha, CXCL6 and beta-defensin was subsequently performed. The mRNA levels of all genes increased rapidly after stimulation for 2-4 h with both LPS and LTA but only the former treatment resulted in sustained responses. In contrast, the increased gene expression for LTA stimulated cells returned to resting levels after 8-16 h with the exception of beta-defensin, which remained up-regulated. The limited and unsustained cytokine response to LTA may explain why mastitis caused by gram-positive bacteria has greater potential for chronic intra-mammary infection than gram-negative infection. It was concluded that bovine mammary epithelial cells have a strong but differential capacity to mount innate immune responses to bacterial cell wall components.

Animals↗
PubMed2005

Dual role of alpha-defensin-1 in anti-HIV-1 innate immunity.

Alpha-defensins are abundant antimicrobial peptides in polymorphonuclear leukocytes and play an important role in innate immunity. We have previously shown that alpha-defensin-1 can inhibit HIV-1 replication following viral entry. Here we examined the molecular mechanism(s) of alpha-defensin-1-mediated HIV-1 inhibition. Alpha-defensin-1 had a direct effect on HIV-1 virions at a low MOI in the absence of serum. The direct effect on HIV-1 virions was abolished by the presence of serum or an increase in virus particles. Studying the kinetics of the HIV life cycle revealed that alpha-defensin-1 inhibited steps following reverse transcription and integration. Analysis of PKC phosphorylation in primary CD4+ T cells in response to alpha-defensin-1 indicated that alpha-defensin-1 inhibited PKC activity. Pretreatment of infected CD4+ T cells with a PKC activator, bryostatin 1, partially reversed alpha-defensin-1-mediated HIV inhibition. Like alpha-defensin-1, the PKC isoform-selective inhibitor Go6976 blocked HIV-1 infection in a dose-dependent manner. Furthermore, kinetic studies and analysis of HIV-1 products indicated that alpha-defensin-1 and Go6976 blocked HIV-1 infection at similar stages in its life cycle, including nuclear import and transcription. Taken together, our studies demonstrate that, in the absence of serum, alpha-defensin-1 may act directly on the virus, but, in the presence of serum, its effects are on the cell, where it inhibits HIV-1 replication. At least 1 of the cellular effects associated with HIV inhibition is interference with PKC signaling in primary CD4+ T cells. Studying the complex function of alpha-defensin-1 in innate immunity against HIV has implications for prevention as well as therapeutics.

Antiviral Agents↗
PubMed2002

Toll-like receptor 4 mediates innate immune responses to Haemophilus influenzae infection in mouse lung.

Toll-like receptors (TLRs) have been implicated in the regulation of host responses to microbial Ags. This study characterizes the role of TLR4 in the innate immune response to intrapulmonary administration of Haemophilus influenzae in the mouse. Two different strains of mice efficiently cleared aerosolized H. influenzae concurrent with a brisk elaboration of IL-1beta, IL-6, TNF-alpha, macrophage-inflammatory protein (MIP)-1alpha, and MIP-2 in bronchoalveolar lavage and a corresponding mobilization of intrapulmonary neutrophils. Congenic strains of mice deficient in TLR4 demonstrated a substantial delay in clearance of H. influenzae with diminished IL-1beta, IL-6, TNF-alpha, MIP-1alpha, and MIP-2 in bronchoalveolar lavage and a notable absence of intrapulmonary neutrophils. In TLR4-expressing animals, but not TLR4-deficient animals, TNF-alpha and MIP-1alpha expression was up-regulated in epithelial cells of the conducting airway in response to H. influenzae which was preceded by an apparent activation of the NF-kappaB pathway in these cells based on the findings of decreased overall IkappaB and an increase in its phosphorylated form. This study demonstrates a critical role of TLR4 in mediating an effective innate immune response to H. influenzae in the lung. This suggests that the airway epithelia might contribute to sensing of H. influenzae infection and signaling the innate immune response.

Administration, Inhalation↗
PubMed2005

Comparison of polychlorinated biphenyl (PCB) induced effects on innate immune functions in harbour and grey seals.

Polychlorinated biphenyls (PCBs) are known to have detrimental effects on the innate immune system of several mammalian species. Top predators such as marine mammals may be badly affected as PCBs can bioaccumulate in their blubber to high concentrations and previous studies have suggested that harbour seals may be particularly vulnerable to the immunotoxic effects of such contaminants. To investigate the effects of PCBs on innate immune functions in phocid seals, blood samples were collected from harbour and grey seals and exposed in vitro to a mixture of Aroclors. Separated mononuclear (PBMCs) and polymorphonuclear (PMNCs) leukocytes from each species were incubated with Aroclors (at 3 and 30 ngml(-1)) for 3 and 24 h incubation periods, after which phagocytosis, respiratory burst and cytotoxic activity were measured. The phagocytic activity of harbour seal PMNCs was decreased at both incubation times and at both Aroclor concentrations tested, but there was no effect on the grey seals. Similarly, the respiratory burst activity of harbour seals was decreased at both incubation times, but only at the higher concentration used. There were no differences in the cytotoxic activity of the PBMCs with respect to incubation times or concentrations in either species. However, differences were observed in the level of cytotoxic activity against YAC-1 target cells, with the grey seal PBMCs showing higher levels of activity. The observed differences in phagocytosis, respiratory burst and cytotoxic activity of the leukocytes following incubation with PCBs may have implications for the previously recorded differences in disease susceptibility between grey and harbour seals.

Animals↗
PubMed2006

Specific recognition of apoptotic cells reveals a ubiquitous and unconventional innate immunity.

The purpose of physiological cell death is the noninflammatory clearance of cells that have become inappropriate or nonfunctional. Consistent with this function, the recognition of apoptotic cells by professional phagocytes, including macrophages and dendritic cells, triggers a set of potent anti-inflammatory responses manifest on multiple levels. The immediate-early inhibition of proinflammatory cytokine gene transcription in the phagocyte is a proximate consequence of recognition of the apoptotic corpse, independent of subsequent engulfment and soluble factor involvement. Here, we show that recognition is linked to a characteristic signature of responses, including MAPK signaling events and the ablation of proinflammatory transcription and cytokine secretion. Specific recognition and response occurs without regard to the origin (species, tissue type, or suicidal stimulus) of the apoptotic cell and does not involve Toll-like receptor signaling. These features mark this as an innate immunity fundamentally distinct from the discrimination of "self" versus "other" considered to be the hallmark of conventional immunity. This profound unconventional innate immune discrimination of effete from live cells is as ubiquitous as apoptotic cell death itself, manifest by professional and nonprofessional phagocytes and nonphagocytic cell types alike. Innate apoptotic immunity provides an intrinsic anti-inflammatory circuit that attenuates proinflammatory responses dynamically and may act systemically as a powerful physiological regulator of immunity.

Animals↗
PubMed2006

Activation of innate immunity by prostate specific antigen (PSA).

BACKGROUND: Prostate specific antigen (PSA) is a serine protease secreted by the prostatic epithelium. The only known function of the protein is to cleave seminogelin. We wished to determine if PSA activated peripheral blood mononuclear cells (PBMC). METHODS: PBMC and selected sub-populations were cultured with purified PSA. Secretion of IFNgamma was measured by cytokine capture flow cytometry and enzyme-linked immunosorbent assay. RESULTS: We observed secretion of IFNgamma and a proliferative response in PBMC cultured with PSA. We found that NK cells were the source of the IFNgamma but NK cells were not directly stimulated by PSA. Rather, a soluble factor secreted primarily by CD14 monocytes in response to PSA stimulated NK cells to secrete IFNgamma. DISCUSSION: PSA induces a pro-inflammatory response that results in the secretion of INFgamma by NK cells. The presence of large amounts of PSA could contribute to the common finding of inflammatory infiltrates in the prostate.

Cell Proliferation↗
PubMed2006

Hepcidin--a peptide hormone at the interface of innate immunity and iron metabolism.

Hepcidin is a cationic amphipathic peptide made in the liver, released into plasma and excreted in urine. Hepcidin is the homeostatic regulator of intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores, but it is also markedly induced during infections and inflammation. Under the influence of hepcidin, macrophages, hepatocytes, and enterocytes retain iron that would otherwise be released into plasma. Hepcidin acts by inhibiting the efflux of iron through ferroportin, the sole known iron exporter that is expressed in the small intestine, and in hepatocytes and macrophages. As befits an iron-regulatory hormone, hepcidin synthesis is increased by iron loading, and decreased by anemia and hypoxia. Hepcidin is also rapidly induced by cytokines, including IL-6. The resulting decrease in plasma iron levels eventually limits iron availability to erythropoiesis and contributes to the anemia associated with infection and inflammation. The decrease in extracellular iron concentrations due to hepcidin probably limits iron availability to invading microorganisms, thus contributing to host defense.

Amino Acid Sequence↗