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At least 415 records · Page 23Linked to original sources
PubMed2006

Age- and breed-dependent adapted immune responsiveness of poultry to intratracheal-administered, pathogen-associated molecular patterns.

Immune modulation of poultry by airborne pathogen-associated molecular patterns (PAMP) was studied. White and Brown layer chicks were exposed intratracheally during 5 consecutive days at 7 wk of age with Escherichia coli-derived lipopolysaccharide (LPS), Saccharomyces cerevisiae-derived 1,3 beta-glucan (BGL), a combination of both, or PBS as a control. Six weeks later, birds received similar or crossover PAMP treatments. Body weight (gain), feed conversion, (primary and secondary) specific antibody responses to model antigens, and natural antibody levels were measured. In general, BGL enhanced but LPS exposure decreased primary immune responses at 7 wk of age, whereas both PAMP-enhanced secondary immune responses but decreased primary immune responses at 13 wk of age. Body weight gain and feed conversion at both ages were negatively affected by LPS, especially in White birds, but not by BGL. Pathogen-associated molecular patterns exposure at 7 wk of age also affected Ab responses at 13 wk of age. Birds exposed to a combination of LPS + BGL at 7 wk of age had significantly lower secondary total and IgG Ab responses at 13 wk of age. Birds from both breeds showed enhanced BW gain after exposure to LPS at 13 wk of age, when initially challenged at 7 wk of age with LPS, BGL, or a combined challenge with both. Pathogen-associated molecular patterns exposure at 7 wk of age affected humoral immunity and BW gain at 13 wk of age in a positive (BGL) or negative (LPS) fashion. Repeated exposure to PAMP did not affect Ab responses, but crossover exposure to PAMP in general enhanced Ab responses. Body weight gain was positively affected by repeated exposure but not by crossover exposure, suggesting adaptation of the birds to early PAMP exposure. Our findings suggest that sensitivity of poultry for immune modulation by airborne PAMP differs between ages, is breed-dependent, and is not irreversible of nature. In addition, our data suggest different adaptation to hygienic conditions, both with respect to immune reactivity and BW gain.

Aging↗
PubMed2006

Adenovirus infection triggers a rapid, MyD88-regulated transcriptome response critical to acute-phase and adaptive immune responses in vivo.

Nearly 50 years ago, the discovery of interferon prompted the notion that host cells innately respond to viral invasion. Since that time, technological advances have allowed this response to be extensively characterized and dissected in vitro. However, these advances have only recently been applied to highly complex, in vivo biological systems. To this end, we exploited high-titer adenovirus (Ad) vectors to globally investigate the innate immune response to nonenveloped viral infection in vivo. Our results indicated a potent cellular transcriptome response shortly after infection, with global assessments revealing significant dysregulation in approximately 15% of the measured transcripts derived from Ad vector-transduced tissue. Bioinformatics-based transcriptome analysis revealed a complex innate response to Ad infection, with induction of proinflammatory responses (and suppression of metabolism and mitochondrial genes) akin to those observed when mice are challenged with lipopolysaccharide. Despite this commonality, there were many unique aspects of the Ad-dependent transcriptome response, including the upregulation of several RNA regulatory mechanisms and apoptosis-related pathways, accompanied by the suppression of lysosomal and endocytic genes. Our results also implicated the Toll-like receptors (TLRs) in these responses, prompting specific investigations into this pathway. By using MyD88KO mice, our results confirmed that Ad-induced dysregulation of five functionally related gene clusters are significantly dependent on this TLR adaptor gene. MyD88 deficiency also resulted in significantly diminished, although not abolished, adaptive and acute-phase immune responses to Ad, confirming the transcriptome data, as well as specifically identifying MyD88 as a significant Ad immunity amplifier and regulator in vivo.

Adenoviridae↗
PubMed2001

Role of interleukin-13 in innate and adaptive immunity.

Initially thought to be functionally redundant with IL-4 as a predominant anti-inflammatory factor secreted during type-2 T-cell responses, IL-13 possesses a number of additional properties that distinguish it from IL-4 in addition to having both anti-inflammatory and immune activating properties. This review centers primarily on the role of IL-13 in the regulation of cellular functions of innate immunity and acquired immunity against certain microbial pathogens. First, we discuss IL-13's regulation of innate cell targets and its impact on inflammation, antigen uptake and antigen presentation. Second, we focus on IL-13's involvement in acquired immunity to infectious helminths and protozoa. The role of this cytokine in immune responses is still being determined but evidence to date suggests this molecule has been conserved as an important regulatory factor involved in both early innate and late adaptive responses.

Adaptation, Physiological↗
PubMed2005

Genomic mining of new genes and pathways in innate and adaptive immunity.

Plant disease resistant (R) genes constitute a large family that mediates host response to bacteria, viruses and fungi. Large mammalian proteins containing a nucleotide binding domain (NBD) and C-terminal leucine-rich repeats (LRRs) are similar in structure to the TLR/NBD/LRR subfamily of R proteins and have been suggested as a link between innate and acquired immunity. Because of our long-term interest in one of these, the class II transactivator (CIITA), and recent reports linking mutations in two new NBD/LRR proteins (Nod2/CARD 15 and CIAS 1/cryopyrin) to various autoimmune and inflammatory disorders, we have performed a comprehensive search of the human genome and found a multigene family which we termed the CATERPILLAR (CARD, Transcription Enhancer, R[purine]-binding, Pyrin, Lots of Leucine Regions)family. The N-termini of these genes are varied although the majority have a pyrin domain and few have a CARD domain. The genomic organization of these genes demonstrates a high degree of conservation with the NBD encoded as a single large exon and the LRRs encoded in two basic arrangements. Detailed analysis and new functional data regarding a number of the CATERPILLAR proteins will be described, including CIITA, cryopyrin and Monarch 1.

Adaptation, Physiological↗
PubMed2001

The art of the probable: system control in the adaptive immune system.

The immune system provides very effective host defense against infectious agents. Although many details are known about the cells and molecules involved, a broader "systems engineering" view of this complex system is just beginning to emerge. Here the argument is put forward that stochastic events, potent amplification mechanisms, feedback controls, and heterogeneity arising from spatially dispersed cell interactions give rise to many of the gross properties of the immune system. A better appreciation of these underlying features will not only add to our basic understanding of how immunity develops or goes awry, but also illuminate new directions for manipulating the system in prophylactic and therapeutic settings.

Adaptation, Physiological↗
PubMed2006

Immunopathogenesis: role of innate and adaptive immune responses.

Hepatitis B virus (HBV) infection in immunocompetent adults usually results in a self-limited, transient liver disease and viral clearance, with only a small percentage (5 to 10%) developing chronic hepatitis associated with viral persistence. In contrast, when neonates are infected, more than 90% become persistently infected, suffering differing degrees of chronic liver disease. Activation of immunity plays a central role in host-virus interactions, greatly influencing viral replication and the clinical outcome of infection. Although all of the specific mechanisms and consequences of this interaction have not been elucidated, the purpose of this article is to describe the basic arms of the immune system as they interact with the HBV and describe the present state of knowledge in this area. These arms may be divided broadly into innate and specific immune responses, and they have different roles and responses in acute and chronic infection.

Adaptation, Biological↗
PubMed2003

Shigellosis: innate mechanisms of inflammatory destruction of the intestinal epithelium, adaptive immune response, and vaccine development.

Acute infectious colitis remains a major pediatric issue of worldwide impact because it still represents a significant public health burden among the larger group of diarrheal diseases with the highest mortality rate. It is also a relevant model of inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis. Among cases of acute colitis of infectious origin, shigellosis is certainly the one that has benefited the most from a significant research effort. Shigella, the causative agent, is a Gram-negative bacterium that has the capacity to invade, disrupt, and cause inflammatory destruction of the intestinal epithelial barrier. The molecular and cellular bases of this invasive phenotype essentially encompass crossing of the epithelial lining, apoptotic killing of macrophages, entry into epithelial cells, and escape into the cytoplasm, followed by cell-to-cell spread. Intracellular colonization is likely to protect the micro-organisms from killing by humoral and cellular effectors of the innate immune response. Concurrently, the capacity of Shigella to reprogram invaded epithelial cells to produce proinflammatory mediators plays a major role in the strong inflammatory profile of the disease. This profile is likely to impact on the nature and quality of the adaptive response, which is dominated by humoral protection at the mucosal level.

Adaptation, Physiological↗
PubMed2003

Adaptive immunity in mice lacking the beta(2)-adrenergic receptor.

The beta-2-adrenergic receptor (beta(2)AR) is expressed by most lymphocyte populations and binds the sympathetic neurotransmitter norepinephrine (NE). Stimulation of the beta(2)AR is reported to be the primary mechanism by which signals from the sympathetic nervous system influence both cell-mediated and humoral immunity. We report here that body/organ weights, lymphoid organ cell number/phenotype/histology, the contact sensitivity response, and the amount, avidity, and isotype of antibody resulting from a T cell-dependent antibody response in beta(2)AR deficient mice (beta(2)AR-/- mice) were all similar to measures made in beta(2)AR+/+ mice. Other members of the adrenergic receptor family did not appear to compensate for the absence in beta(2)AR expression. In contrast, beta(2)AR-/- B cells cultured in vitro were unable to respond to NE in a manner similar to beta(2)AR+/+ B cells. Thus, mice in which expression of the beta(2)AR gene is defective from early development to adulthood may no longer require that NE stimulate the beta(2)AR to maintain immune homeostasis, and this may be due to a non-adrenergic mechanism that provides compensation in vivo.

Adaptation, Physiological↗
PubMed2000

Heat shock proteins: the fountainhead of innate and adaptive immune responses.

The ability of heat shock proteins to (1) chaperone peptides, including antigenic peptides; (2) interact with antigen-presenting cells through a receptor; (3) stimulate antigen-presenting cells to secrete inflammatory cytokines; and (4) mediate maturation of dendritic cells, makes them a unique starting point for generation of immune responses. These properties also permit the use of heat shock proteins for development of a new generation of prophylactic and therapeutic vaccines against cancers and infectious diseases.

Adaptation, Physiological↗
PubMed2001

Lack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected with Helicobacter pylori.

To study the role of T cell responses in Helicobacter pylori gastritis, C57BL/6 wild-type and interferon regulatory factor-1-deficient (IRF-1(-/-)) mice were infected with the mouse-adapted H. pylori Sydney strain. Mice lacking the transcription factor IRF-1 are defective in Th1 development and are therefore biased to mount a Th2-type response. After 4 months of infection, C57BL/6 mice developed severe gastritis and atrophy and mounted a Th1-type response towards H. pylori. The Th1 response was abrogated in IRF-1(-/-) mice. This defective Th1 response was associated with the total lack of gastritis and atrophy in IRF-1(-/-) mice despite severe colonization with H. pylori. In addition, IRF-1(-/-) mice did also not develop a Th2 reaction, since they failed to generate H. pylori-specific antibodies and to produce IL-4 in response to H. pylori antigens in vitro. Thus, the transcription factor IRF-1 is necessary for the development of gastritis and atrophy in H. pylori-infected wild-type mice, suggesting a role of Th1 cells in the pathogenesis of H. pylori-associated diseases.

Animals↗
PubMed2005

B-1a and B-1b cells exhibit distinct developmental requirements and have unique functional roles in innate and adaptive immunity to S. pneumoniae.

B-1a and B-1b lymphocytes were found to exhibit specialized roles in providing immunity to Streptococcus pneumoniae and differ dramatically in their developmental requirements. Transgenic mice overexpressing CD19 (hCD19Tg) generated B-1a cells and natural antibodies that provided protection during infection, while CD19-deficient (CD19(-/-)) mice lacked B-1a cells, lacked natural antibodies, and were more susceptible to infection. By contrast, pneumococcal polysaccharide (PPS) immunization protected CD19(-/-) mice during lethal challenge, whereas hCD19Tg mice remained unprotected. This resulted from differences in the B-1b subset: the key population found to produce protective PPS-specific antibody in both wild-type and CD19(-/-) mice. Thus, CD19(-/-) mice generated B-1b cells and protective adaptive PPS-specific antibody responses, whereas hCD19Tg mice lacked B-1b cells and adaptive PPS-specific antibody responses. This reciprocal contribution of B-1a and B-1b subsets to innate and acquired immunity reveals an unexpected division of labor within the B-1 compartment that is normally balanced by their coordinated development.

Animals↗
PubMed2005

How do adaptive immune systems control pathogens while avoiding autoimmunity?

Immune systems face a daunting control challenge. On the one hand, they need to minimize damage from pathogens, without wasting energy and resources, but on the other must avoid initiating or perpetuating autoimmune responses. Finally, because pathogens interfere with immune function, immune systems must be robust against sabotage. We describe here how these challenges are met by two immune systems, the intracellular RNA interference system and the vertebrate CD8 T-cell response. We extrapolate from these two systems to propose principles for strategically robust control.

Adaptation, Physiological↗
PubMedDate not supplied

Energetic and nutritional regulation of the adaptive immune response and trade-offs in ecological immunology.

Ecological Immunology views immunocompetence as a costly process involving trade-off decisions among competing nutrient demands by different life-history traits. This review examines immunocompetence fitness costs in light of recent work on the role the energetic and nutritional status of the host plays in the regulation of the adaptive T-helper lymphocyte response. Three phenotypically distinct T-lymphocyte populations have been identified: the Th1 response, important in protecting against intracellular infections; the Th2 response, important in protecting against noninvasive infections such as helminthes; and the Th3 or Treg population, which downregulates polarized Th1 or Th2 responses. A strong Th1 response is protective against intracellular infections, while a Th2 response is protective against noninvasive infections. Adequate zinc and energy intake leads to a dominant Th1 response and a downregulated Th2 response, while deficiencies of either of these results in activation of the Th2 response and downregulation of the Th1 response. In contrast, adequate vitamin A intake leads to an activated Th2 response and downregulation of the Th1 response, while vitamin A deficiency reverses these patterns. These differential immune regulatory effects of energy and nutrient intake will have distinct effects on specific stages of the natural history of different pathogen infections where the protective roles of the Th1-Th2 responses are distinct. Accordingly, fitness costs of immunocompetence are more complex than currently proposed since trade-offs in energetic and nutritional resources produce cross-regulatory effects on immune system subcomponents.

Animals↗
PubMed2006

T cell- and B cell-independent adaptive immunity mediated by natural killer cells.

It is commonly believed that only T lymphocytes and B lymphocytes expressing recombination-dependent antigen-specific receptors mediate contact hypersensitivity responses to haptens. Here we found that mice devoid of T cells and B cells demonstrated substantial contact hypersensitivity responses to 2,4-dinitrofluorobenzene and oxazolone. Those responses were adaptive in nature, as they persisted for at least 4 weeks and were elicited only by haptens to which mice were previously sensitized. No contact hypersensitivity was induced in mice lacking all lymphocytes, including natural killer cells. Contact hypersensitivity responses were acquired by such mice after adoptive transfer of natural killer cells from sensitized donors. Transferable hapten-specific memory resided in a Ly49C-I(+) natural killer subpopulation localized specifically in donor livers. These observations indicate that natural killer cells can mediate long-lived, antigen-specific adaptive recall responses independent of B cells and T cells.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Some general pathological and biological categories: health, disease, homeostasis, sanogenesis, adaptation, immunity. New approaches and definitions].

The article outlines new approaches to definition of categories of homeostasis, health, disease and sanogenesis in terms of relationships between human body and environment. According to these definitions, health is the state of the body with unaffected functional dynamic homeostasis securing optimal functioning for productive relations with the environment; disease is the state of the body with affected functional dynamic homeostasis and its inability to accomplish functions for productive relations with the environment. These formulations reflect biological and social aspects of the above categories.

Adaptation, Physiological↗
PubMed1999

Innate and adaptive immune responses co-operate to protect cattle against Theileria annulata.

For many years it was assumed that Theileria annulata resembled T. parva, parasitizing lymphocytes and causing lymphoproliferative disease, with the two species being controlled by similar protective immune responses. Patricia Preston et al. here review the evidence that has led to a different view of T. annulata. It is now thought that the schizonts of T. annulata inhabit macrophages and B cells, and that tropical theileriosis is not a lymphoproliferative disease. Both innate and adaptive responses contribute to recovery from infection and resistance to challenge and cytokines produced by infected and uninfected cells influence the outcome of infection. Partial protection has been stimulated recently by defined recombinant antigens; efficacy depended upon the delivery system.

Animals↗