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PubMedDate not supplied

Gene array technology to determine host responses to Salmonella.

Gene expression array technology is a powerful new tool that has already been used to expand our understanding of host-pathogen interactions. There has been a rapid increase in published reports describing use of this approach to profile host responses to pathogenic bacteria and viruses. The large number of array studies currently in progress coupled with increasing accessibility of this new technology promises a plethora of gene expression data on host response to infection in the near future. Recent insights into macrophage and epithelial cell responses to Salmonella infection garnered from array studies are outlined and used as a basis to discuss various future research directions using gene arrays that will advance the field of cellular microbiology. There is an exciting potential for the gene expression data generated in such studies to provide insights into host physiology, the pathophysiology of disease and novel therapeutics.

Animals↗

PubMed1996

Infectivity and host responses in Creutzfeldt-Jakob disease.

The relationship between viral titer and host responses was evaluated in Creutzfeldt-Jakob Disease (CJD). Rapid clearing of 97% of the virus from hamster brain occurred within 5 days, and residual virus was dispersed equally to both hemispheres. Exponential replication began only after a long eclipse phase of approximately 30 days, and by 100 days showed an > 3 log increase in titer. However, from 100 to 135 days, titers were restricted to plateau levels of approximately 10(8)/g. In comparison, previous studies show no appreciable eclipse phase and > or = 100-fold higher brain titers in hamster scrapie. Our calculations also revealed an effective doubling time (ti) of 7.6 days in CJD and a markedly different ti of approximately 3 days in scrapie. Thus different initiation and replication programs are encoded by each of these strains. The most pertinent host molecular responses included early astrocytic activity by 54 days, unaccompanied by morphological or behavioral changes. Changes in host PrP were minimal until 87 days when titers were already 2 x 10(7)/g. In the next 20 days 60% of brain PrP became resistant to limited proteolysis but total PrP did not increase. These fulminant PrP changes preceded viral arrest and subsequent spongiform degeneration. Because these and other data are not consistent with PrP itself being the infectious agent, we discuss a model in which progressive PrP and glial activation are part of a final host strategy to contain a virus that is innocuous at low titers. This strategy is flawed because PrP is an independent provocateur of self-destruction in the brain. However, in the periphery this strategy may eliminate rare infected cells.

Animals↗

PubMedDate not supplied

The involvement of class Ib molecules in the host response to infection with Salmonella and its relevance to autoimmunity.

Class I molecules with limited polymorphism have been implicated in the host response to infectious agents. Following infection with Salmonella typhimurium, mice develop a CD8+ CTL response that specifically recognizes bacteria infected cells. An immunodominant component of the CTL response recognizes a peptide epitope derived from the Salmonella GroEL molecule that is presented by the non-polymorphic MHC class Ib molecule Qa-1. T cells recognizing the bacterial peptide also cross-recognize a homologous peptide from the mammalian hsp60 molecule. Since Qa-1 has a functional equivalent in humans, this observation may be relevant not only to the host response involved in clearing infection but also in understanding the link between infection with Gram-negative pathogens and autoimmune disease.

Animals↗

PubMed1983

Immunoperoxidase localization of lymphocyte subsets in the host response to melanoma and nevi.

Using an avidin:biotin immunoperoxidase system with monoclonal antibodies to lymphocyte subsets, we have investigated the host response to malignant melanoma and melanocytic nevi in frozen sections. Eight primary melanomas, eight metastases, three dysplastic nevi, and two dermal nevi were studied with antibodies T11, T4, T8, and B1. Sections were read in a semiquantitative manner by two observers. Virtually all lymphocytes in these lesions were T-cells (T11 positive). In all primary melanomas, in the majority of metastases, and in all dysplastic nevi, both T4- and T8-positive cells were present. In two of eight metastases, tumor cells stained with T4, and in one case, melanoma cells stained with B1 antibody. The host response to melanoma involves primarily T-cells and includes both the helper:inducer (T4) and suppressor:cytotoxic (T8) subsets.

Horseradish Peroxidase↗

PubMed2006

Roles of macrophages and neutrophils in the early host response to Bacillus anthracis spores in a mouse model of infection.

The development of new approaches to combat anthrax requires that the pathogenesis and host response to Bacillus anthracis spores be better understood. We investigated the roles that macrophages and neutrophils play in the progression of infection by B. anthracis in a mouse model. Mice were treated with a macrophage depletion agent (liposome-encapsulated clodronate) or with a neutrophil depletion agent (cyclophosphamide or the rat anti-mouse granulocyte monoclonal antibody RB6-8C5), and the animals were then infected intraperitoneally or by aerosol challenge with fully virulent, ungerminated B. anthracis strain Ames spores. The macrophage-depleted mice were significantly more susceptible to the ensuing infection than the saline-pretreated mice, whereas the differences observed between the neutropenic mice and the saline-pretreated controls were generally not significant. We also found that augmenting peritoneal neutrophil populations before spore challenge did not increase resistance of the mice to infection. In addition, the bacterial load in macrophage-depleted mice was significantly greater and appeared significantly sooner than that observed with the saline-pretreated mice. However, the bacterial load in the neutropenic mice was comparable to that of the saline-pretreated mice. These data suggest that, in our model, neutrophils play a relatively minor role in the early host response to spores, whereas macrophages play a more dominant role in early host defenses against infection by B. anthracis spores.

Animals↗

PubMed1991

Host responses and neuroendocrinological changes in pyrexia in childhood.

Host responses and neuroendocrinological changes during pyrexia in childhood were studied. Serum IL-1 beta could not be detected in most subjects either during pyrexia or in afebrile periods. IL-1 beta was detected in two cases, increasing during pyrexia and decreasing during the afebrile period. Plasma ACTH increased during pyrexia, but this was not statistically significant. Serum cortisol during pyrexia increased to around twice the normal value, and many subjects showed a high level of arginine vasopressin. The subjects, who did not develop dehydration, showed a decrease in serum osmolality and serum sodium during the pyrexia period. Serum Fe and Zn decreased, but serum Cu increased during both periods. It could not be confirmed that IL-1 activates the hypothalamic-pituitary-adrenal axis during pyrexia. It is concluded that AVP is important in the control of fever and the maintenance of homeostasis of body fluid during pyrexia.

Acute Disease↗

PubMed2001

Analysis of host responses of guinea pigs during Helicobacter pylori infection.

Host responses of guinea pigs infected with Helicobacter pylori were investigated. Passaged H. pylori colonised the stomach for up to 13 weeks after infection, but after 1 month the number of bacteria fell sharply. Specific antibodies, predominantly of the IgG2 subtype, were present from week 3 onwards. Antibodies to urease A and flagella were abundant. Severe inflammation of the gastric mucosa and damage to the stomach epithelium was seen. Infiltrates of mononuclear cells and eosinophils were found near the parietal glands. As infection progressed, inflammation and tissue damage became more localised and more variable between individual animals. These parameters can be used as markers for colonisation of the stomach by H. pylori.

Animals↗

PubMed2004

Sepsis and the lung host response.

Sepsis is the leading cause of death in critically ill patients and is the most common risk factor for the development of acute lung injury in medical patients. Initially investigators hypothesized that an excessive proinflammatory response contributed to the pathogenesis of sepsis. However, this hypothesis overlooked the beneficial effects of proinflammatory mediators and the detrimental effects of an excessive anti-inflammatory response. This has led to a new hypothesis where sepsis is characterized by imbalances of the pro- and anti-inflammatory responses, with tissue injury the result of an excessive proinflammatory response and impaired pulmonary host defense the result of an excessive anti-inflammatory response. This article reviews clinical studies and animal models which show that sepsis results in an impaired lung host response to bacteria. Information in this article should provide the reader with an increased understanding of the pathogenesis of sepsis and the realization that new therapeutic strategies for sepsis need to take into account the need to balance pro- and anti-inflammatory responses to maintain pulmonary host defenses and prevent the development of acute lung injury.

Journal Article↗

PubMed2002

Neutrophil-mediated host response to Porphyromonas gingivalis.

Periodontal diseases are infections initiated by specific species of microorganisms and are among the most common human infections. The pathogenesis of periodontitis is mediated by interactions between host and microbial factors, complicated by genetic and environmental risk factors. Periodontal disease also represents a unique model in which to study the roles of bacterial and host-related factors, a model in which patients do not suffer from life-threatening disease. The aim of this paper is to focus on recent findings relating to neutrophil-mediated host response mechanisms in Porphyromonas gingivalis-induced periodontal disease. Virulence factors of Porphyromonas gingivalis such as the gingipains, fimbrillin peptides, capsule polysaccharides, lipopolysaccharides, haemagglutinating and haemolysing activities, toxic products of metabolism, outer membrane vesicles, and other enzymes have important roles in eliciting host responses in various ways. These factors significantly affect epithelial/endothelial cells, but their major effect is observed on the modulation of neutrophil response. Periodontitis represents an important model for neutrophil-mediated host tissue injury. In this model, neutrophils, primed or stimulated by the presence or persistence of infection, express an elevated and excessive response. This, in turn, leads to tissue destruction mediated by neutrophil activity. It is essential to understand the mechanisms underlying the interactions between the neutrophils and the microbial virulence factors to be able to develop rational, novel treatment strategies.

Adhesins, Bacterial↗

PubMed2006

The mammalian host response to borrelia infection.

Tick-borne relapsing fever (RF) and Lyme disease (LD) are spirochetal infections of humans caused by different Borrelia species in endemic areas throughout the world. Our laboratory is studying the response of mammalian hosts to borrelia infection in RF and LD. For this, we use mice and non-human primates infected with B. burgdorferi sensu stricto strain N40 (N40) and the Oz1 strain of Borrelia turicatae (Bt), agents of LD and RF in North America, respectively. Our results have revealed that outbred non-human primates are significantly less susceptible than outbred mice to persistent infection with N40. In contrast, the majority of mice inoculated with the RF agent B. turicatae clear the infection, with the notable exception of residual brain or blood infection in up to 25% of cases. Little if any tissue injury occurs in immunocompetent animals with either LD or RF. In contrast, impairment of specific antibody production results in significant tissue injury, most notably in the heart, in both LD and RF. The inflammatory infiltrate is rich in plasma cells, activated macrophages and T cells, and there is significant deposition of antibody and complement, including membrane attack complex, in inflamed tissues and spirochetes. Significant loss of cardiomyocytes with apoptosis and caspase activation was observed in the heart of immunosuppressed non-human primates infected with N40 and in B cell-deficient mice infected with B. turicatae. Unlike the heart, the brain of B cell-deficient mice infected with B. turicatae showed prominent microglial activation but no detectable tissue injury. Tissues from immunosuppressed non-human primates infected with N40 produce large amounts of immunoglobulin and the B cell chemokine CXCL13, both of which significantly correlate with the spirochetal load. We conclude that the main response of mammalian hosts in LD and RF is the production of specific antibody to clear the infection. Failure of this response leads to persistent infection, which can lead to tissue injury, most notably in the heart.

Animals↗

PubMed1999

Temporal expression of an H2-linked locus in host response to mouse malaria.

The action of host genes in response to malarial infection is complex. Two mouse loci, Char1, and Char2, have previously been shown to control peak parasitemia and host survival. Recent analysis of host response to mouse malaria has demonstrated that the action of several loci is time dependent. Char1 and Char2 act prior to peak parasitemia. Analysis of additional crosses revealed significant linkage to Chromosome 17 on the day following peak parasitemia. This H2-linked locus acts late in infection and is therefore crucial in clearing parasites from the circulation. The cloning of this gene will lead to a greater understanding of the host-parasite interaction, and the kinetics of host gene expression during an immune response.

Animals↗

PubMed1988

The effects of E series prostaglandins on blastogenic responses in vitro and graft vs. host responses in vivo.

In this study the ability of prostaglandin E1 (PGE1), Misoprostol (a stable analog of PGE1), and 16,16-dimethyl PGE2 (a stable analog of PGE2) to suppress immune responses in vitro and in vivo was determined. All of the compounds caused a titratable (10(-6) to 10(-9) M) suppression of Con A blastogenesis and the mixed lymphocyte response whereas there was only slight inhibition of the LPS response. When either 16,16-dimethyl PGE2 (30 ug/mouse) or Misoprostol (60 ug/mouse) was administered daily in vivo, there was a significant suppression of splenomegaly in F1 mice (C57Bl/6 x CBA) which had been injected with parental (C57Bl/6) spleen cells. We conclude that prostaglandins of the E series can function as immunosuppressive reagents both in vitro and in vivo. In the future they may serve to augment existing forms of immunosuppressive therapy.

Animals↗

PubMed2000

Antivector and antitransgene host responses in gene therapy.

Current viral gene therapy vectors effectively transfer genes in vivo at the price of eliciting innate and acquired host responses against the vector and/or transgene. Antigens present in the viral vector and the expression of the transgene both cause cellular and humoral immune responses dependent on the viral vector, the route of administration, and the genotype and infection history of the host. In general, adenoviral vectors cause strong immune responses, which result in only transient expression of the therapeutic gene. Adeno-associated virus and retrovirus vectors elicit weaker immune responses and can therefore result in long-term gene transfer and expression. Methods to avoid host responses, including modification of viral vector and immunosuppression of the host, can increase the longevity and efficiency of gene transfer.

Adjuvants, Immunologic↗

PubMedDate not supplied

Local cellular host response induced by Nocardia-delipidated cell mitogen in Lewis lung carcinoma-bearing mice.

Various Nocardial fractions have been shown to exert inhibitory effects against several experimental tumors, via a host response mechanism. With the aim of obtaining further information on the mechanism of action of these immunomodulators, we examined in the present study the local cellular host response induced by intratumoral administration of one of these fractions, the Nocardia-delipidated cell mitogen (NDCM), at the site of the tumor (Lewis lung carcinoma-3LL). The tumor itself was found to provoke a scanty cellular infiltration surrounding the tumor mass, mainly composed of lymphocytes. The site of the tumor in NDCM-treated mice was surrounded by a very thick rim of inflammatory cells, consisting of macrophages and lymphocytes. Although recognized decades ago, the existence of tumor infiltrating leukocytes still constitutes a puzzle. The composition and significance of these host cells, in both non-treated and treated tumors has not yet been elucidated. Since lymphocytes were also found around non-treated tumors and they apparently did not prevent tumor development, it is possible that macrophages play a more important role in the NDCM-elicited host defense against the Lewis lung carcinoma.

Animals↗

PubMed2003

IL-10 modulates host responses and lung damage induced by Pneumocystis carinii infection.

Host responses to Pneumocystis carinii infection mediate impairment of pulmonary function and contribute to the pathogenesis of pneumonia. IL-10 is known to inhibit inflammation and reduce the severity of pathology caused by a number of infectious organisms. In the present studies, IL-10-deficient (IL-10 knockout (KO)) mice were infected with P. carinii to determine whether the severity of pathogenesis and the efficiency of clearance of the organisms could be altered in the absence of IL-10. The clearance kinetics of P. carinii from IL-10 KO mice was significantly enhanced compared with that of wild-type (WT) mice. This corresponded to a more intense CD4(+) and CD8(+) T cell response as well as an earlier neutrophil response in the lungs of IL-10 KO mice. Furthermore, IL-12, IL-18, and IFN-gamma were found in the bronchoalveolar lavage fluids at earlier time points in IL-10 KO mice suggesting that alveolar macrophages were activated earlier than in WT mice. However, when CD4(+) cells were depleted from P. carinii-infected IL-10 KO mice, the ability to enhance clearance was lost. Furthermore, CD4-depleted IL-10 KO mice had significantly more lung injury than CD4-depleted WT mice even though the intensity of the inflammatory responses was similar. This was characterized by increased vascular leakage, decreased oxygenation, and decreased arterial pH. These data indicate that IL-10 down-regulates the immune response to P. carinii in WT mice; however, in the absence of CD4(+) T cells, IL-10 plays a critical role in controlling lung damage independent of modulating the inflammatory response.

Adjuvants, Immunologic↗

PubMed1984

Host responses in periodontal diseases.

Great progress has been made in our understanding of the pathogenesis of periodontal disease, the primary role of bacteria as etiologic agents, and the critical modifying role of host responses. It is useful to consider several stages in the pathogenesis of periodontal disease - (a) colonization, (b) invasion, (c) destruction, and (d) healing - and to place into perspective the various host responses as they may affect each of these four stages (Table 5). With respect to colonization, although very little direct evidence is available, it is reasonable to suggest that antibodies, either secretory or serum-derived, acting by virtue of their ability to block attachment, could inhibit colonization by immune reduction of adherence mechanisms. With respect to invasion of the tissue, it appears that phagocytes, particularly the neutrophils, are important, acting in concert with opsonic antibody and complement in ingesting and killing the periodontal microflora before or during the early invasive process. A major advance in our understanding of the pathogenesis of periodontal diseases is the realization that the virulence of periodontopathic bacteria relates to their leukaggressive properties, allowing them to evade neutrophil protective mechanisms. Invasion of the periodontal tissues by bacterial products may be inhibited by the complexing of these products with antibody with the formation of antigen-antibody complexes that are phagocytosed and digested, particularly by scavenger phagocytes such as the macrophage. With respect to the destructive phase of periodontal disease, it is clear that the direct effect of lymphocytes mediated either through direct cytotoxic activity, or through biologically-active destructive lymphokines (such as alpha-lymphotoxin and osteoclast activating factor), can lead to tissue destruction. Macrophages, through the production of monokines, collagenase, and reactive oxygen species, can also lead to tissue destruction. The direct effects of bacterial toxins or enzymes which can lead to tissue destruction can be inhibited by complexing with antitoxic or enzyme-neutralizing antibodies. With respect to healing and fibrosis, very little direct information is available; however, it is possible that the lymphocytes and macrophages affect fibrosis by the production of chemotactic factors for fibroblasts which would be expected to bring them to the area of periodontal inflammation and also by production of fibroblast-activating factors, which then cause the fibroblasts to proliferate and produce collagen which replaces lost collagen or results in fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aggressive Periodontitis↗

PubMed1981

Regulatory effect of H2-D region antigens in the graft-vs-host response: F1 hybrid resistance to alloreactive T cells.

The role of donor and host H2D alleles in the graft-vs-host response was evaluated by measurement of DNA synthetic response of donor lymph node cells in lethally irradiated hosts and by a mortality assay in sublethally irradiated F1 hosts. Comparison of the potency of graded doses of B10.A, B10.A(2R), and (B10.A X B10.A(2R))F1 cells in (B10 vs B10.A)F1 and other hosts expressing foreign KbIb revealed a deficient response of 10(6) B10.A(2R) cells, but only when the host was heterozygous d/b at H2-D. Studies with TI congenic donors failed to implicate T region antigens in this effect. These results are interpreted to suggest that under the conditions of these experiments there is F1 hybrid resistance to alloaggressive T lymphocytes that are homozygous in the Db region.

Animals↗

PubMed1989

Ethanol and soluble mediators of host response.

Lymphokines serve to modulate host inflammatory response by providing a communication link among cells involved in resistance to infection. In the alcoholic, this system may be impaired due to a combination of the direct effects of ethanol on immunocompetent cells and the soluble factors involved in cell-cell interactions. In this paper, we review the literature on this subject, describe an ethanol-related impairment of migration inhibitory factor activity in the rat, and present a possible mechanism for this alteration.

Alcoholism↗