PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “host response”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMedDate not supplied

Inflammation and the host response to injury: an overview of the multicenter study of the genomic and proteomic response to burn injury.

Inflammation and the Host Response to Injury is a prospective, multicenter, federally funded collaborative study of the genomic and proteomic basis for injury response. This study has brought together clinical specialists in burn injury with experts in genomics, proteomics, and bioinformatics to answer questions related to immunoinflammatory responses to injury. The purpose of this report is to describe the structure, organization, goals, and current progress of this Glue Grant project.

Burns↗
PubMed1999

Tissue transglutaminase is expressed as a host response to tumor invasion and inhibits tumor growth.

A stable extracellular matrix (ECM) constitutes an important part of host response mechanism against tumor growth and invasion. Tissue transglutaminase (TG), a calcium-dependent enzyme, can cross-link all major ECM proteins to form a stable ECM, because these cross-links are resistant to proteolytic and mechanical damage. TG can also enhance stability and strength of the ECM by its ability to facilitate the activation of transforming growth factor-beta. We hypothesized that TG ECM-promoting abilities form an important part of the host response mechanism against tumor growth. Increased expression of TG was observed in the ECM of the host tumor interface of subcutaneously implanted rat mammary adenocarcinoma R3230 Ac. TG expression was also detected in the endothelial cells and macrophages. We also detected the cross-link product at the host tumor interface and within the tumor tissue, showing that TG was active. Western blots showed TG was degraded into three fragments of 55-, 50-, and 20-kDa forms. When recombinant wild-type TG was applied to R3230 Ac implanted in rat dorsal skin flap window chamber, it caused significant growth delay at day 7 compared with recombinant inactive TG controls. Collagen was detected in increased amounts in TG treated tumors, suggesting augmentation of production and stability of the ECM. We conclude that TG forms a distinct part of host response system against and acts to inhibit tumor growth.

Adenocarcinoma↗
PubMed1991

Dependence among host response parameters used to diagnose urinary tract infection.

The host-response parameters fever, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) are activated in concert by cytokines such as interleukin-6 (IL-6). Il-6 is secreted in response to Escherichia coli infection of the urinary tract. This study tested the hypothesis that the level of fever, CRP, and ESR is coregulated in individual patients. Body temperature, CRP, ESR, pyuria, and renal concentrating capacity were analyzed in 692 children with first-time urinary tract infections. The association of the parameters was evaluated by correlation and multiple regression analysis. The body temperature, CRP, and ESR were significantly correlated (r = .54, .58, and .58; P less than .001), and variation in CRP and ESR explained approximately 40% of the variation in fever. In contrast, the renal concentrating capacity and pyruia were weakly or not at all correlated with the febrile response (r = -.22; P less than .001), and less than 10% of the variation in renal concentrating capacity was explained by the other parameters. The results suggest that fever, CRP, and ESR describe the same aspect of the host response to UTI.

Adolescent↗
PubMed2002

Host responses to Renibacterium salmoninarum and specific components of the pathogen reveal the mechanisms of immune suppression and activation.

During infection, Renibacterium salmoninarum survives within the pronephric macrophages of salmonid fish. Therefore, to study the initial phases of the interaction we infected macrophages with live bacteria and analysed the responses of host and pathogen. It was found that the expression of msa encoding the p57 antigen of R. salmoninarum, was constitutive, while the expression of hly and rsh, encoding haemolysins, and lysB and grp was reduced after infection. Macrophages showed a rapid inflammatory response in which the expression of interleukin-1beta (IL-1beta), major histocompatibility complex class II (MHC II), inducible cyclo-oxygenase (Cox-2), and inducible nitric oxide synthase (iNOS) was enhanced, but tumour necrosis factor-alpha (TNF-alpha) expression was greatly reduced initially and then increased. After 5 days, except for TNF-alpha and MHC II, expression returned to levels approaching those of uninfected macrophages. We propose that R. salmoninarum survives initial contact with macrophages by avoiding and/or interfering with TNF-alpha-dependent killing pathways. The effects of specific R. salmoninarum components were studied in vivo by injecting fish with DNA vaccine constructs expressing msa, hly, rsh, lysB, or grp. We found that msa reduced the expression of IL-1beta, Cox-2, and MHC II but stimulated TNF-alpha while hly, rsh and grp stimulated MHC II but down-regulated TNF-alpha. Constructs expressing hly or lysB stimulated iNOS expression and additionally, lysB stimulated TNF-alpha. The results show how p57 suppresses the host immune system and suggest that the immune mechanisms for the containment of R. salmoninarum infections rely on MHC II- and TNF-alpha-dependent pathways. Moreover, prolonged stimulation of TNF-alpha may contribute to the chronic inflammatory pathology of bacterial kidney disease.

Animals↗
PubMed2005

Surfactant protein A limits Pneumocystis murina infection in immunosuppressed C3H/HeN mice and modulates host response during infection.

The development of Pneumocystis murina pneumonia and host response were characterized over time and at different levels of infection in corticosteroid immunosuppressed surfactant protein A (SP-A) knockout and wild-type (WT) mice. Infection increased over time in both strains of mice; however, significantly more cyst forms were detected in the knockout mice at intermediate and late stages of infection. In mice with heavy infections, TNF-alpha and IFN-gamma protein concentrations were significantly higher in pulmonary lavage fluid from knockout mice. There was a significant positive correlation between TNF-alpha and IFN-gamma concentrations and the level of infection in knockout mice, but not in WT mice. No significant differences were detected in IL-1 levels between the two strains of mice at any of the time points or at any level of infection. At heavier infection levels, significantly more MIP-2 protein was detected in the lungs of knockout mice, but a significant positive correlation between MIP-2 concentrations and the infection level was detected in both groups of mice. At the intermediate stage of infection, a significantly higher percentage of neutrophils was detected in the lungs of knockout mice than in WT mice. There was no difference in SP-D levels between WT and KO mice with identical levels of infection. These data support a protective role for SP-A in host defense against Pneumocystis and suggest that the effects of SP-A on the host response vary based on the intensity of the infection.

Adrenal Cortex Hormones↗
PubMed2005

Host response to microbial challenge following resective/non-resective periodontal therapy.

BACKGROUND: The host response to microbial challenge depends on the recruitment of homing leucocytes and may be related to the experience to infectious insults over years. PURPOSE: The aim of this study was to investigate the soft tissue reactions to de novo plaque formation at sites treated with either open flap debridement or with the use of resective means during periodontal therapy. MATERIAL AND METHODS: Fifteen patients, who had been treated for periodontal disease (severe generalized chronic periodontitis), participated in the study. Surgical therapy was performed using either gingivectomy (GV) or open flap debridement (OFD) procedures in a split mouth design. After 6 months of healing (day 0), two gingival biopsies were obtained, one from the GV- and one from the OFD-treated sites. The experimental gingivitis model was applied and plaque accumulation was allowed for 3 weeks. New biopsies were obtained from the remaining quadrants on day 21 of plaque formation. The biopsies were snap frozen and prepared for immunohistochemical analysis. RESULTS: Following 3 weeks of plaque accumulation, the size of the lesion in OFD sites was more than twice as large than that in GV sites (0.42 versus 0.19 mm2). In the GV units, the lesion was characterized by almost similar proportions of T cells (CD3+, 6.0%) and B cells (CD19+, 6.6%), while the ICT in OFD sites was dominated by B cells (13.8%). During the 3-week period of plaque formation the increase in cell densities of T and B cells was three times larger in OFD than in GV sites. The proportion of ELAM-1 (CD62+ cells) decreased in GV (-0.4%) and increased in OFD (0.9%) sites. CONCLUSIONS: The host response that occurred in the gingival sites treated with OFD was more pronounced than the reaction that under similar experimental conditions took place in the regenerated gingiva at sites treated by resective means.

Adult↗
PubMed2004

Initiation of the host response against murine gammaherpesvirus infection in immunocompetent mice.

Murine gammaherpesvirus 68 (gammaHV-68) provides a useful model for understanding the initiation of the host response against the gammaherpesviruses. Its value as a model for such studies lies in large part with the inherent difficulties in investigating human responses against EBV and HHV-8 during the first few days following infection. While studies aimed at defining the initiation of gammaHV-68 infection are far from complete, an unexpected trend in this early host response has already emerged. Despite viral replication and the beginnings of viral latency at the site of infection during the first few days following infection, the early host response seems surprisingly inadequate. For example, the pro-inflammatory response is quite limited, and with the exception of the type I interferons, it is not at all clear what innate responses are necessary to provide protection from acute infection. This confusion results from the lack of any significant effect on acute viral replication in several strains of mice which have been made genetically deficient in the expression of particular pro-inflammatory molecules. It is likely that these unexpected results reflect the ability of gammaherpesviruses to carefully control the initial response so that they are efficacious pathogens even in immunocompetent hosts.

Animals↗
PubMed1996

Host response to initial and challenge infections, following treatment, of Gyrodactylus bullatarudis and G. turnbulli (Monogenea) on the guppy (Poecilia reticulata).

The host response of Poecilia reticulata Peters against two species of Gyrodactylus (G. bullatarudis Turnbull, 1956 and G. turnbulli Harris, 1986) was investigated by comparing the dynamics of infrapopulations arising from initial infections, challenge infections begun 1 day after formalin treatment of 3-day-old initial infections and challenge control infections. The primary host response of P. reticulata to Gyrodactylus was shown to be non-(Gyrodactylus)-species-specific. Observations of differences in host-site specificities of initial and challenge infection infrapopulations indicated that the host response is largely localised to areas of heavy infection. The exact nature of the response remains unknown.

Animals↗
PubMed1976

Is multiple sclerosis an age-dependent host response to measles?

Several lines of evidence support the possibility that multiple sclerosis (M.S.) may be an age-dependent host response to measles. In animals, measles evokes different responses depending upon age at inoculation. In man, measles is already known to produce at least two age-dependent responses: risk of subacute sclerosing panencephalitis is increased among those who have had measles before 2 years of age and risk of measles encephalitis increases with age, at least during adolescence. Studies of immigrant populations indicate that an event at or before adolescence but not infancy affects risk of M.S. In the tropics where M.S. is rare, measles tends to be acquired very early in life, usually before the age of 3, whereas in temperate areas, measles tends to be acquired later, after the age of 5. A retrospective study has shown that M.S. patients tend to have had measles later than controls. Mechanisms which might underlie an age-dependent host response to measles include maturation of an immune system (k.g., number of available B cells) or change in the metabolic state of a target cell (e.g., oligocytes which change from laying down myelin to maintaining it). If the hypothesis that M.S. is a host response to later measles infection is valid, then mass measles vaccination programmes should produce a decline in the rate of M.S., but the effect may not be discernible before 1980.

Adolescent↗
PubMed1999

Viral modulation of the host response via crmA/SPI-2 expression.

Viruses have evolved numerous strategies to modulate the host response to infection. Poxviruses cause acute infections and need to replicate quickly to promote efficient transmission. Consequently, it is not surprising to learn that poxviruses encode a large number of proteins designed to target various arms of the host inflammatory response. One of the earliest described and most well-studied viral modulatory proteins is crmA/SPI-2. While the biochemical targets and possible modes of action have been well characterized in vitro, the role that crmA/SPI-2 plays during natural infection is less clear. It may have effects in modulating host responses involving apoptosis and inflammation. It is important to further understand the precise mode of action of viral proteins, such as crmA/SPI-2, because this may lead to better therapeutic strategies to combat a range of inflammatory and autoimmune diseases.

Animals↗
PubMed1976

Host response to tumor-associated fetal antigens: kinetics and components.

Using a colony-inhibition bioassay that measures the contribution of the host response in transplantation immunity to tumor-associated fetal antigens (TAFA), I evaluated the occurrence of TAFA during different developmental stages of murine fetal liver cells. A maximum concentration of TAFA was present at approximately 15 days' gestation. A similar age-equivalence phase of gestation was also found in pig fetal liver. Host-response kinetics to TAFA were examined, and results indicated a similar pattern of activity for tumor- or fetal-immunized groups with a transient immune suppression in the middle of the study period. I detected specific antibodies generated by tumor and fetal cell immunization by a complement-dependent serum microcytotoxicity assay. The specificity of the reaction was evaluated further by absorption studies that demonstrated specific cross-reactive antibodies to fetal and tumor cell targets. Adoptive transplanted immunity to TAFA was indirectly evaluated by a modified Winn assay which indicated that a cellular immune mechanism was an important component of the host response to TAFA.

Animals↗
PubMed1997

Intramucosal acidosis and systemic host responses in abdominal aortic aneurysm surgery.

OBJECTIVES: To assess the specific host responses to systemic endotoxemia and tumor necrosis factor (TNF) activation after abdominal aortic aneurysm surgery by measuring antiendotoxin core antibodies (EndoCab) immunoglobulin (Ig)G and IgM, and soluble p55TNF receptor concentrations. The role of the gut in initiating these immune responses was evaluated by correlating the systemic markers to changes in the intramucosal pH of the sigmoid colon. DESIGN: Retrospective, reevaluation study. SETTING: Vascular unit of a university hospital. PATIENTS: Eleven patients who underwent abdominal aortic aneurysm repair surgery were selected from a larger patient cohort (n = 42) on the basis of their clinical outcome (four patients had fatal complications and seven patients had an uneventful recovery). INTERVENTIONS: After induction of anesthesia, intramucosal pH of the sigmoid colon was measured using tonometry. Blood samples were obtained from indwelling catheters or direct venipuncture preoperatively, during surgery, and daily until postoperative day 5. MEASUREMENTS AND MAIN RESULTS: Those patients who died developed intramucosal acidosis of the sigmoid colon intraoperatively. Significant consumption of both IgG and IgM EndoCab antibodies was found in all patients. By measuring the concentration of antibodies to a neutral antigen, i.e., tetanus toxoid, the consumption of IgG EndoCab antibody concentrations was shown to be a specific host response. In all patients, reciprocal changes in the serum concentrations of p55TNF receptor and interleukin (IL)-6 were observed. The percentage increase in p55TNF receptor and the concentration of IL-6 were significantly higher in the nonsurvivor group by 48 hrs. There were significant correlations between, intramucosal pH and EndoCab antibodies, intramucosal pH and p55 TNF receptor, and p55 TNF receptor and IL-6. CONCLUSIONS: The development of colonic ischemia is associated with a significant consumption of IgG EndoCab antibodies and a simultaneous increase in soluble p55TNF receptor. This study provides further support for the concept that gut-derived endotoxin and the generation of TNF may play a role in the pathogenesis of complications after abdominal aortic aneurysm surgery.

Acidosis↗
PubMed1979

Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia.

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.

Animals↗
PubMed2004

The development of early host response to Pseudomonas aeruginosa lung infection is critically dependent on myeloid differentiation factor 88 in mice.

Toll-like receptors (TLR) induce distinct patterns of host responses through myeloid differentiation factor 88 (MyD88)-dependent and/or -independent pathways, depending on the nature of the pathogen. Pseudomonas aeruginosa is a cause of serious lung infection in immunocompromised individuals and cystic fibrosis patients. The role of the TLR-MyD88 pathway in P. aeruginosa-induced lung infection in vivo was examined in this study. MyD88-/- mice demonstrated an impaired clearance of P. aeruginosa from the lung. Little or no neutrophil recruitment was observed in the airways of MyD88-/- mice following P. aeruginosa lung infection. This observation was associated with a reduced production of inflammatory mediators that affect neutrophil recruitment, including macrophage-inflammatory protein-2, tumor necrosis factor, and interleukin-1beta in the airways of MyD88-/- mice. Similarly, MyD88-/- mice showed inhibited NF-kappaB activation in the lung following P. aeruginosa infection. Interestingly, P. aeruginosa infection induced a 7.5-fold increase of TLR2 mRNA expression in the lungs of MyD88+/+ mice. Furthermore, host responses to P. aeruginosa lung infection in TLR2-/- and TLR4 mutant mice were partially inhibited compared with the responses of respective control mice. Taken together, our results indicate that the MyD88-dependent pathway is essential for the development of early host responses to P. aeruginosa infection, leading to the clearance of this bacterium, and that TLR2 and TLR4 are involved in this process.

Adaptor Proteins, Signal Transducing↗
PubMed1998

Host response to tissue engineered devices.

The two main components of a tissue engineered device are the transplanted cells and the biomaterial, creating a device for the restoration or modification of tissue or organ function. The implantation of polymer/cell constructs combines concepts of biomaterials and cell transplantation. The interconnections between the host responses to the biomaterial and transplanted cells determines the biocompatibility of the device. This review describes the inflammatory response to the biomaterial component and immune response towards transplanted cells. Emphasis is on how the presence of the transplanted cell construct affects the host response. The inflammatory response towards a biomaterial can impact the immune response towards transplanted cells and vice versa. Immune rejection is the most important host response towards the cellular component of tissue engineered devices containing allogeneic, xenogeneic or immunogenic ex vivo manipulated autologous cells. The immune mechanisms towards allografts and xenografts are outlined to provide a basis for the mechanistic hypotheses of the immune response towards encapsulated cells, with antigen shedding and the indirect pathway of antigen presentation predominating. A review of experimental evidence illustrates examples of the inflammatory response towards biodegradable polymer scaffold materials, examples of devices appropriately integrated as assessed morphologically with the host for various applications including bone, nerve, and skin regeneration, and of the immune response towards encapsulated allogeneic and xenogeneic cells.

Journal Article↗
PubMed1990

Principal lymphocyte subpopulation in local host response to human oesophageal cancer.

We investigated what subpopulations of tumour-infiltrating lymphocytes (TIL) play a key role in in vivo function and what determines the degree of local host response represented by lymphocyte infiltration in human oesophageal cancer. We examined the increased subpopulation of TIL in "good responders" (GR) (patients with intensively TIL infiltrated tumours) when compared with "poor responders" (PR) (patients with weakly TIL infiltrated tumours). The frequency of each subpopulation was determined by quantitative flow-cytometric measurement on TIL separated from fresh tumours. Of TIL in GR, the frequency of CD3+ cells increased significantly (P less than 0.05) but the frequencies of CD16+, Leu7-, and CD16+ Leu7- cells were low and did not increase significantly compared with those in PR. With respect to T-cell subsets of TIL in GR, the frequency of CD8+ cells was significantly higher than that in PR (P less than 0.01), and CD4+/CD8+ ratio was lower than that in PR (P less than 0.025). On two-colour analyses, most of CD8+ cells (cytotoxic/suppressor T-cells: Tc/s) did not co-express CD11b and the frequency of CD8+ CD11b- cells (cytotoxic T-cell: Tc) increased significantly compared with that in PR. Clinicopathological and phenotypic analysis of peripheral blood lymphocytes revealed that there are no major differences in general immunocompetence between GR and PR. These results suggest that Tc/s, especially Tc, might play a key role in local host response. They also suggest that not only the general immune status of the host but also the identification of class I major histocompatibility complex antigens by the host at the tumour site may strongly affect the degree of host response in oesophageal cancer.

Aged↗