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Results for “host response”

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PubMed2000

CXC chemokine receptor CXCR2 is essential for protective innate host response in murine Pseudomonas aeruginosa pneumonia.

Pulmonary infection due to Pseudomonas aeruginosa has emerged as a leading cause of mortality. A vigorous host response is required to effectively clear the organisms from the lungs. This host defense is dependent on the recruitment and activation of neutrophils and macrophages. A family of chemotactic cytokines (chemokines) has been shown to participate in this protective response. In this study, we assessed the role of the ELR(+) (glutamic acid-leucine-arginine motif positive) CXC chemokines and their CXC chemokine receptor (CXCR2) in lung antibacterial host defense. The intratracheal administration of Pseudomonas to mice resulted in the time-dependent influx of neutrophils to the lung, peaking at 12 to 24 h after inoculation. The influx of neutrophils was associated with a similar time-dependent expression of the ELR(+) CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolysaccharide-induced CXC chemokine (LIX). Selective neutralization of MIP-2 or KC resulted in modest changes in neutrophil influx but no change in bacterial clearance or survival. However, neutralization of CXCR2 resulted in a striking increase in mortality, which was associated with a marked decrease in neutrophil recruitment and bacterial clearance. Conversely, the site-specific transgenic expression of KC resulted in enhanced clearance of bacteria after Pseudomonas challenge. This study indicates that ELR(+) CXC chemokines are critical mediators of neutrophil-mediated host defense in Pseudomonas pneumonia.

Animals↗

PubMed2003

Kinome analysis of host response to mycobacterial infection: a novel technique in proteomics.

An array of mammalian phospho-specific antibodies was used to screen for a host response upon mycobacterial infection, reflected as changes in host protein phosphorylation. Changes in the phosphorylation state of 31 known signaling molecules were tracked after infection with live or heat killed Mycobacterium bovis BCG or after incubation with the mycobacterial cell wall component lipoarabinomannan (LAM). Mycobacterial infection triggers a signaling cascade leading to activation of stress-activated protein kinase and its subsequent downstream target, c-Jun. Mycobacteria were also shown to inhibit the activation of protein kinase C epsilon and to induce phosphorylation of proteins not yet known to be involved in mycobacterial infection, such as the cytoskeletal protein alpha-adducin, glycogen synthase kinase 3beta, and a receptor subunit involved in regulation of intracellular Ca(2+) levels. The mycobacterial cell wall component LAM has been identified as a trigger for some of these modulation events.

Antibody Specificity↗

PubMed2005

Polymorphism of host response genes: implications in the pathogenesis and treatment of acute renal failure.

Acute inflammatory disorders are the result of an interaction between genetic and environmental factors, and are often characterized by an imbalance between pro- and anti-inflammatory host immune responses. Over the past decade, polymorphisms of host response genes have been explored as genetic risk and prognostic markers in the course and severity of acute inflammatory disorders. Increasing evidence supports an important role for inflammatory mechanisms in the pathogenesis of acute renal failure (ARF) following both ischemic and nephrotoxic injury. The use of genetic epidemiology may become a useful tool to identify patients with an altered susceptibility to developing hospital-acquired ARF, and stratify those who may benefit from preventive therapies that modulate host immune responses in a favorable way. This review summarizes the existing experimental and clinical studies supporting the role of inflammation in ARF and critically appraises studies that have examined polymorphism of immune response genes as potential determinants of susceptibility to and severity of acute inflammatory disorders. Conclusions are drawn on the application of genetic epidemiology to the field of ARF and the rationale for further research on the role of genetic markers in ARF.

Acute Kidney Injury↗

PubMed1995

Comparison of splenectomy effects as an indication for host response to growth of primary and metastatic tumour cells in two murine tumour systems.

The tumour-host relation is of extreme complexity; moreover, it may change during tumour progression. Information regarding this relation may be of importance in appreciating the efficiency of immunotherapy. In the present study, the effect of splenectomy on tumour growth in two murine tumour progression models, the Lewis lung carcinoma and AKR lymphoma, was examined. The effect of spleen ablation on growth of cells derived from primary and metastatic tumour cells was tested. The data obtained showed a differential effect of splenectomy on the growth of primary versus metastatic tumour cells in the two tumour systems, indicating a differential host response induced by the two cell types and/or a differential tumour cell sensitivity to immune reactions. Surprisingly, the spleen appeared to have a defensive role against metastatic tumour cells and a growth enhancing influence on primary tumour cells. The instability of the tumour-host relation may have important implications for the chances of immunotherapy to serve as an efficient cancer treatment.

Animals↗

PubMed2006

Limited contribution of Toll-like receptor 2 and 4 to the host response to a fungal infectious pathogen, Cryptococcus neoformans.

The present study was designed to elucidate the role of Toll-like receptor (TLR) 2 and TLR4 in the host response to Cryptococcus neoformans. Both TLR2 knockout (KO) and TLR4KO mice produced interleukin-1beta (IL-1beta), IL-6, IL-12p40 and tumor necrosis factor-alpha (TNF-alpha) in sera and cleared this fungal pathogen from infected lungs at a comparable level to control littermate (LM) mice. Synthesis of these cytokines was not significantly different in the lungs of these KO mice and LM mice, although IL-1beta, IL-6 and IL-12p40 tended to be lower in TLR2KO, but not TLR4KO, mice than in controls. In addition, there was no significant reduction detected in the synthesis of IL-12 and TNF-alpha by bone marrow-derived dendritic cells from TLR2KO and TLR4KO mice upon stimulation with live yeast cells. Finally, HEK293 cells expressing either TLR2/dectin-1 or TLR4/MD2/CD14 did not respond to C. neoformans in the activation of nuclear factor kappa B (NFkappaB) detected by a luciferase assay. Our results suggest that TLR2 and TLR4 do not or only marginally contribute to the host and cellular response to this pathogen.

Animals↗

PubMed1988

Host responses to Borrelia burgdorferi in dogs and horses.

By using paired sera the IgM and IgG host responses were analyzed in dogs with ELISA and Western blot techniques. Antibodies in clinical seropositive dogs bound to 4-25 IgM and up to 40 or more IgG antigenic determinants. Early IgM response to the 41-kDa flagellin persisted for at least 9 months and involved as many as seven other peptides. IgG response expanded later in the disease and involved more immunogens than are currently recognized in late human disease. A percentage of asymptomatic dogs that later developed clinical symptoms were seropositive. Immunoblot studies suggested that B. burgdorferi is persistent in both asymptomatic and weakly reactive animals and if untreated could lead to disease expression. Clinical seropositive, asymptomatic seronegative, and experimentally infected horses were similarly studied. In experimentally inoculated animals IgG antibodies were initially bound to flagellin and later to the 34- and 31-kDa polypeptides, even though ELISA values were considered only slightly reactive.

Animals↗

PubMed1987

Natural killer cells in the host response to melanoma.

Using an immunoperoxidase technique, we have investigated natural killer (NK) cells in the host response to malignant melanomas and melanocytic nevi in frozen sections. Eight primary melanomas, 12 metastatic melanomas, and 31 dysplastic nevi were studied. NK cells were identified phenotypically using an antibody, B73.1, against an Fc receptor present only on NK cells and neutrophils. Rare NK cells were identified in three of 31 dysplastic nevi and in one of eight melanomas. In contrast, significant numbers of NK cells were identified in ten of 12 metastases.

Humans↗

PubMed1988

Biocompatibility--the interaction of biomaterials and host response.

Future developments for better biocompatibility of dental implants are possible and are discussed here. On each level of local host response, which is subdivided into four phases, improvements of knowledge in basic mechanisms concerning the interaction of biomaterial and host are necessary. For the development of new biomaterials, the limits for load with foreign ions and particles acting on cellular and extracellular matrix should be determined. An example is given for ZrO2-containing glass ceramics. Biochemistry of soft and hard tissue bonding to biomaterials should be investigated. Biomechanical properties of implants could be adapted to individual needs of patients. New composite materials are candidates for the design of long-term functioning implants.

Animals↗

PubMed2004

Immunization with the C-Domain of alpha -Toxin prevents lethal infection, localizes tissue injury, and promotes host response to challenge with Clostridium perfringens.

Clostridium perfringens gas gangrene is characterized by rapid tissue destruction, impaired host response, and, often, death. Phospholipase C (alpha -toxin) is the virulence factor most responsible for these pathologies. The present study investigated the efficacy of active immunization with the C-terminal domain of alpha -toxin (Cpa247-370) in a murine model of gas gangrene. Primary end points of the study were survival, progression of infection, and tissue perfusion. Secondary end points, which were based on findings of histologic evaluation of tissues, included the extent of tissue destruction and microvascular thrombosis, as well as the magnitude of the tissue inflammatory response. Survival among C-domain-immunized animals was significantly greater than that among sham-immunized control animals. Furthermore, immunization with the C-domain localized the infection and prevented ischemia of the feet. Histopathologic findings demonstrated limited muscle necrosis, reduced microvascular thrombosis, and enhanced granulocytic influx in C-domain-immunized mice. We conclude that immunization with the C-domain of phospholipase C is a viable strategy for the prevention of morbidity and mortality associated with C. perfringens gas gangrene.

Animals↗

PubMed1998

Effect of immune T cells derived from mucosal or systemic tissue on host responses to Porphyromonas gingivalis.

The purpose of this study was to compare the effects of immune T cells derived from mucosal and systemic tissues on specific humoral responses to the periodontal pathogen Porphyromonas gingivalis and to determine the effect these responses have on periodontal bone loss in an experimental rat model. T cells were derived from either the spleen or Peyer's patches of conventional Fischer rats given live P. gingivalis by the oral route and were adoptively transferred into groups of nude Fischer rats. A group of nude rats to which no T cells were transferred served as control. Within 24 h of the adoptive cell transfer, animals from all groups were orally challenged with live P. gingivalis. Serum and salivary responses were seen in rats given immune T cells, whereas a low, variable serum IgM and no serum IgG or salivary IgA response was detected in the control nude rats, indicating that the major host responses to P. gingivalis whole-cell antigens were T-cell dependent. Rats given immune Peyer's patch-derived T cells exhibited a different serum IgG and salivary IgA immune response pattern than animals given immune splenic T cells. A higher serum IgG, especially IgG2b, antibody response and less horizontal bone loss was seen in rats given splenic than Peyer's patch-derived T cells. Although some differences were seen in the levels of salivary IgA early in the study in the two experimental groups, the levels of IgA were comparable by the termination of the experimental period. Furthermore, no difference was seen in the amount of vertical bone support in these two groups, which was greater than in the controls. These results suggest a role for serum IgG and salivary IgA in periodontal disease protection. The presence of high serum IgG2b antibody activity suggest the involvement of Th1-like cells in the response, whereas salivary IgA antibodies indicates the participation of Th2-like cells. These results suggest that the balance between Th1 and Th2-like cells within the systemic and mucosal compartments and the humoral immune responses to P. gingivalis they mediate are important in determining whether the responses induced are protective against experimental bone loss after oral challenge with the periodontal pathogen P. gingivalis.

Alveolar Bone Loss↗

PubMed2001

Host responses to Plasmodium yoelii hepatic stages: a paradigm in host-parasite interaction.

The liver stage of malaria, caused by the genus Plasmodium, is clinically silent, but immunologically significant. Ample evidence exists for an effective CD8(+) T cell response to this stage as well as the involvement of gammadeltaT cells and NK1.1(int) cells in immunized animal models. In contrast, there is little information concerning responses in a naive host. Here we report that several host gene expressions in the liver, spleen, and kidney of BALB/c mice are altered during the liver stage of Plasmodium yoelii infection. Really interesting new gene 3 (Ring3), semaphorin subclass 4 member G, glutamylcysteine synthetase, and p45 NF erythroid 2 were all up-regulated 24 h after infection with P. yoelii. Semaphorin subclass 4 member G expression was elevated in the kidney, whereas Ring3 was elevated in both spleen and kidney. The expression of TNF-alpha (TNF-alpha and IFN-gamma) were down-regulated in all three tissues tested except in infected spleen where IFN-gamma was elevated. P. yoelii-related host gene changes were compared with those in Toxoplasma gondii-infected livers. Ring3 expression increased 5-fold over control values, whereas expression of the other transcripts remained unchanged. TNF-alpha and IFN-gamma expressions were increased in the Toxoplasma-infected livers. The uniform increase of Ring3 expression in both Plasmodium- and Toxoplasma-infected livers suggests an innate immune response against parasitic infections, whereas the other gene expression changes are consistent with Plasmodium parasite-specific responses. Taken together, these changes suggest the immune responses to P. yoelii infection are both parasite and organ specific.

Animals↗

PubMed1988

A role for elevated plasma corticosterone in modulation of host response during infection with Trichinella pseudospiralis.

Suppression of host inflammatory response in mice infected with Trichinella pseudospiralis was associated with host plasma corticosterone levels significantly higher than those seen in uninfected mice or in mice infected with T. spiralis. Increases in the population of mitochondria and depletion of lipid droplets in cells of the zona fasciculata were seen in the adrenals of mice infected with T. pseudospiralis. Elevations in enteritis, myositis and myocarditis accompanied 100% mortality in adrenalectomized mice infected with T. pseudospiralis, while lower levels of inflammation and no mortality were observed in sham operated or intact animals infected with this parasite. The severe myositis normally accompanying infection with T. spiralis was suppressed by concurrent infection with 1000 or 2000 T. pseudospiralis to levels equivalent to those seen in animals receiving 0.15 and 0.41 mg cortisone acetate/25 g mouse/day, respectively.

Adrenal Glands↗

PubMed1994

Pathogenesis and host response in Pneumocystis carinii pneumonia.

Pneumocystis carinii (PC) pneumonia is recognized as the leading cause of opportunistic pulmonary infections in immunocompromised hosts during the past decade. Although much remains unknown about pathogenesis and host response in PC, recent years, studies of PC have provided us with an increasing base of knowledge about this organism and its relationship to the host. These studies have led to a better understanding of mechanisms of PC attachment and injury to host cells. New information about the interaction of PC with pulmonary surfactant provides insight about the pathophysiology of PC pneumonia. The interplay of the organism, host inflammatory cells, release of cytokines, generation of toxic metabolites, and involvement of both cellular and humoral immunity is complex, but understanding the pathogenesis of PC pneumonia is necessary in order to develop new therapies for this disorder.

Animals↗

PubMed1993

Vitamin A deficiency impairs some aspects of the host response to influenza A virus infection in BALB/c mice.

We examined the impact of vitamin A deficiency on the host response to an acute, viral infection of the respiratory tract by infecting BALB/c mice with a mouse-adapted strain of influenza A virus. Several indicators of the severity of infection were examined, including the rate of virus clearance from the lungs, the extent of inflammatory lesions, and percentage of survival. None of these was affected by vitamin A deficiency. Following the acute phase of infection, however, the regeneration of normal, respiratory epithelium was impaired and adenomatoid, metaplastic lesions developed within inflammatory foci in the lungs of deficient animals. The antibody response to infection was also characterized: the influenza A-specific immunoglobulin A (IgA) response in the respiratory tract was markedly decreased by vitamin A deficiency, but tracheal and lung lavage IgG titers were not affected. The serum IgM and IgG responses, and the serum hemagglutination-inhibition response, were also diminished by vitamin A deficiency. Decreased mucosal IgA titers and impaired regeneration of normal respiratory epithelium could impair recovery from a primary infection and increase susceptibility to opportunistic secondary infections.

Animals↗

PubMed1993

The role of the host response in periodontal disease progression: implications for future treatment strategies.

In this paper, we review the relevant aspects of host responses in periodontal diseases as we understand them today. Discussion will focus on neutrophil function, lymphocytes and the immune response, macrophage function, cytokines and complement, fibroblasts and growth factors, and regeneration. Recent literature and concepts will be presented with an emphasis on future directions and application to treatment regimens.

Forecasting↗

PubMed2004

Tissue adhesiveness and host response of in situ photopolymerizable interpenetrating networks containing methylprednisolone acetate.

Interpenetrating networks (IPNs) of varying formulations were investigated as candidates for an in situ photopolymerizable drug delivery matrix containing poly(ethylene glycol) diacrylate and gelatin. The anti-inflammatory agent methylprednisolone acetate was loaded into the IPN. Bond strength between the IPN and tissue (i.e., muscle, dermis, skin) was determined by a modified American Society for Testing and Materials peel test at constant peel rate. The IPNs provided adhesion values of up to 5.7N, which were three- to fivefold lower than that of the commercial tissue bioadhesive. The subcutaneous cage implant system was utilized to assess material host response and drug efficacy in vivo. IPN formulations elicited a more intense acute inflammatory response than the empty cage controls. Methylprednisolone acetate loaded within the IPNs lowered the level of inflammatory response to levels that were comparable to the empty cage baseline controls. In conclusion, a methodology was developed to quantify the tissue adhesiveness of an in situ photopolymerized IPN matrix containing anti-inflammatory agents. The efficacy of drug-loaded IPN in affecting the host inflammatory response was demonstrated in vivo.

Biocompatible Materials↗

PubMed2002

Respiratory syncytial virus--viral biology and the host response.

Respiratory syncytial virus (RSV) is the most important cause of respiratory tract infection in infants. We have an incomplete understanding of the reasons why some infants are more severely affected by RSV than others. There is no effective antiviral treatment for the infection. Advances in our understanding of the biology of RSV, particularly in relation to the attachment protein G and the fusion protein F, have revealed potential targets for new antiviral therapies and vaccine development. In response to RSV infection an intense inflammatory response is triggered, mediated initially by the infected airway epithelial cells. Cell mediated responses are important in controlling the extent of infection and in viral clearance. Humoral responses are important in protection. There is early evidence that genetic variation of the host response can influence the outcome of RSV-induced bronchiolitis.

Epithelial Cells↗

PubMedDate not supplied

Analysis of host response to hepatectomy by simultaneous measurement of cytokines in the portal vein, caval vein and radial artery.

We analysed the host response to hepatectomy by simultaneous measurement of various cytokines and their antagonists in the portal vein, caval vein and radial artery in 10 patients with hepatocellular carcinoma. Concentrations of tumour necrosis factor-alpha (TNF), interleukin (IL) 1 beta, IL-2, IL-6, IL-10, soluble TNF receptor type I (sTNF-R), soluble IL-2 receptor (sIL-2R), IL-1 receptor antagonist (IL-1ra), soluble CD14 (sCD14) and endotoxin were determined just before and 1 h after hepatectomy. The values of IL-6, sTNF-R and IL-1ra were significantly increased after hepatectomy at each sampling site. In contrast, the levels of sIL-2R and sCD14 after hepatectomy were significantly decreased, and the levels of IL-1 beta, IL-2 and IL-10 were below the detection limits. Differences in cytokine concentrations between sampling sites revealed that the surgical stress of hepatectomy induced significant IL-1ra production in the liver and sTNF-R and IL-6 production in the lungs. These results suggest that hepatic resection is followed by the production of cytokine antagonists, such as IL-1ra, sTNF-R and IL-6, which could represent an important regulatory mechanism against surgical stress.

Aged↗