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Results for “host response”

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PubMed1970

Synergy among lymphoid cells mediating the graft-versus-host response. I. Synergy in graft-versus-host reactions produced by cells from NZB-Bl mice.

The ability of spleen cells from young (3 month) and old (1 yr) NZB mice to induce GVH reactions in newborn C57BL/6N mice was compared quantitatively using the Simonsen spleen assay. Young NZB cells were five times more reactive than cells from older mice. The minimum number of cells producing detectable reactions was 2 x 10(6) for the young and 10 x 10(6) for the old. Young and old cells combined and injected together produced GVH reactions quantitatively similar to those obtained with inocula composed of young cells alone. Mixtures of two cell populations producing no detectable reactions when injected separately into different recipients (1 x 10(6) young cells and 4 x 10(6) old cells) produced reactions approximately equal to those obtained with 5 x 10(6) young cells. As few as 0.25 x 10(6) young cells were sufficient to effect a reaction when combined with 4.75 x 10(6) old unreactive cells. Viability of both cell populations was essential for GVH reactivity. This evidence of synergy in GVH reactions indicates that old NZB spleen cells can be rendered immunologically more reactive in the presence of a normally reactive population.

Age Factors↗

PubMed2002

Comparison of in vitro-cultured and wild-type Perkinsus marinus. II. Dosing methods and host response.

Endoparasites must breach host barriers to establish infection and then must survive host internal defenses to cause disease. Such barriers may frustrate attempts to experimentally transmit parasites by 'natural' methods. In addition, the host's condition may affect a study's outcome. The experiments reported here examined the effect of dosing method and host metabolic condition on measures of virulence for the oyster parasite Perkinsus marinus. Oysters, Crassostrea virginica, were challenged with wild-type and cultured forms of P. marinus via feeding, shell-cavity injection, gut intubation and adductor-muscle injection. For both parasite types, adductor-muscle injections produced the heaviest infections followed by shell-cavity injection, gut intubation, and feeding. There was no difference in parasite burdens between oysters fed cultured cells by acute vs chronic dosing, and parasite loads stabilized over time, suggesting a dynamic equilibrium between invasion and elimination. P. marinus distribution among tissues of challenged oysters indicated that parasites invaded the mantle and gill, as well as the gut, which has been considered the primary portal of entry. Frequency distributions of P. marinus in oysters challenged with 3 different culture phases indicated an aggregated distribution among hosts and suggested that stationary-phase parasites were easiest for the oyster to control or eliminate and log-phase parasites were the most difficult. Host metabolic condition also affected experimental outcomes, as indicated by increased infection levels in oysters undergoing spawning and/or exposed to low oxygen stress.

Animals↗

PubMed2006

PDT-associated host response and its role in the therapy outcome.

BACKGROUND AND OBJECTIVES: The outcome of the treatment of solid tumors by photodynamic therapy (PDT) is critically dependent on the contribution from the host. This host response is provoked by the rapidly induced massive tumor tissue injury delivered by PDT that is experienced as a local trauma threatening the integrity and homeostasis at the affected site. STUDY DESIGN/MATERIALS AND METHODS: Mouse tumor models were extensively employed in pre-clinical studies investigating various aspects of host-tumor interaction following PDT, but important input was also derived from clinical data. RESULTS: The recognition of this PDT-inflicted insult by innate immune sensors detecting danger signals from the distressed/altered tumor tissue, triggers host-protecting responses dominantly manifested as acute inflammation that are elicited and orchestrated by the innate immune system. To secure the affected PDT-targeted site, the inflammatory reaction attacks tumor vasculature and then neutralizes the focal source of danger signals by eliminating the injured tumor cells. CONCLUSION: The provoked highly intensified phagocytosis of dead tumor cells occurring in the context of a vigorous innate immune reaction emerges as a key factor responsible for the development of tumor antigen-specific adaptive immune response that contributes to the eradication of PDT-treated cancers.

Acute-Phase Reaction↗

PubMed2003

Co-expression of bfl-1 enhances host response in the herpes simplex virus-thymidine kinase/ganciclovir gene therapy system.

Anticancer suicide gene therapy using herpes simplex virus-thymidine kinase (HSV-tk) and ganciclovir (GCV) features the unique advantage of being able to elicit brisk host immune response against tumors and the host response reportedly can be potentiated with the co-expression of other appropriate immune- or apoptosis-related genes. We introduced a novel antiapoptotic gene, bfl-1, to test its applicability in the HSV-tk/GCV system. CT-26 murine colon cancer cells transfected with HSV-tk, alone or in combination with bcl-xL or bfl-1, were either grown in vitro or injected into syngeneic mice, followed by GCV administration. The co-expression of bfl-1 was associated with the upregulation of CD95 and CD40 ligand (CD40L) in vitro and with pronounced intratumoral T-lymphocyte infiltration in vivo. These results add to the previous findings that antiapoptotic genes can be used as an adjunctive component in the HSV-tk/GCV system to enhance host immune response against tumors.

Adenocarcinoma↗

PubMed1994

Role of macrophages in the host response to Lewis lung peritoneal carcinomatosis.

Lewis lung (3LL) peritoneal carcinomatosis elicits a complex host response in the peritoneal compartment. The response was delayed, showing few inflammatory cells through day 6 after lethal challenge with 3LL cells. Responses began in about half the mice on day 7 and had appeared in all mice by day 11. On day 7, some mice still showed no detectable 3LL growth in the pertioneal lavage fluid, and no differences in the peritoneal cell populations as compared with the control group. Other tumor-bearing mice, however, had evidence of 3LL cells and hemorrhagic ascites in the peritoneal compartment, with increased numbers of peritoneal macrophages (PM) and polymorphonuclear neutrophils (PMN). By day 11, all tumor-bearing mice had 3LL growth and hemorrhagic ascites. On days 7-11, there was a major influx of macrophages with a later influx of PMN between days 11 and 14. Two distinct PM populations were detected on day 7 in mice that showed detectable 3LL peritoneal carcinomatosis: resident PM, which did not express the Mac-2 antigen, and recruited PM, which were Mac-2+. At least some resident PM remained in the peritoneal compartment through day 14. Analysis of the kinetics of the cytotoxic capabilities of PM from tumor-bearing mice showed that by day 7 macrophages were able to kill the B16 melanoma tumor target, but not the 3LL target. The PM, however, were able to be activated further to kill the 3LL target by treatment in vitro with lipopolysaccharide and interferon gamma. No inhibition of PM tumoricidal activity could detected in the peritoneal wash of tumor-bearing mice. A lack of activation of PM from 3LL tumor-bearing mice may be involved in progression of peritoneal carcinomatosis.

Animals↗

PubMed1989

Host response in women with symptomatic urinary tract infection.

The agreement between clinical signs and host response was analysed in 174 women with symptomatic urinary tract infection. C-reactive protein (CRP) confirmed the clinical diagnosis in that 94% of non-pregnant and 91% of pregnant women with acute pyelonephritis had serum levels greater than or equal to 30 mg/l, compared with only 5% of cystitis patients. There was a significant increase in the erythrocyte sedimentation rate (ESR) and reduction of the renal concentrating capacity in patients with acute pyelonephritis, although the overlap with the cystitis group was greater than for CRP. The transient decrease in urine osmolality was unrelated to age, as were CRP, ESR and the total white blood cell count. Pregnant women had higher ESR but lower CRP levels than non-pregnant women with acute pyelonephritis. The renal concentrating capacity was more reduced in those infected with Escherichia coli expressing adhesins specifically recognizing Gal alpha 1----4Gal beta-containing receptors on uroepithelial cells.

Adolescent↗

PubMed1985

An innate host response to the neoplastic cell: syngeneic rat tumor cells can elicit a rapid de novo lymphoid procoagulant response.

To analyze unique molecular differences between normal and neoplastic cells, we have examined host responses to tumor cells. The present study provides the first evidence for an innate rapid recognitive response of the lymphoid system to some syngeneic tumors. The lymphoid procoagulant (PCA) response, a T cell-instructed monocyte response that activates proteases of the coagulation cascade culminating in thrombin formation, is considered a component of classic delayed-type hypersensitivity responses. We have demonstrated that three syngeneic rat mammary carcinomas elicit this cellular response in vitro in lymphoid cells of the unimmunized rat. The response was rapid, reaching maximum within 6 hr. Analysis was compounded by the constitutive PCA activity of some tumors; however, the PCA product produced in the response to tumor challenge in vitro was newly biosynthesized and was of lymphoid cell origin, differing from the PCA of tumor cells. The lymphoid PCA response was prothrombinase-like and did not require vitamin K for biosynthesis, nor were other gamma-carboxylation-dependent extrinsic pathway proteases other than prothrombin required for thrombin generation. Both in vivo and in vitro derived mammary carcinoma cells elicited the response, whereas a fibrosarcoma and nontransformed syngeneic cells did not. Tumor shed substances, which were devoid of PCA and sedimentable only in part at 100,000 X G, induced this cellular response. The same stimuli shed from tumor cells did not directly elicit a PCA response from elicited peritoneal macrophages; however, in the presence of T lymphocytes a PCA response of these macrophages was produced. This study provides novel information to indicate that a T-enriched lymphocyte-dependent monocyte-macrophage response to some tumors, before effective in vivo immunization, may participate in initial local protease generation and fibrin deposition, both thought to play a significant role in the local pathobiology of tumors.

Adenocarcinoma↗

PubMed1996

Varicella-zoster virus: aspects of pathogenesis and host response to natural infection and varicella vaccine.

Events in the pathogenesis of infection and the host response to VZV are very closely linked. Our experiments demonstrate that CD4- and CD8+ T-lymphocyte populations that are targets of cell-associated VZV viremia also mediate protection against severe infection. Diminished cell-mediated immunity predisposes the host to progressive primary or recurrent VZV disease because infected lymphocytes persist in the circulation and carry the virus to major organs, causing pneumonitis, hepatitis, or other life-threatening complications. The live attenuated varicella vaccine induces cell-mediated immunity and protects against or significantly reduces the morbidity associated with primary VZV infections. The universal administration of varicella vaccine is likely to generate new insights about host-virus interactions, particularly in relation to how VZV immunity is maintained, that will be relevant to the design of vaccines for other human herpesviruses.

Animals↗

PubMed1982

Behaviorally conditioned suppression of a graft-versus-host response.

Cyclophosphamide (CY), previously used to condition suppression of humoral immune responses, was used to condition suppression of a graft-versus-host response (GvHR). Female (Lewis x Brown Norway) F1 rats were conditioned by pairing consumption of a saccharin solution with an intraperitoneal injection of CY at 50 mg/kg of body weight 48 days before immunization. On day 0, all animals were injected with a suspension of splenic leukocytes (2 x 10(7) cells per footpad) obtained from female Lewis donors. The regional GvHR was assessed on day 5 by weighing popliteal nodes. Conditioned animals given a single low-dose injection of CY and reexposed to conditioned stimuli had lymph node weights significantly lower than control groups and did not differ from animals given three injections of CY during the ongoing GvHR. The results suggest that conditioned immunosuppression, previously demonstrated in thymus-dependent and thymus-independent humoral immune responses, also affects the popliteal GvHR, a cellular immune response.

Animals↗

PubMed1995

Temporal pattern of host responses against intrastriatal grafts of syngeneic, allogeneic or xenogeneic embryonic neuronal tissue in rats.

The host response to immunologically incompatible intrastriatal neural grafts was studied using immunohistochemical techniques. Dissociated ventral mesencephalic tissue from embryonic donors of either syngeneic, allogeneic or xenogeneic (mouse) origin was stereotaxically implanted into adult rats. The brains were analysed 4 days, 2 weeks or 6 weeks after grafting with antibodies against the following antigenic structures: major histocompatibility complex (MHC) class I antigens; MHC class II antigens; complement receptor (CR) 3 (marker for microglia and macrophages); helper T-lymphocyte antigen-cluster of differentiation (CD) 4; cytotoxic T-lymphocyte antigen-CD8; tyrosine hydroxylase (TH) (marker for transplanted dopaminergic neurons). The number of surviving TH-positive cells was not different at the various time points in either the syngeneic or allogeneic groups, whereas the xenogeneic cells were all rejected by 6 weeks. The host reactions were similar in character in the syngeneic and allogeneic groups. At 4 days after implantation, there were increased levels of expression of MHC class I and II antigens. In and around the grafts, there were cellular infiltrates consisting of activated microglia, macrophages, CD4- and CD8-positive lymphocytes. At 6 weeks, MHC expression was reduced and the cellular infiltrates had subsided with only low numbers of activated microglia cells and CD8-positive lymphocytes remaining. In the xenogeneic group, at 4 days, some grafts contained cavities, possibly reflecting acute rejection. At later stages, the xenografts were heavily infiltrated by macrophages, activated microglial cells and T-lymphocytes, and at 6 weeks all the xenografts were rejected. Taken together, the results suggest that there is an inflammation caused by the implantation process which leads to an accumulation of host defence cells. This, in turn, leads to increased MHC expression in and around the grafts. In syngeneic grafts, these reactions are short lasting and weak; for allografts slightly more pronounced and longer lasting than syngeneic grafts, but not sufficient to cause rejection. For xenografts, the reactions are more intense and lead to transplant rejection. Thus, a strong sustained inflammatory response may be an important determinator for the failure of histoincompatible neural grafts. It can be speculated that a short-term anti-inflammatory treatment of graft recipients may be a sufficient immunosuppressive regimen to allow long-term graft survival.

Animals↗

PubMedDate not supplied

Effects of sleep on endotoxin-induced host responses in healthy men.

OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.

Adult↗

PubMed1991

Effect of cancer therapy on host response and immunobiology.

The advances in bioengineering and hybridoma technology and the acquisition of basic knowledge about human antitumor defenses have facilitated the development of biologic therapies as a fourth cancer treatment approach. It is becoming important, therefore, to reconsider how conventional therapies affect host responses. It is apparent from the work of many laboratories that both the biologic agents and certain anticancer agents can cause augmentation of antitumor host defenses. These augmenting effects are generally seen at less than maximally tolerated doses. In contrast, at maximally tolerated doses these agents may induce long-lasting untoward effects, some of which (eg, long-term immunodepression) seem incongruent with effective host response-based therapies. This review examines developments in these areas over the past year and suggests that the maximal benefit may not be derived from the combination of chemotherapeutic agents with biologic therapies unless the optimal conditions for their administration in such combinations are redefined.

Antineoplastic Agents↗

PubMed1996

Host response assessment in recurring periodontitis.

Data derived from periodontitis patients have provided support for a relationship between the distribution of selected members of the periodontopathic microbiota and antibody levels to the intact bacteria in both serum and GCF. These data are consistent with the systemic antibody as a reflection of the host response to an infectious process associated with an episode of disease activity. The purpose of this report is to address the concept that the host antibody responses may help to elucidate the specific etiologic agents and be used to model the risk for future periodontal disease progression in recurring periodontitis. These findings from one study in adult periodontitis patients indicated that elevations in certain antibody specificities are most closely associated with patients exhibiting a risk of disease recurrence. Furthermore, analysis of the frequency of antibody elevations suggested that patients capable of maintaining elevated antibody to these pathogens post-treatment, may be indicative of an individual at less risk. A 2nd investigation was implemented to address questions concerning host-parasite interactions in A. actinomycetemcomitans-associated recurring periodontitis. The results showed distinctive characteristics of local and systemic antibody responses and A. actinomycetemcomitans infection in patients with varying extents of recurrent disease. These longitudinal studies developed evidence for the potential of local and/or systemic antibody responses as indicators of periodontal disease recurrence.

Actinobacillus Infections↗

PubMed2002

Molecular and cellular interactions between Brucella abortus antigens and host immune responses.

Host protection against Brucella abortus, is thought to be mediated primarily by a Th1 type immune response. Unfortunately, only few specific bacterial antigens involved in stimulating protective cellular immunity against Brucella are known. Therefore, identifying bacterial proteins that induce a T-lymphocyte mediated response is critical to determine Brucella immunity. Several library screening methods are discussed that have been used to identify Brucella proteins that stimulate T lymphocytes including cellular immunoblotting, Escherichia coli expressed Brucella proteins, green fluorescence reporter systems, and signature tagged mutagenesis. Future studies would likely examine how bacterial proteins expressed within host cells aid pathogen survival and/or induce host responses. Some of these newly identified bacterial gene products may serve as antigens to activate a protective host immune response. Also, identifying Brucella proteins expressed at particular times during infection will also yield insights into Brucella pathogenesis.

Animals↗

PubMed2001

[Role of host response during severe bacterial infection].

Explosion of knowledge both in human genomics and in host inflammatory response explains the increasing interest in infectious disease genetics over the last 5 years. However, twin and adoptee studies have suggested more than 15 years ago, that host genetic factors are major determinants of susceptibility to infectious diseases in humans. Recently, candidate gene studies (association studies) and human genomewide analysis have been used to identify infectious diseases susceptibility and resistance genes. Rarely, a single gene defect has been directly related to devastating consequences such as interferon-gamma receptor mutations leading to fatal infections with ubiquitous mycobacteria. For clinical practice, gene polymorphisms of specific host immune defence elements appear to be of major importance. These genetic variants, which modify the regulation or function of the mediators, have been associated with susceptibility and/or outcome of severe sepsis and septic shock. All steps of the host response to bacteria may be affected by genetic factors. For example, Fc gamma receptor, Toll like receptor or mannose binding protein mutations have been shown to modify the detection of pathogens leading to pneumococcal severe infections, Gram-negative bacteria septic shock, and meningococcal disease, respectively. Polymorphisms of cytokine genes (TNF-alpha, TNF-beta, IL-1-ra) have been reported to influence the level of secreted mediators and to unbalance the inflammatory cascade. Coagulation response to sepsis may also be affected by gene variants such as the plaminogen activator inhibitor 1 (PAI-1) common functional polymorphism which increases the risk of death from meningococcal infection or severe trauma. The impact of these findings on the understanding of infectious disease pathogenesis and on the design of future preventive and therapeutic strategies should be considerable.

Bacterial Infections↗

PubMed2005

Role of early stress in the individual differences in host response to viral infection.

Early negative life events, especially during the neonatal period, resulted in long lasting, irreversible effects on well being. The goal of the following study was to examine the lifelong effects of neonatal stress on the response to an influenza viral infection. Mouse pups were repeatedly separated from their dams between postnatal days 1-14 (maternal separation, MSP). As adults, these mice were infected with influenza A/PR8 virus and lung cytokine and plasma corticosterone responses to the viral infection were measured. The results indicated that MSP augmented several aspects of the response to infection. First, infection-induced lung proinflammatory cytokine (interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-alpha) mRNA expression was higher in MSP mice compared to controls. In addition, MSP augmented infection-induced lung IL-12 and interferon (IFN)-gamma, but had no effect on IL-18 mRNA. Interestingly, MSP-induced increase in IL-1, TNF-alpha and IFN-gamma mRNA expression was evident in females, but not in males. These findings suggest that MSP disrupted the regulation of innate resistance resulting in enhanced cytokine responses in the lungs during an infectious challenge. These changes in host response to the viral infection were accompanied by an increase in viral replication in lungs of MSP mice. Interestingly, influenza-induced corticosterone secretion was blunted in MSP mice, suggesting that the increase in immune reactivity to the virus was due to lack of glucocorticoid feedback control. These data demonstrate that neonatal stress has implications for host resistance to infection throughout life. Thus, long lasting effects of negative life events on health and disease may be the basis for the individual differences in host susceptibility to infection.

Age Factors↗

PubMed1977

Association of graft survival with host response to hepatitis B infection in patients with kidney transplants.

We studied the relation of host response to hepatitis B infection before transplantation with survival of kidney grafts in 79 patients receiving 87 transplants. Antibody to hepatitis B surface antigen (anti-HBs) signaled early graft rejection (median survival congruent to two months), whereas hepatitis B surface antigen (HBsAg) signaled delayed rejection (greater than 22 months). Patients with neither HBsAg nor anti-HBs had graft survival times (median congruent to 16 months) similar to the HBsAg carriers but significantly longer than the anti-HBs-positive patients (p less than 0.01). Similar results were observed when patients who received HLA-identical kidneys or had anti-HLA antibodies before transplantation were excluded. The highest probability of graft rejection was in patients with anti-HBs who received kidneys from male donors. The probability that such grafts would survive for four months was less than 20 per cent. HLA-nonidentical kidneys transplanted into patients with anti-HBs have a poor prognosis, whereas such grafts in HBsAg carriers have as good a prognosis as grafts in uninfected recipients.

Antibodies, Viral↗

PubMed1998

Local host response in osteosarcoma after chemotherapy referred to radiographs, CT, tumour necrosis and patient survival.

PURPOSE: The necrotic effect of chemotherapy on primary osteosarcoma has been shown to be predictive of the final outcome. Little attention has been paid to the local response of the host (LHR), which reflects the tumour-host relationship. DESIGN: A four-step grading system was developed based on distinct histological patterns of the LHR around the lesion. These responses were correlated with the chemotherapy-induced necrosis or chemosensitivity and analysed in an attempt to ascertain their influence on the patient prognosis. The ability of conventional radiographs and computed tomography to measure LHR was studied. METHODS: The grading system was applied to macroslides of specimens obtained from 72 patients with stage II B primary osteosarcoma in various limbs after wide resection and complete courses of pre- and postoperative chemotherapy who were treated between 1985 and 1991 with a median follow-up of 5 years and 9 months. The histological specimens were blindly reviewed by two pathologists and two experienced musculoskeletal oncologists to assign a grade of response. The results were correlated with tumour necrosis, patient survival and response features on conventional radiographs and CT images. RESULTS: Significant correlation was found between LHR and tumour necrosis or chemosensitivity (r=0.55) and between LHR and CT response (r=0.56). There was no correlation between LHR and the findings on conventional radiographs. A grade 4 LHR was predictive of long-term survival. CONCLUSIONS: The LHR to preoperative chemotherapy has a prognostic influence on patient survival and can be predicted by CT.

Adolescent↗