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Results for “host response”

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PubMed2025

Activation and modulation of the host response to DNA damage by an integrative and conjugative element.

Mobile genetic elements help drive horizontal gene transfer and bacterial evolution. Conjugative elements and temperate bacteriophages can be stably maintained in host cells. They can alter host physiology and regulatory responses and typically carry genes that are beneficial to their hosts. We found that ICEBs1, an integrative and conjugative element (ICE) of Bacillus subtilis, inhibits the host response to DNA damage (the SOS response). Activation of ICEBs1 before DNA damage reduced host cell lysis that was caused by SOS-mediated activation of two resident prophages. Further, activation of ICEBs1 itself activated the SOS response in a subpopulation of cells, and this activation was attenuated by the functions of the ICEBs1 genes ydcT and yddA (now ramT and ramA; ram for RecA modulator). Double-mutant analyses indicated that RamA functions to inhibit and RamT functions to both inhibit and activate the SOS response. Both RamT and RamA caused a reduction in RecA filaments, one of the early steps in activation of the SOS response. We suspect that there are several different mechanisms by which mobile genetic elements that generate single-stranded DNA (ssDNA) during their life cycle inhibit the host SOS response and RecA function, as RamT and RamA differ from the known SOS inhibitors encoded by conjugative elements.IMPORTANCEBacterial genomes typically contain mobile genetic elements, including bacteriophages (viruses) and integrative and conjugative elements, that affect host physiology. ICEs can excise from the chromosome and undergo rolling-circle replication, producing ssDNA, a signal that indicates DNA damage and activates the host SOS response. We found that following excision and replication, ICEBs1 of B. subtilis stimulates the host SOS response and that ICEBs1 encodes two proteins that limit the extent of this response. These proteins also reduce the amount of cell killing caused by resident prophages following their activation by DNA damage. These proteins are different from those previously characterized that inhibit the host SOS response and represent a new way in which ICEs can affect their host cells.

Bacillus subtilis↗

PubMed2005

HIV-1 burden influences host response to co-infection with Neisseria gonorrhoeae in vitro.

There is considerable evidence that co-infection with the sexually transmitted pathogen Neisseria gonorrhoeae (Gc) can increase the likelihood of both transmitting and acquiring HIV-1 worldwide. However, less information is available on how host immune response to co-infection differs with immune response to HIV-1 infection alone. To evaluate HIV-1 burden effects on host response to co-infection with Gc, we performed gene-expression profiling of human PBMCs infected over a broad range of viral titers (HIV-1 series) and upon exposure to a single infectious dose of Gc (HIV-1/Gc series). The transcriptional profiles differed substantially between each series (P < 0.0001). Major shifts in the transcriptional landscape were identified in contour plots based on fold stimulation and hierarchical clustering. Prominent regions of transcriptional activity were evaluated for statistical enrichment to identify up-regulated pathways associated with immune response, infection and T-cell stimulation. Notably, gene enrichment was dependent on HIV-1 burden and shifted during co-infection to reveal a disproportionate effect on lymphocyte signaling, apoptosis and proteasome activity. Further evaluation of these findings may help to better understand the role of viral burden in defining cellular contribution to host immune response upon co-infection with secondary sexually transmitted pathogens.

Cells, Cultured↗

PubMed1998

Modulation of the host response in the treatment of periodontitis.

Periodontitis has two distinct but interconnected etiologic components: periodontopathic bacteria adjacent to the periodontal tissues, and host-mediated connective tissue-destructive responses to the specific causative bacteria and their metabolic products. Although past and existing therapies have focused primarily on the causative microbial challenge, the host component of periodontal destruction has recently been intensely studied. New treatment strategies that focus on attenuating destructive host responses are emerging. Host modulatory agents, when used adjunctively, may enhance clinical therapeutic responses and make these responses more predictable in the susceptible host. The ongoing development of safe, effective pharmacotherapies that specifically target host response mechanisms, and the introduction of such pharmacotherapies as adjuncts to traditional, antimicrobial interventions may represent a new, integrated approach in the long-term treatment and management of this chronic disease.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1999

Characterization of the memory/activated T cells that mediate the long-lived host response against tuberculosis after bacillus Calmette-Guérin or DNA vaccination.

The memory/activated T cells, which mediate the long-lived host response against tuberculosis, in mice immunized with either bacillus Calmette-Guérin (BCG) or mycobacterium heat-shock protein 65 (hsp 65) antigen expressed from plasmid DNA (DNA-hsp 65), were characterized. Protection against Mycobacterium tuberculosis challenge by DNA-hsp 65 vaccination was associated with the presence of lymph node T-cell populations in which CD8+/CD44hi interferon-gamma (IFN-gamma)-producing/cytotoxic cells were prominent even after 8 or 15 months of plasmid DNA-mediated immunizations, whereas after BCG vaccination the majority were CD4+/CD44lo IFN-gamma-producing T cells. When the cells were separated into CD4+CD8- and CD8+CD4- and then into CD44hi and CD44lo types, CD44lo cells were essentially unable to transfer protection in adoptive transfer experiments, the most protective CD44hi cells were CD8+CD4- and those from DNA-vaccinated mice were much more protective than those from BCG-immunized mice. The frequency of protective T cells and the level of protection were increased up to 8 months and decreased after 15 months following DNA or BCG immunizations.

Animals↗

PubMed2006

Tensile strength and host response towards silk and type i polypropylene implants used for augmentation of fascial repair in a rat model.

OBJECTIVE: We compared host response, architectural integration and tensile strength of two different macroporous silk constructs to a polypropylene type I implant in a rat model for augmentation of primary fascial defect repair. MATERIALS AND METHODS: Animals were sacrificed on days 7, 14, 30 and 90 after implantation. The explants were evaluated macroscopically for infections, herniations and adhesions, mechanically for tensile strength, and histopathologically, to evaluate collagen deposition and inflammatory response. RESULTS: The tensile strength of the explants showed a gradual increase for all materials. All implants uniformly shrank around one fifth by 90 days. In the silk implants, the inflammatory reaction showed a remarkable higher number of foreign body giant cells that characteristically spread from the periphery into implants. Collagen deposition was comparable for all the materials. In Silk a higher grade of neovascularisation was observed. CONCLUSION: Silk explants expressed high tensiometric strength, which was associated with a marked fibrotic process. The silk implants induced a strong foreign body reaction accompanied by microscopic signs of architectural degradation at 90 days. Polypropylene explants showed a more moderate foreign body reaction without architectural disturbance.

Abdominal Wall↗

PubMed2005

Host response modulation in the management of periodontal diseases.

OBJECTIVE: To review the biological mechanisms and clinical utility of therapeutic modulation of the host response in the management of periodontal diseases. MATERIAL AND METHODS: A search of MEDLINE-PubMed was performed up to and including December 2004. The search was limited to in vitro, experimental animal and clinical studies published in English. The selection criteria included all levels of available evidence: systematic reviews, randomised-controlled clinical trials, controlled clinical trials, prospective and retrospective cohort studies and case reports of human and experimental animal studies. RESULTS: Six targets for non-microbial chemotherapeutic intervention were identified. Clinical trials have demonstrated the ability of non-steroidal anti-inflammatory drugs to slow periodontal disease progression. However, recently reported serious adverse effects preclude the use of cyclooxygenase-2 inhibitors as an adjunct to periodontal therapy. Adjunctive use of subantimicrobial dose doxycycline to non-surgical periodontal therapy is beneficial in the management of chronic periodontitis over 12 months. Controversial data exist on the effects of bisphosphonate administration as an adjunct to periodontal therapy. Evidence on modulation of other host mediators including lipoxins, cytokines and nitric oxide synthase is limited to animal research. CONCLUSION: After validation in long-term clinical trials, adjunctive host modulation therapy may prove advantageous in the management of periodontal diseases.

Animals↗

PubMed2000

Host response to cytomegalovirus infection as a determinant of susceptibility to coronary artery disease: sex-based differences in inflammation and type of immune response.

BACKGROUND: Positive and negative associations between cytomegalovirus (CMV) infection and coronary artery disease (CAD) have been reported. We postulated that the susceptibility to CMV-induced CAD might relate to patterns of inflammatory and immune responses to CMV infection and that sex might have an effect on these responses. METHODS AND RESULTS: In 151 men and 87 women being evaluated for CAD, blood samples were tested for humoral (Ab+) and cellular (Tc+) responses to CMV and for C-reactive protein (CRP). In men, an elevated CRP level was a significant determinant of CAD even after adjustment for CAD risk factors (OR, 3.1; 95% CI, 1.21 to 7. 97). CMV seropositivity was associated with elevated CRP levels on multivariate analysis (P:=0.006). In contrast, in women, CMV seropositivity was independently predictive of CAD (OR, 41.8; 95% CI, 4.12 to 423.74). CRP level in women with CAD was >25% higher than those without CAD, but the difference did not reach statistical significance. Importantly, compared with CMV Ab-/Tc- women, CAD prevalence was higher in Ab+/Tc- and Ab+/Tc+ (13% versus 68% and 64%, both P:<0.005) but not in Ab-/Tc+ women (25%). There were no differences in age, smoking, diabetes, hypertension, and hypercholesterolemia among women with different types of immune responses to CMV infection. CONCLUSIONS: The mechanisms by which CMV predisposes to CAD in men and women may be different. In men, CMV appears to contribute to CAD risk, insofar as it predisposes to inflammation. In women, other mechanisms, possibly related to the type of immune response generated by the host, appear to be responsible for the proatherogenic effects of CMV.

Adult↗

PubMed1997

Comparison of the roles of reactive oxygen and nitrogen intermediates in the host response to Mycobacterium tuberculosis using transgenic mice.

OBJECTIVE: To study the role of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) in host response to Mycobacterium tuberculosis. DESIGN: M. tuberculosis infection (i.v.) was compared in B6 control and two strains of knockout (KO) mice. X-CGD mice with a nonfunctional allele for the gp91phox subunit of the phagocyte oxidase cytochrome b are unable to produce ROI whereas iNOS KO mice lack a functional inducible nitric oxide synthase (iNOS) gene and fail to make RNI. RESULTS: M. tuberculosis growth was markedly enhanced in the lungs of X-CGD mice compared to B6 mice, but was controlled in the spleen and liver. In iNOS KO mice, M. tuberculosis growth was exacerbated in the spleen, but was unremarkable in the lungs compared to B6 mice until later (Day 60) in the infection. In vitro, X-CGD alveolar and peritoneal macrophages (M phi) produced no ROI, but did produce RNI and inhibited growth of M. tuberculosis when activated with interferon gamma. iNOS KO M phi produced ROI, but failed to produce RNI and could not cope with M. tuberculosis in vitro when activated. The inhibition of M. tuberculosis growth observed in activated B6 and X-CGD M phi) was reversed in the presence of aminoguanidine. CONCLUSION: These KO mouse strains demonstrate the relative potent effects of ROI and RNI in resistance to M. tuberculosis and should prove useful for the study of regulatory and compensatory mechanisms of immunity.

Animals↗

PubMed2001

Early recruitment of neutrophils determines subsequent T1/T2 host responses in a murine model of Legionella pneumophila pneumonia.

The contribution of neutrophils to lethal sensitivity and cytokine balance governing T1 and T2 host responses was assessed in a murine model of Legionella pneumophila pneumonia. Neutrophil depletion by administration of granulocyte-specific mAb RB6-8C5 at 1 day before infection rendered mice approximately 100-fold more susceptible to lethal pneumonia induced by L. pneumophila. However, this treatment did not alter early bacterial clearance, despite a substantial decrease in neutrophil influx at this time point. Cytokine profiles in the lungs of control mice demonstrated strong T1 responses, characterized by an increase of IFN-gamma and IL-12. In contrast, neutrophil-depleted mice exhibited significantly lower levels of IFN-gamma and IL-12, and elevation of T2 cytokines, IL-4 and IL-10. Immunohistochemistry of bronchoalveolar lavage cells demonstrated the presence of IL-12 in neutrophils, but not alveolar macrophages. Moreover, IL-12 was detected in lavage cell lysates by ELISA, which was paralleled to neutrophil number. However, intratracheal administration of recombinant murine IL-12 did not restore resistance, whereas reconstitution of IFN-gamma drastically improved bacterial clearance and survival in neutrophil-depleted mice. Taken together, these data demonstrated that neutrophils play crucial roles in primary L. pneumophila infection, not via direct killing but more immunomodulatory effects. Our results suggest that the early recruitment of neutrophils may contribute to T1 polarization in a murine model of L. pneumophila pneumonia.

Animals↗

PubMed1993

Outcome of intra-abdominal infection in pigs depends more on host responses than on microbiology.

OBJECTIVE: To assess the effects of mortality of the presence and proliferation of bacteria, and the host's response to infection, in pigs with peritonitis. DESIGN: Laboratory study. SETTING: University hospital. MATERIAL: 71 Swedish Landrace pigs, 63 with peritonitis and 8 without (controls). INTERVENTIONS: Induction of peritonitis by intraperitoneal infusion of equal amounts of Escherichia coli and Bacteroides fragilis (10(9) to 10(11) bacteria/animal); sterile faeces were added in half the experiments. MAIN OUTCOME MEASURES: Microbiological events were quantified as the area under the bacterial concentration curve from 0-6 hours. Host responses were quantified with a score of 8 physiological variables measured between 4-6 hours after the induction of peritonitis. RESULTS: Of the 63 infected animals, 37 (59%) died within 6-24 hours and both the physiological response and the bacterial load were significantly higher in those that died. Logistic regression analysis with death as the dependent variable showed that the physiology score carried more predictive information than the quantification of bacterial load. CONCLUSION: The quantification of local events within the abdomen is of only limited predictive value compared with the extent of the physiological alterations.

Animals↗

PubMed2005

Comparison of host response to polypropylene and non-cross-linked porcine small intestine serosal-derived collagen implants in a rat model.

OBJECTIVE: To compare the host response, architectural integration and tensile strength of polypropylene and porcine small intestine submucosa-derived implants in a rat model. DESIGN: Experimental study. SETTING: Center for Surgical Technologies, Faculty of Medicine, Katholieke Universiteit Leuven, Belgium. SAMPLE: Forty-eight adult male Wistar rats weighing 220-250 g randomised to receive either implant. METHODS: Full thickness abdominal wall defects were primarily repaired with polypropylene mesh (Marlex) (MX group) or porcine small intestine submucosa (Surgisis) (SIS group). Animals were sacrificed at 7, 14, 30 and 90 days after implantation. MAIN OUTCOME MEASURES: The presence of herniation, infection and intra-peritoneal adhesions. Change in thickness and tensile strength of implant. Histopathological and immunohistochemical appearances of inflammatory response and collagen deposition. RESULTS: Implants from the SIS group showed a short term increase in thickness in the first 14 days. Formation of adhesions was significantly more intense in the MX group at 30 days, and more extensive in the SIS group at 90 days. Tensile strength increased over time in both groups but was significantly lower in the SIS group than the MX group at 30 days. Implants in the MX group showed a more pronounced inflammatory response and more pronounced new vessel formation than the SIS group. Collagen formation was initially more fibrous and better organised in the MX group but became greater in the SIS group at 90 days. CONCLUSIONS: Biologically derived implant material induced a less pronounced inflammatory response and differences in collagen deposition. At 30 days tensile strength was weaker in the biological implant group but was equivalent by 90 days. These differences may have implications for the in vivo performance of the materials.

Abdominal Wall↗

PubMed1966

Leukocytes and interferon in the host response to viral infections. II. Enhanced interferon response of leukocytes from immune animals.

Glasgow, Lowell A. (University of Rochester School of Medicine and Dentistry, Rochester, N.Y.). Leukocytes and interferon in the host response to viral infections. II. Enhanced interferon response of leukocytes from immune animals. J. Bacteriol. 91:2185-2191. 1966.-The production of interferon was studied under in vitro conditions in peritoneal leukocytes or macrophages from mice immunized with Chikungunya virus (CV). Cultures of leukocytes obtained from animals immune to CV produced 2- to 10-fold greater amounts of interferon when exposed to an inoculum of CV than similar cell preparations from nonimmune, control animals. The viral inhibitor produced in increased quantity by CV-immune leukocytes had the biological and biochemical properties of interferon. The enhanced interferon production was inhibited by actinomycin D. This response of immune leukocytes was specific, and was initiated only by CV; it was not observed in leukocytes from animals immunized against other viruses which were challenged with CV. The presence of neutralizing antibody could not be related to this response. The observed increase in interferon production was not dependent upon an enhanced virus uptake. The data are presented as a possible new dimension of the "immune response" and may suggest a mechanism for the phenomenon of "tissue immunity."

Animals↗

PubMed1972

Synergy among lymphoid cells mediating the graft-versus-host response. 3. Evidence for interaction between two types of thymus-derived cells.

Two types of thymus-derived (T) lymphocytes have been shown to cooperate in the induction of graft-versus-host responses. One cell type is found in highest concentrations in the peripheral blood and lymph node, is extremely sensitive to anti-thymocyte serum (ATS) in vivo, and is probably part of the recirculating lymphoid cell pool (3). The second cell type, found in highest concentrations in the thymus and spleen, is relatively resistant to small doses of ATS in vivo. Both cell types are substantially depleted after neonatal thymectomy. Moreover, since synergism was also obtained using appropriate mixtures of cells from either parental strain in F(1) hosts, it was possible to show that the nonrecirculating cells determined the specificity of the response and were probably the precursors of effector cells in this response. The recirculating T cell appeared to amplify this response. The implications of these data are discussed.

Animals↗

PubMed2003

Overexpression of Toll-like receptor 4 amplifies the host response to lipopolysaccharide and provides a survival advantage in transgenic mice.

Toll-like receptors are transmembrane proteins that are involved in the innate immune recognition of microbial constituents. Among them, Toll-like receptor 4 (Tlr4) is a crucial signal transducer for LPS, the major component of Gram-negative bacteria outer cell membrane. The contribution of Tlr4 to the host response to LPS and to infection with virulent Salmonella typhimurium was studied in four transgenic (Tg) strains including three overexpressing Tlr4. There was a good correlation between the level of Tlr4 mRNA expression and the sensitivity to LPS both in vitro and in vivo: Tg mice possessing the highest number of Tlr4 copies respond the most to LPS. Overexpression of Tlr4 by itself appears to have a survival advantage in Tg mice early during infection: animals possessing more than two copies of the gene survived longer and in a greater percentage to Salmonella infection. The beneficial effect of Tlr4 overexpression is greatly enhanced when the mice present a wild-type allele at natural resistance-associated macrophage protein 1, another critical innate immune gene involved in resistance to infection with Salmonella. Tlr4 and natural resistance-associated macrophage protein 1 exhibit functional epistatic interaction to improve the capacity of the host to control bacterial replication. However, this early improvement in disease resistance is not conducted later during infection, because mice overexpressing Tlr4 developed an excessive inflammatory response detrimental to the host.

Adjuvants, Immunologic↗

PubMed2005

Activation of MAPK kinase pathway by Gal/GalNAc adherence lectin of E. histolytica: gateway to host response.

Amoebiasis caused by the protozoan parasite Entamoeba histolytica is one of the leading parasitic causes of morbidity and mortality in the developing countries. Among the variety of virulence factors, an adherence lectin (Gal/GalNAc, 260 kDa) has been known to mediate colonization and subsequent host responses. It is a major cell surface antigen which is universally recognized by the immune sera of patients with amoebic liver abscess (ALA). The role of this lectin in cytolysis and phagocytosis of human colonic mucin glycoproteins has also been established. The objective of the present study was to elucidate the signal transduction events induced in response to Entamoeba histolytica derived Gal/GalNAc lectin in the target epithelial cells. We have attempted to define a pathway in target cells that could link this immunodominant antigen to a known biological pathway for target cell activation and triggering of subsequent disease pathology/parasite survival. Lectin stimulated cells showed immediate rise in (Ca2+)i concentration corresponding to 1517.31+/-16.3 nM (approximately) at 0-2 min. The intracellular calcium also extruded from the cells as was measured by increase in calcium green-1 fluorescence. Expression of several protein kinases was checked by western blotting to delineate the signaling pathway. Results showed that the expression of PLA2, PI3K, Ras p21, Ras GAP, ERK-MAPK, p38MAPK and PKC was significantly increased. Expression of Raf-1 and MEK-1 was also found to be significant, as determined by intensity analysis. Overall, it indicated activation of MAPKinase pathway which is implicated in a variety of cellular functions. On the basis of our observations it can be stated that there is a calcium mediated activation of PKC in target cells, by lectin, which inturn activates cyclic nucleotides and other protein kinases. These protein kinases further phosphorylated downstream signals in a sequential manner, thus leading to the activation of MAPKinase cascade. Activation of MAPK cascade, in our studies, is implicated in a variety of physiological cellular functions including apoptosis, proliferation, cytoskeleton rearrangements and permeability changes. However, future screening of the genes responsible for the transcription and translation of new proteins and their biological functions in response to lectin stimulation will prove useful in understanding this host-parasite relationship.

Animals↗

PubMed2003

Hypertonic saline enhances host response to bacterial challenge by augmenting receptor-independent neutrophil intracellular superoxide formation.

OBJECTIVE: This study sought to determine whether hypertonic saline (HTS) infusion modulates the host response to bacterial challenge. METHODS: Sepsis was induced in 30 Balb-C mice by intraperitoneal injection of Escherichia coli (5 x 107 organisms per animal). In 10 mice, resuscitation was performed at 0 and 24 hours with a 4 mL/kg bolus of HTS (7.5% NaCl), 10 animals received 4 mL/kg of normal saline (0.9% NaCl), and the remaining animals received 30 mL/kg of normal saline. Samples of blood, spleen, and lung were cultured at 8 and 36 hours. Polymorphonucleocytes were incubated in isotonic or hypertonic medium before culture with E. coli. Phagocytosis was assessed by flow cytometry, whereas intracellular bacterial killing was measured after inhibition of phagocytosis with cytochalasin B. Intracellular formation of free radicals was assessed by the molecular probe CM-H(2)DCFDA. Mitogen-activated protein (MAP) kinase p38 and ERK-1 phosphorylation, and nuclear factor kappa B (NFkappaB) activation were determined. Data are represented as means (SEM), and an analysis of variance test was performed to gauge statistical significance. RESULTS: Significantly reduced bacterial culture was observed in the animals resuscitated with HTS when compared with their NS counterparts, in blood (51.8 +/- 4.3 vs. 82.0 +/- 3.3 and 78.4 +/- 4.8, P = 0.005), lung (40.0 +/- 4.1 vs. 93.2 +/- 2.1 and 80.9 +/- 4.7, P = 0.002), and spleen (56.4 +/- 3.8 vs. 85.4 +/- 4.2 and 90.1 +/- 5.9, P = 0.05). Intracellular killing of bacteria increased markedly (P = 0.026) and superoxide generation was enhanced upon exposure to HTS (775.78 +/- 23.6 vs. 696.57 +/- 42.2, P = 0.017) despite inhibition of MAP kinase and NFkappaB activation. CONCLUSIONS: HTS significantly enhances intracellular killing of bacteria while attenuating receptor-mediated activation of proinflammatory cascades.

Analysis of Variance↗

PubMed2002

Characterization of subcutaneous Contramid implantation: host response and delivery of a potent analog of the growth hormone-releasing factor.

Cross-linked high amylose starch (Contramid) was investigated as a solid implant for evaluation of host response in mice and as a possible delivery system for a human growth hormone-releasing factor analog (Hex-hGRF) release profile in pigs. Seventy mice were administered subcutaneously one 3 mm diameter Contramid pellet and host reaction was evaluated over 6 months. Thirty pigs were divided into four groups. All animals of the three implanted groups were administered subcutaneously 15 mg Hex-hGRF, (1) one pure Hex-hGRF implant; (2) four 30/70 w/w Hex-hGRF/Contramid implants; or (3) eight 15/85 w/w Hex-hGRF/Contramid implants. The fourth group (n=6) was injected subcutaneously twice daily with 10 microg/kg of Hex-hGRF over 5 consecutive days. Serum insulin-like growth factor-I (IGF-I) was monitored over 1 month. In mice, no adverse reaction occurred after implantation. Macroscopic and microscopic inflammatory reactions were always localized. Polymorphonuclear cells (PMNs) and macrophages predominated within and around the pellets, respectively. Thin fibrovascular septas eventually subdivided Contramid pellets which were progressively phagocytosed by macrophages. In pigs, serum IGF-I concentrations were increased over a 10 day period in all implanted groups. The initial IGF-I peak observed in the daily injected group was avoided in both Contramid implant groups but not in the pure Hex-hGRF implant group. These encouraging results warrant the development of Contramid implants as a sustained delivery system for peptidic drugs.

Animals↗

PubMed1993

Modulation of host response during infection with Trichinella pseudospiralis using immuno-stimulant drug.

Infection of the mouse with Trichinella pseudospiralis is accompanied by pronounced suppression of host inflammatory response. This study examines the effect of infection with this parasite on one major component of cell mediated immunity: delayed type hypersensitivity (DTH) reaction and the effect of administration of immunostimulant drug (Levamisole) on host response to T. pseudospiralis infection. Serum cortisol levels and the response of skin test to phytohaemagglutinin were used to construct the time table of drug regimen. Three groups were studied; group I (infected mice), group II (received levamisole on day 6 p.i.) and group II (received Levamisole on day 14 p.i.) Early administration of Levamisole restored DTH response to normal and histopathological examination of infected muscles revealed evident collagen deposition around the muscle larvae.

Animals↗