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Results for “Cross Protection”

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PubMed1990

Human parainfluenza virus induces a type-specific protective immune response.

Induction of type-specific and cross-protective immune responses against human parainfluenza viruses have been investigated. The envelope glycoproteins HN (76 kDa) and F0 (62 kDa) from parainfluenza type 2 virus were selectively solubilized with octylglucoside. Detergent-soluble envelope glycoproteins were used as vaccine antigens for intranasal immunization of hamsters. The immunized animals showed complete protection from challenge infection with prototype live virus but failed to demonstrate a significant level of protection against either human parainfluenza type 1 or type 3 virus. The sera and bronchial lavages of immunized animals also showed type-specific neutralizing antibodies. A similar type-specific protective immune response was also noted after primary infection with live virus. The results indicate that a multivalent parainfluenza virus vaccine is probably required for protection against natural infection.

Animals↗

PubMed1976

Oral vaccination against Porteus mirabilis.

Mice given a single dose of proteus vaccine orally were protected against 1 MLD (minimum lethal dose) of autologous Proteus mirabilis by the fourth day after vaccination. Three doses of oral vaccine induced protection against 1 MLD autologous challenge for 7 days after vaccination and partial protection for a further 8 weeks. Cross-protection against different strains of Pr. mirabilis and against some strains of Pseudomonas aeruginosa, Serratia marcescens and Providencia species was found in mice immunized orally on three consecutive days with a bivalent proteus vaccine.

Administration, Oral↗

PubMed1978

Teratocarcinoma cell variants rejected by syngeneic mice: protection of mice immunized with these variants against other variants and against the original malignant cell line.

We reported previously that, by mutagenesis of a malignant teratocarcinoma cell line, it is possible to obtain a number of variant clones that are incapable of forming progressive tumors. Each of these "tum-" variants is rejected in syngeneic mice and stimulates the production of immune memory cells (self-protection). We show here that four different tum- clones confer an immune protection against each other although this cross-protection is invariably weaker than the self-protection. Moreover, mice immunized with living tum- cells are partially protected against the original malignant teratocarcinoma cells, even though the latter cells are incapable of conferring any immune protection when injected after being killed by irradiation. These results indicate that each tum- variant carries at least one specific transplantation antigen that is absent from the original tumor cell line and from most other tum- variants. Other tumor-specific transplantation antigens are probably present on all the tum- variants and also on the malignant teratocarcinoma cell line.

Animals↗

PubMed2003

Induction of an adaptive tolerance response in the foodborne pathogen, Campylobacter jejuni.

In this study we aimed to determine if Campylobacter had the ability to induce an adaptive tolerance response (ATR) to acid and/or aerobic conditions. Campylobacter jejuni CI 120 was grown to the appropriate phase in Brucella broth under microaerobic conditions. Cells were initially adapted to a mild stress (pH 5.5) for 5 h prior to challenge at pH 4.5, a lethal pH. Survival was examined by determining the numbers of viable cells on Campylobacter blood free selective agar base. Stationary phase cells adapted at pH 5.5 induced an ATR that enabled a 100-fold greater survival compared to an uninduced culture. Aerobic adaptation also protected the cells against acid challenge. The cross protection provided a 500-fold increase in survival when compared to unadapted cells. The incorporation of chloramphenicol during the induction period eliminated the ATR and resulted in death kinetics similar to an uninduced culture. These data suggest that Campylobacter spp. have the ability to induce an ATR to sublethal treatments, which increased their ability to withstand subsequent stresses.

Adaptation, Physiological↗

PubMed2003

A single arginine residue is required for the interaction of the electron transferring flavoprotein (ETF) with three of its dehydrogenase partners.

The interaction of several dehydrogenases with the electron transferring flavoprotein (ETF) is a crucial step required for the successful transfer of electrons into the electron transport chain. The exact determinants regarding the interaction of ETF with its dehydrogenase partners are still unknown. Chemical modification of ETF with arginine-specific reagents resulted in the loss, to varying degrees, of activity with medium chain acyl-coenzyme A dehydrogenase (MCAD). The kinetic profiles showed the inactivations followed pseudo-first-order kinetics for all reagents used. For activity with MCAD, maximum inactivation of ETF was accomplished by 2,3-butanedione (4% residual activity after 120 min) and it was shown that modification of one arginine residue was responsible for the inactivation. Almost 100% restoration of this ETF activity was achieved upon incubation with free arginine. However, the same 2,3-butanedione modified ETF only possessed decreased activity with dimethylglycine-(DMGDH, 44%) and sarcosine- (SDH, 27%) dehydrogenases unlike the abolition with MCAD. Full protection of ETF from arginine modification by 2,3-butanedione was achieved using substrate-protected DMGDH, MCAD and SDH respectively. Cross-protection studies of ETF with the three dehydrogenases implied use of the same single arginine residue in the binding of all three dehydrogenases. These results lead us to conclude that this single arginine residue is essential in the binding of the ETF to MCAD, but only contributes partially to the binding of ETF to SDH and DMGDH and thus, the determinants of the dehydrogenase binding sites overlap but are not identical.

Acyl-CoA Dehydrogenase↗

PubMed2004

Chronic HIV-2 infection protects against total CD4+ cell depletion and rapid disease progression induced by SHIV89.6p challenge.

OBJECTIVE: To better understand HIV-1 sexual transmission risk, we have studied the susceptibility of HIV-2-exposed, uninfected (EU) female pig-tailed macaques to intravaginal (IVAG) re-challenge with the homologous HIV-2 strain, followed by heterologous SHIV89.6p. METHODS: Nine female macaques, previously protected by a post-exposure prophylaxis (PEP) regimen, along with one mock-treated EU animal, were re-exposed to HIV-2 by the IVAG route approximately 1.5 years later. A single follow-up challenge was performed approximately 1 year later with SHIV89.6p to assess susceptibility of chronic HIV-2-infected animals to further re-infection and pathogenic effects with a heterologous virus, somewhat mimicking HIV-1. RESULTS: Eight of ten macaques (80%) became infected systemically with HIV-2, and plasma or cervicovaginal vRNA levels did not appreciably differ from prior historic non-PEP control macaques. Interestingly, all eight HIV-2-infected females were susceptible to SHIV89.6p infection by either intravenous (n = 4) or IVAG exposure (n = 4) after one inoculation. Plasma vRNA levels in these groups were controlled by week 8 and there were no decrease in CD4+ T cells > 50%. The remaining two HIV-2 EU macaques, inoculated intrarectally with SHIV89.6p, were unable to control virus replication and succumbed to disease by week 25 or week 61. CONCLUSIONS: Our findings demonstrate that successful PEP regimens to prevent an initial infection do not have any lasting protective effects. The observed lack of cross-protection against SHIV89.6p transmission among chronic HIV-2-infected macaques provides modeling support for limited epidemiologic data indicating that human HIV-2 infection does not protect against HIV-1 infection, but may serve to alter overt clinical outcome.

Animals↗

PubMed1979

Evaluation of Pseudomonas aeruginosa toxin A in experimental rat burn wound sepsis.

The search for methods to achieve control of Pseudomonas aeruginosa infection continues with the introduction of aluminum-absorbed toxoid developed from P. aeruginosa exotoxin. This toxoid induces significant titers of neutralizing and precipitating antibodies for toxin A when given with appropriate adjuvants. These experiments show that immunization with aluminum phosphate-absorbed toxoid failed to protect burned rats infected with P. aeruginosa. These and previous experiments show that active immunization with live P. aeruginosa provides good strain-specific protection in the same model. No cross-protection was demonstrated between strains of P. aeruginosa in these experiments.

Animals↗

PubMed1977

Purification of histamine receptor (VI). An improved double labeling method with "double protection".

Studies were done on the specific labeling of the histaminergic H1-receptor of the longitudinal smooth muscle of cat small intestine. A procedure involving 'double protection' combined with the double labeling technique was developed. The first protection was the usual with a protective antihistamine, promethazine, and the second was cross protection of non-specific sites with non-hitaminergic drugs, thioriazine and atropine. Muscle tissue protected with promethazine against non-radioactive dibenamine was treated with 3H-dibenamine in the presence of these second protectors. The second protectors covered non-receptor sites which had been protected from non-radioactive dibenamine with promethazine. The dose-response curves were carefully checked in each experiment to confirm that the second protectors did not interfere with the specific coverage provided by the first protector. Finally 14C-dibenamine was applied to measure non-specific binding after which the labeled muscles were fractionated and the radioactivity was counted. The specificity of labeling achieved in the receptor-rich fraction by this method is discussed.

Animals↗

PubMed1982

Protective antigenic determinant of streptococcal M protein shared with sarcolemmal membrane protein of human heart.

We present definitive evidence that at least one protective antigenic determinant on type 5 M protein of group A streptococci evokes antibody that is cross-reactive with human heart tissue. One of nine rabbits immunized with a peptide fragment of type 5 M protein (pep M5) produced antibody that cross-reacted by immunofluorescence with sarcolemmal membranes of human heart. The cross-reactive antibody could be removed by absorbing the antiserum with sarcolemmal membranes, types 5 and 19 streptococci, or their pepsin-extracted M proteins, but with no other serotypes tested. Although each of the pep M5 immune sera was opsonic for type 5 streptococci, only the heart-reactive antiserum opsonized type 19 streptococci. The opsonization of type 19 streptococci was abolished by absorbing the antiserum with sarcolemmal membranes isolated from human heart tissue. Purified heart-reactive antibodies eluted from sarcolemmal membranes opsonized both types 5 and 19 streptococci, indicating that the heart cross-reactive determinant of type 5 M protein is cross-protective. The cross-reactive antigen was purified by affinity chromatography from detergent extracts of sarcolemmal membranes and determined to be a complex protein composed of four subunits apparently linked by disulfide bonds.

Antigens, Bacterial↗

PubMed1988

Delta and non-A, non-B hepatitis viruses.

A review is given on the current knowledge of the hepatitis delta virus (HDV), the only hepatotropic non-A and non-B (NANB) virus characterized, although the infection it causes requires infection with hepatitis B virus (HBV). Studies in chimpanzees have provided the most data now available on the putative NANB agents. Histologic and electron microscopic changes occurring in HDV and NANB hepatitis have been shown to be comparable, and some biologic, epidemiologic and clinical features are similar. However, the lack of cross-protection between NANB and HDV hepatitis in cross-challenge transmission experiments and the lack of hybridization between HDV-RNA and nucleic acids from NANB material indicate that HDV and the putative NANB agents are minimally, if at all, related.

Animals↗

PubMed1992

Immunization of pigs against Actinobacillus pleuropneumoniae with two recombinant protein preparations.

Two Actinobacillus pleuropneumoniae serotype 7 antigens were expressed in Escherichia coli and tested for their protective efficacy in an experimental pig model. The antigens used were a fusion protein containing the carboxy-terminal 70% of the +/- 103 kDa cytolysin and a full length 60 kDa protein which has been shown previously to bind transferrin. Pigs were immunized twice with 25 micrograms of either or both preparations. All pigs developed a strong humoral immune response comparable to that induced by infection. Upon challenge with an A. pleuropneumoniae serotype 7 strain, all immunized groups were less affected by the disease and showed significantly lower mortality than the controls (p less than 0.1). Pigs receiving both antigens had a tendency to recover faster than the controls or animals which were vaccinated with only one antigen. Protection was serotype-specific since no cross-protection was detected following challenge with an A. pleuropneumoniae serotype 1 strain. A dose-response experiment using the single antigens at 200, 50 or 12.5 micrograms per dose showed no difference in protection among the groups.

Actinobacillus pleuropneumoniae↗

PubMed2005

Clearance of Bordetella parapertussis from the lower respiratory tract requires humoral and cellular immunity.

Bordetella parapertussis and Bordetella pertussis are closely related species that cause whooping cough, an acute, immunizing disease. Their coexistence in the same host populations at the same time and vaccine studies showing that B. pertussis vaccines have little effect on B. parapertussis infection or disease suggest that the protective immunity induced by each does not efficiently cross protect against the other. Although the mechanisms of protective immunity to B. pertussis have been well studied, those of B. parapertussis have not. The present study explores the mechanism by which B. parapertussis is cleared from the lower respiratory tract by anamnestic immunity. Serum antibodies are necessary and sufficient for elimination of this bacterium, and CD4(+) T cells, complement, and neutrophils are required for serum antibody-mediated clearance. Mice lacking immunoglobulin A had no defect in their ability to control or clear infection. Interestingly, serum antibody-mediated clearance of B. parapertussis did not require Fc receptors that are required for antibody-mediated clearance of B. pertussis. Together these data support a model for the mechanism of protective immunity to B. parapertussis that is similar but distinct from that of B. pertussis.

Adoptive Transfer↗

PubMed2000

Gamma interferon is not required for mucosal cytotoxic T-lymphocyte responses or heterosubtypic immunity to influenza A virus infection in mice.

Heterosubtypic immunity (HSI) is defined as cross-protection against influenza virus of a different serotype than the virus initially encountered and is thought to be mediated by influenza virus-specific cytotoxic T lymphocytes (CTL). Since gamma interferon (IFN-gamma) stimulates cytotoxic cells, including antigen-specific CTL which may control virus replication by secretion of antiviral cytokines such as tumor necrosis factor alpha and IFN-gamma, we have investigated the mechanism of HSI by analyzing the role of IFN-gamma for HSI in IFN-gamma gene-deleted (IFN-gamma(-/-)) mice. It has been reported that IFN-gamma is not required for recovery from primary infection with influenza virus but is important for HSI. Here, we conclusively show that IFN-gamma is not required for induction of secondary influenza virus-specific CTL responses in mediastinal lymph nodes and HSI to lethal influenza A virus infection. Although T helper 2 (Th2)-type cytokines were upregulated in the lungs of IFN-gamma(-/-) mice after virus challenge, either Th1- or Th2-biased responses could provide heterosubtypic protection. Furthermore, titers of serum-neutralizing and cross-reactive antibodies to conserved nucleoprotein in IFN-gamma(-/-) mice did not differ significantly from those in immunocompetent mice. These results indicate that lack of IFN-gamma does not impair cross-reactive virus-specific immune responses and HSI to lethal infection with influenza virus. Our findings provide new insight for the mechanisms of HSI and should be valuable in the development of protective mucosal vaccines against variant virus strains, such as influenza and human immunodeficiency virus.

Adaptation, Physiological↗

PubMed1993

Plasmodium falciparum sporozoite immunization protects against Plasmodium berghei sporozoite infection.

Irradiated sporozoites are generally thought to elicit protective immune responses that are parasite stage and species specific. But immunization with Plasmodium falciparum sporozoites delivered by the bite of infected mosquitoes protects an average of 60% mice from Plasmodium berghei sporozoite infection. Protection appears to be specific as P. falciparum sporozoite-immunized mice protected against P. berghei remain susceptible to Plasmodium yoelii sporozoite infection. Passively transferred immunoglobulin from P. falciparum sporozoite-immunized mouse serum protected naive mice against challenge with P. berghei sporozoites, indicating that cross-protection is mediated, at least in part, by anti-sporozoite antibody. Antibody-mediated protection may not be due to cross-reaction between P. falciparum and P. berghei CS proteins because mice immunized with the recombinant P. falciparum CS protein repeat vaccine candidate, R32tet32, remain susceptible to P. berghei sporozoite infection.

Animals↗

PubMed2006

Vaccination with a gE-negative bovine herpesvirus type 1 vaccine confers insufficient protection to a bovine herpesvirus type 5 challenge.

In the present study, cross-protection to bovine herpesvirus type 5 (BHV-5) induced by bovine herpesvirus type 1 (BHV-1) vaccination was examined following inoculation of rabbits and calves with a glycoprotein E (gE)-negative BHV-1 vaccine and subsequent challenge with BHV-5. Rabbits (n=5) and calves (n=8) were vaccinated [five rabbits intranasally (IN), four calves IN and four intramuscularly (IM)] with 7.1 log(10)median tissue culture infective dose (TCID(50)) of the BHV-1 vaccine. Rabbits and calves were challenged IN [rabbits 2 weeks post-vaccination (pv); calves 5 weeks pv] with 9.1log(10)TCID(50) of BHV-5. Two out of five vaccinated rabbits died after challenge with typical BHV-5 disease, as did 3/5 non-vaccinated controls. In calves, 4/8 vaccinated animals displayed mild signs of disease, whereas 6/6 non-vaccinated controls developed signs of disease, so severe that 2/6 had to be killed. Besides, nasal virus shedding post-challenge was not reduced by vaccination. At necropsy, on day 21 post-challenge, typical BHV-5 lesions were evident in brain tissues of both vaccinated and non-vaccinated calves. Dexametasone administration at 180 days post-infection did not reactivate clinical signs despite BHV-5 shedding in nasal secretions of both vaccinated and non-vaccinated calves. These results show that the BHV-1 vaccine evaluated here did not confer protection to BHV-5 in rabbits. In calves, BHV-1 vaccination did confer some protection to BHV-5 induced clinical disease, but it did not prevent infection and had no effect on nasal virus shedding or on the development of encephalitic lesions.

Administration, Intranasal↗

PubMed1991

Immunity to Haemonchus contortus and the cellular response to helminth antigens in the mammary gland of non-lactating sheep.

Cellular exudates induced by infusion with helminth antigens were examined in non-lactating mammary glands of ewes immune to infection with the abomasal nematode, Haemonchus contortus. Secondary immunological responsiveness was expressed in two ways. Firstly, antigens from adult H. contortus elicited larger eosinophil-rich cellular exudates in immune compared to non-immune ewes. In this situation, secondary responsiveness in the mammary gland must have been generated through abomasal infection with the parasite. Secondly, repeated infusion with the antigens from adult H. contortus increased the size of cellular exudates in both immune and non-immune ewes. Eosinophils predominated but numbers of macrophages and lymphocytes were also increased. In this second situation, secondary responsiveness must have been either supplemented in immune ewes or derived completely in non-immune ewes by contact with helminth antigens through the mammary gland. The helminth antigens which induce eosinophil exudates in the mammary gland may not be potently protective against H. contortus. Furthermore, eosinophil exudation may not be an in vivo correlate of immunity which is directly useful for discriminating protective antigens and applicable to vaccine development. Infusion with antigens from adult forms of either H. contortus or Trichostrongylus colubriformis elicited cellular exudates equally well in immune ewes primed by infusion with H. contortus adult antigens 7 days beforehand. In addition, antigens from infective larvae of H. contortus elicited cellular exudates more potently than antigens from adult worms. However, vaccination with irradiated larvae has shown that species-specific protective immunity for H. contortus is stronger than cross-protective immunity conferred by T. colubriformis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Oral cholera vaccine--for whom, when, and why?

The search for a safe, effective, well tolerated, low cost vaccine against the ancient cholera enemy has been ongoing since the 19th century and has been revitalized in the past two decades since the advent of recombinant technology. Large-scale field trials have readily demonstrated the tolerability and safety of oral cholera vaccine in various forms. Variable levels of protection have been shown and one challenge has been to demonstrate whether this is a cost effective treatment in differing environments including its use in endemic and epidemic areas as well as for travelers. A review of recent literature was undertaken to assess the effectiveness and uses of currently available oral cholera vaccine. While the evidence does not support the creation of formal guidelines, some clear recommendations can be made. There is undoubtedly the potential to reduce the burden of illness both in endemic and epidemic situations. For travelers, certain higher risk groups may benefit from protection against cholera. More significantly, the short term cross-protection afforded by whole cell, B subunit (WC BS) oral cholera vaccine formulations against enterotoxigenic E. coli, (ETEC), the commonest causative agent of traveler's diarrhoea, may prove to be the most important raison d'être.

Administration, Oral↗

PubMed2006

Immunization with murine breast cancer cells treated with antisense oligodeoxynucleotides to type I insulin-like growth factor receptor induced an antitumoral effect mediated by a CD8+ response involving Fas/Fas ligand cytotoxic pathway.

We have demonstrated that in vivo administration of phosphorothioate antisense oligodeoxynucleotides (AS[S]ODNs) to type I insulin-like growth factor receptor (IGF-IR) mRNA resulted in inhibition of C4HD breast cancer growth in BALB/c mice. The present study focused on whether in vivo administration of C4HD tumor cells pretreated with IGF-IR AS[S]ODN and irradiated could provide protection against C4HD wild-type tumor challenge and also on elucidating the mechanism mediating this effect. Our results showed that mice immunized with IGF-IR AS[S]ODN-treated C4HD cells experienced a growth inhibition of 53.4%, 61.6%, and 60.2% when compared with PBS-treated mice, wild-type C4HD cell-injected mice, or phosphorothioate sense oligodeoxynucleotide-treated C4HD cell-injected mice, respectively. The protective effect was C4HD-specific, because no cross-protection was observed against other syngeneic mammary tumor lines. The lack of protection against tumor formation in nude mice indicated that T cells were involved in the antitumoral response. Furthermore, cytotoxicity and splenocyte proliferation assays demonstrated that a cellular CD8(+)-dependent immune response, acting through the Fas/Fas ligand death pathway, could be mediating the antitumor effect induced by immunization with AS[S]ODN-treated cells. Immunization also induced splenocytes to produce Ag-dependent IFN-gamma, indicating the presence of a type 1 response. We demonstrated for the first time that IGF-IR AS[S]ODN treatment of breast cancer cells induced expression of CD86 and heat shock protein 70 molecules, both involved in the induction of the immunogenic phenotype. Immunization with these tumor immunogens imparted protection against parental tumor growth through activation of a specific immune response.

Animals↗