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Results for “BALB/c mouse model”

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PubMed1996

Highly virulent strains of herpes simplex virus fail to kill mice following infection via gingival route.

Virulence of herpes simplex virus (HSV) in mice has been demonstrated to be dependent on the site of infection. In this experiment, pathogenesis of HSV was studied in 2 different routes of infection in a mouse model system. When BALB/c mice were infected with 5 x 10(3) plaque-forming units (PFU) of virulent HSV type 1 Miyama GC+ strain (HSV-1-GC+) intraperitoneally, all mice were dead in 6 to 9 days. HSV-1-GC+ was recovered from organs such as the cerebrum, cerebellum, brainstem, and spleen 2 to 5 days after infection, but not from other organs such as trigeminal ganglia. However, if mice were infected in the maxillary gingiva with 1.0 x 10(7) PFU of HSV-1-GC+, all mice survived. HSV-1-GC+ was recovered from the trigeminal ganglia and brainstem 2 to 5 days after infection, but not from other organs tested. When mice were infected in maxillary gingiva with HSV-1-GC+, followed by the intraperitoneal injection of 6 mg of cyclophosphamide 72 hrs after virus infection, all mice were dead within days. Immunofluorescent and hematoxylin-eosin staining of gingival tissue sections revealed that when mice were infected in maxillary gingiva with HSV-1-GC+, 3 times as many gamma delta T-cells and 5 times as many polymorphonuclear cells can be detected in sections of maxillary gingiva when compared with non-infected mice. These data show that the gingiva of mice is considerably more resistant to infection with HSV, compared with the peritoneal cavity, and suggest the possible presence of an oral defense mechanism which might be different from that in the peritoneal cavity.

Animals↗

PubMed2006

Inhibitory effect of DA-9201, an extract of Oryza sativa L., on airway inflammation and bronchial hyperresponsiveness in mouse asthma model.

Asthma is one of the major public health problems worldwide and the morbidity and mortality of asthma has increased in the past two decades. Accumulating data suggest that unnecessary immune responses and inflammation should be suppressed to treat asthma. The purpose of this study is to investigate the anti-asthmatic effects of DA-9201, an ethanolic extract of black rice (Oryza sativa L. var japonica), on an ovalbumin (OVA)-induced mouse model of asthma. Balb/c mice immunized with OVA were administered with DA-9201 (30, 100 or 300 mg/kg, p.o.) or dexamethasone (3 mg/kg, p.o.) and challenged with 1% aerosolized OVA for 30 min. The effects on airway inflammation, airway hyperresponsiveness (AHR), antibody profiles and cytokines were evaluated. DA-9201 treatment significantly reduced the number of eosinophils in bronchoalveolar lavage fluid (BALF) and ameliorated the AHR. Lung histological features also showed that DA-9201 reduced airway inflammation. Furthermore, DA-9201 treatment decreased IFN-gamma as well as IL-4, IL-5 and IL-13 levels in the supernatant of cultured splenocytes, and suppressed the level of OVA-specific IgG, IgG2a, IgG1 and total IgE in plasma. DA-9201 showed anti-asthmatic effects by suppressing unnecessary immune responses, airway inflammation, eosinophilia, AHR and IgE level. These results suggest DA-9201 might be beneficial for the treatment of asthma.

Animals↗

PubMed2000

In vivo biodistribution of a humanized anti-Lewis Y monoclonal antibody (hu3S193) in MCF-7 xenografted BALB/c nude mice.

The biodistribution characteristics of a humanized anti-Lewis(y) antibody (hu3S193) radiolabeled to three radioisotopes, 125I, 111In, and 90Y, were examined in a BALB/c nude mouse xenograft model of breast cancer. The immunoreactivity of both 125I- and 111In-bound hu3S193 exceeded 50% and was 20% for 90Y. In vivo, labeled antibody was shown by gamma camera imaging and immunohistochemical and autoradiographic techniques to localize to Lewis(y)-expressing breast xenografts with minimal normal tissue uptake. Maximal radioisotope uptake peaked at 48 h for all three isotopes; however, the percentage of injected dose/gram and tumor retention were greater for 111In- and 90Y-bound antibody than for 125I-bound antibody. Although immunoreactivity of 111In- and 125I-labeled hu3S193 in serum was stable over a 5-day period, the amount of unlabeled 111In in serum was lower than 125I, which together with higher tumor uptake indicates better retention of 111In-labeled hu3S193 and catabolites within the tumor cells. Superior tumor uptake and retention of 111In-labeled hu3S193 and similar blood clearance compared with 125I-labeled hu3S193, suggest that radiometals are the preferred radioisotope for this antibody-antigen system. Humanized 3S193 is a promising new construct for the targeting and potential therapy of Lewis(y)-expressing tumors.

Adenocarcinoma↗

PubMed2000

Pyelonephritic potential of Pseudomonas aeruginosa in ascending mouse model.

The suitability of female BALB/c and Swiss Webster (LACA) strains of mice for an ascending model of pyelonephritis for human uroisolate of Pseudomonas aeruginosa, was assessed. A fresh isolate of Ps. aeruginosa elaborating virulence factors like elastase, protease, phospholipase C, pyochelin and haemolysin was selected and introduced transuretherally in mice without any manipulation of the urinary tract. This isolate was able to colonize and persist in the renal tissue till day 12 post infection. Histopathologically, severe renal lesions i.e., abscesses formation was observed. The LACA strain was found to be more susceptible to infection with the selected Ps. aeruginosa isolate.

Animals↗

PubMed2003

Novel vitamin E analogue decreases syngeneic mouse mammary tumor burden and reduces lung metastasis.

A nonhydrolyzable ether analogue of RRR-alpha-tocopherol, 2,5,7,8-tetramethyl-2R-(4R, 8R, 12-trimethyltridecyl)chroman-6-yloxyacetic acid, called RRR-alpha-tocopheryloxyacetic acid or RRR-alpha-tocopherol ether-linked acetic acid analogue (alpha-TEA), exhibits antitumor activity in vitro and in vivo using a syngeneic BALB/c mouse mammary tumor model (line 66 clone 4 stably transfected with green fluorescent protein). Treatment of cells with 5, 10, and 20 micro g/ml alpha-TEA for 3 days produced 6, 34, and 50% apoptosis, respectively, and treatment of cells with 10 micro g/ml for 2, 3, 4, and 5 days produced 20, 35, 47, and 58% apoptosis, respectively. A liposomal formulation of alpha-TEA administered by aerosol reduced s.c. tumor growth and lung metastasis. Alpha-TEA-treated animals showed a significant decrease in tumor volumes over 17 days of aerosol treatment (P < 0.001). Forty percent of aerosol as well as untreated control mice had visible, macroscopic lung metastases versus none (0%) of the alpha-TEA-treated mice. On the basis of fluorescence microscopic examination of the surface (top and bottom) of flattened whole left lung lobes, an average of 60 +/- 15 and 102 +/- 17 versus 11 +/- 4 fluorescent microscopic metastases was observed in aerosol control and untreated control versus alpha-TEA-treated animals, respectively. Alpha-TEA formulated in ethanol + peanut oil (5 mg/mouse/day) delivered by gavage did not reduce s.c. primary tumor burden; however, fluorescent microscopic lung metastases were significantly reduced (P < 0.0021). In summary, alpha-TEA formulated in liposomes and delivered by aerosol is a potent antitumor agent and reduces lung metastasis.

Administration, Oral↗

PubMed1998

[Effect of adenosine on intravascular accumulation of leukocytes and tissue damage in striated muscle in endotoxemia].

Under the experimental conditions of endotoxinemia, the therapeutic use of an intravenous infusion of adenosine (110 micrograms x kg-1 x min-1) has been investigated in the microcirculation model of the BALB/c mouse. Injection of S. abortus-equi endotoxin (2 mg x kg-1 body wt. i.v.) elicited a significant increase of sticking leukocytes in postcapillary venules of striated skin muscle, which was associated with a swelling of microvascular endothelium and striated skin muscle. Infusion of adenosine effectively attenuated the endotoxin induced enhancement of leukocyte sticking and preserved microvascular endothelial and striated muscle integrity. These results imply the use of adenosine as therapeutic concept during endotoxinemia.

Adenosine↗

PubMed2005

Neovastat (AE-941) inhibits the airway inflammation and hyperresponsiveness in a murine model of asthma.

Matrix metalloproteinase (MMP)-9 plays an important role in the pathogenesis of bronchial asthma. Neovastat, having significant antitumor and antimetastatic properties, is classified as a naturally occurring multifunctional antiangiogenic agent. We evaluated the therapeutic effect of Neovastat on airway inflammation in a mouse model of asthma. BALB/c mice were immunized subcutaneously with ovalbumin (OVA) on days 0, 7, 14, and 21 and challenged with inhaled OVA on days 26, 29, and 31. Neovastat was administrated by gavage (5 mg/kg body weight) three times with 12 h intervals, beginning 30 min before OVA inhalation. On day 32, mice were challenged with inhaled methacholine, and enhanced pause (Penh) was measured as an index of airway hyperresponsiveness. The severity of airway inflammation was determined by differential cell count of bronchoalveolar lavage (BAL) fluid. The MMP-9 concentration in BAL fluid samples was measured by ELISA, and MMP-9 activity was measured by zymography. The untreated asthma group showed an increased inflammatory cell count in BAL fluid and Penh value compared with the normal control group. Mice treated with Neovastat had significantly reduced Penh values and inflammatory cell counts in BAL fluid compared with untreated asthmatic mice. Furthermore, mice treated with Neovastat showed significantly reduced MMP-9 concentrations and activity in BAL fluid. These results demonstrate that Neovastat might have new therapeutic potential for airway asthmatic inflammation.

Airway Resistance↗

PubMed2005

[RNA interference inhibits replication and expression of hepatitis B virus in mice].

OBJECTIVE: To develop a mouse model of acute hepatitis B virus infection and to observe the RNA interference-mediated inhibition of HBV replication and expression in the mouse model. METHODS: Thirty Balb/c mice were randomly divided into 5 equal groups: group A to be injected with pHBV1.3, naked plasmid containing 1.3 time HBV ayw type whole genome eukaryotic expression vector, via the caudal vein as infection group; group B to be injected with pHBV1.3 and pSI-C, plasmid expressing HBV-C specific short hairpin RNA, as interference group; group C to be injected with pHBV1.3 and pSI-C mut, a mutant RNAi vector, as mutant interference group; group D to be injected with pHBV1.3 and pGFP, siRNA transcription vector targeting green fluorescence protein (GFP); and group E to be injected with PBS as blank controls. Six days after blood was collected and the mice were killed and their livers were taken out. ELISA was used to measure the concentration of HBsAg in the serum. Immunohistochemistry and RT-PCR were used to detect the expression of HBcAg and HBV C mRNA in the liver. RESULTS: Three days after injection the HBsAg expression in the sera of the infection group was strongly positive. Six days after injection expression of HBsAg was negative in the interference group and blank control group, and was positive in the infection group, mutant interference group, and irrelevant group, however, with significantly lower OD values in the latter 2 groups compared with in the infection group (both P < 0.05). Six days after injection immunohistochemistry showed that HBcAg expression in liver was positive in the infection group, weakly positive in the mutant interference group and irrelevant interference group, and was negative in the blank control group and interference group. RT-PCR showed clear expression of HBV C mRNA in the infection group, mutant interference group, and irrelevant interference. CONCLUSION: RNAi technique specifically and effectively inhibits the replication and expression of HBV. siRNA has significant potential to become a new type antiviral drug. The establishment of an animal model of acute HBV infection in mice by hydrodynamic injection of naked plasmid has solved, to a certain degree, the problem of lack of appropriate animal model of HBV infection.

Animals↗

PubMed2006

Effects of cytotoxic T lymphocyte antigen 4 (CTLA4) signaling and locally applied steroid on retinal dysfunction by recoverin, cancer-associated retinopathy antigen.

PURPOSE: To assess the cytotoxic T lymphocyte antigen 4 (CTLA4) pathway in the recoverin peptide (R64; AYAQHVFRSF) mouse model of cancer-associated retinopathy (CAR) and to assess the protective effects of subconjunctival triamcinalone injections in this model. METHODS: To study the role of the CTLA4 pathway on the R64-induced mouse model of CAR, BALB/c mice were immunized with R64. The mice were further intraperitoneally treated with anti-CTLA4 antibody to get stronger immunoreaction. The development of CAR was evaluated by electroretinogram (ERG) examinations 21 days after treatment. A cytotoxicity assay was employed to detect induction of R64-specific cytotoxic T lymphocytes (CTLs). Immunoblotting to assess the development of anti-recoverin antibody and a T cell proliferation assay to determine the activity of lymphocytes against R64 were examined in two experimental groups, anti-CTLA4 antibody treated and untreated mice.To study the protective effect of subconjunctival triamcinalone in this model, mice immunized with R64 peptide and anti-CTLA4 antibody were either treated with 50 mg/kg/body weight of triamcinalone or phosphate buffered saline (PBS). These mice were assayed using ERG and histological examination 35 days after the first R64 immunization. RESULTS: When mice were challenged with R64 peptide and anti-CTLA4 antibody, R64 peptide-specific CTLs were induced and decreased b-wave amplitudes were observed in ERG. Conversely, no CAR symptoms were detected in mice not treated with anti-CTLA4 antibody. Anti-CTLA4 antibody treatment did not give any significant differences in T cell proliferation and humoral reaction against recoverin. Subconjunctival triamcinalone treated mice show a trend toward improved survival of outer nuclear layer cell bodies, but did not show significant improvement of ERG amplitudes compared to the untreated mice. CONCLUSIONS: Inhibition of the CTLA4 pathway is essential for the development of recoverin-induced murine CAR, suggesting that strengthening negative T cell signaling through CTLA4 may lessen the retinal degenerations in CAR-affected subjects. The positive effects of attenuation of the CTLA4 pathway must be weighed against a potential negative effect on survival since this pathway may also provide natural immunotherapy against the underlying malignancy. Subconjunctival injections of triamcinalone may have beneficial effects on the integrity of the outer nuclear layer (ONL) of the retina in the CAR model, although there was no significant effect on the ERG recordings.

Animals↗

PubMed1993

Specific V beta T cell subsets mediate the immediate hypersensitivity response to ragweed allergen.

T and B cell responses after sensitization to ragweed (RW) were examined in a mouse model in which BALB/c mice were exposed to the allergen by ultrasonic nebulization. Sensitization resulted in the stimulation of an IgE anti-RW response and was paralleled by a rise in IgG1 anti-RW titers. Skin testing for immediate cutaneous hypersensitivity revealed the presence of allergic type I reactions to RW. Sensitization to RW in this way was also associated with the development of increased airways responsiveness as determined by electrical field stimulation of preparations of tracheal smooth muscle. Histologic examination of the airways and the lung indicated the presence of a mononuclear cell infiltrate in the mucosa and submucosa of the airways that was accompanied by an enlargement of local draining lymph nodes of the airways and the lung. T cell populations were analyzed for the frequency of V beta-expressing T cells. Such analysis indicated that RW sensitization stimulated the expression of V beta 8.1+, V beta 8.2+, and V beta 13+ T cells in the local lymphoid tissue and of V beta 8.1+, V beta 8.2+, V beta 8.3+, V beta 9+ and V beta 14+ T cells in the spleen. Co-culture of these T cell populations with RW-primed B cells indicated that in the presence of RW, V beta 8.2 T cells stimulated IgE and IgG1 production, whereas the other T cell populations showed a different stimulation profile for Ig isotypes and IgG subclasses. The transfer of V beta 8.2 T cells from sensitized but not from nonsensitized control mice stimulated an allergen-specific IgE and IgG1 response and increased airways responsiveness in naive recipients. These data provide additional support for the pivotal role of specific V beta-expressing T cell subpopulations in the stimulation of IgE/IgG1 production and increased airways responsiveness.

Aerosols↗

PubMed2004

Development of a model of seizure-induced hippocampal injury with features of programmed cell death in the BALB/c mouse.

Although mice are amenable to gene knockout, they have not been exploited in the setting of seizure-induced neurodegeneration due to the resistance to injury of key mouse strains. We refined and developed models of seizure-induced neuronal death in the C57BL/6 and BALB/c strains by focally evoking seizures using intra-amygdala kainic acid. Seizures in adult male BALB/c mice, or C57BL/6 mice as reference, caused ipsilateral death of CA1 and CA3 neurons within the hippocampus. Termination of seizures by lorazepam was more effective than diazepam in both strains, largely restricting neuronal loss to the CA3 sector. Electroencephalography (EEG) recordings defined injurious and non-injurious seizure patterns, which could not be separated adequately by behavioral observation alone. Degenerating neurons in the hippocampus were positive for DNA fragmentation and approximately a third of these exhibited morphologic features of programmed cell death. Western blot analysis revealed the cleavage of caspase-8 after seizures in both strains. These data refine our C57BL/6 model and establish a companion model of focally evoked limbic seizures in the BALB/c mouse that provides further evidence for activation of programmed cell death after seizures.

Animals↗

PubMed2003

Characterization of transmission of Pneumocystis carinii f. sp. muris through immunocompetent BALB/c mice.

By using mouse models, it has been shown that Pneumocystis carinii f. sp. muris can be transmitted to immunocompetent mice that are exposed to immunosuppressed mice with active P. carinii pneumonia. We sought to determine whether P. carinii f. sp. muris could be transmitted between normal mice. The rationale for these experiments was to demonstrate whether the normal host could serve as the reservoir of organisms that produce Pcp when the organism is acquired by the immunosuppressed host. Under the conditions of these experiments, normal mice are able to be infected by brief cohousing with P. carinii-infected SCID mice. There was active replication of organisms in the normal host such that the organism could be transmitted to other normal mice, again with active replication. Mice that had seroconverted after exposure to P. carinii-infected SCID mice were more resistant to infection when reexposed. Infection in normal mice was well tolerated with minimal effects on dynamic lung compliance. We speculate, based on these results, that transmission from normal host to normal host, as an asymptomatic or minimally symptomatic infection, could be a way to maintain this opportunistic pathogen in the environment.

Animals↗

PubMed1984

Carcinoembryonic antigen production, secretion, and kinetics in BALB/c mice and a nude mouse-human tumor model.

Carcinoembryonic antigen (CEA) is currently being used as a target antigen in the radioimmunodetection of cancer. Circulating CEA may adversely affect the outcome of such studies by formation of intravascular immune complexes. The following studies were undertaken to expand our knowledge of the production, secretion, and pharmacokinetics of CEA, since these factors should have a direct bearing on the serum levels of CEA encountered in radioimmunodetection. The production of CEA was assessed in nude mice given implants of the T-380 CEA secreting human colon tumor. Serum CEA rose linearly as the tumors enlarged; however, the concentration of CEA per g of extracted tumor remained constant throughout the weight range studied. The secretory rate of the T-380 tumor was determined by surgically removing all blood flow to the liver and gastrointestinal tract of the nude mouse model. This procedure removes the known sites of CEA degradation. Serum CEA levels rose progressively following surgery, the values being directly related to the tumor size. The secretory rate was also proportional to tumor size but was a constant 13.8 +/- 3.6 (S.D.) ng/g tumor/hr when expressed on a per g tumor basis. To determine if the serum levels of CEA observed in patients could be due to unique differences in the clearance rates of each patient's CEA, serum from three patients with CEA levels of 2150, 709, and 58 ng/ml was administered i.v. to groups of mice at the original and diluted concentrations. The kinetics of all samples followed a single exponential clearance pattern with a half-time of about 2.5 hr. This was dramatically different from the kinetics of tumor-extracted CEA which exhibited a multiexponential pattern, the first component having a half-time of 3 min. These data suggest that CEA secreted by a tumor is in some way different from that adhering to the tumor. If the secreted CEA truly has a monoexponential clearance with a fixed rate as the experiments suggest, the absolute values of serum CEA are either entirely a function of the tumor secretory rate, or else the product having the short half-time is not measured in serum samples obtained from patients.

Animals↗

PubMed2002

Dermal infection with vaccinia virus reveals roles for virus proteins not seen using other inoculation routes.

Previously, we developed a model for testing the virulence and immunogenicity of vaccinia virus (VV) mutants based on the intradermal injection of BALB/c mouse ear pinnae. The model is characterized by a local infection in the inoculated skin without signs of systemic illness, mimicking dermal vaccination with VV. Here a further characterization of this model is presented, including the responses of mice to infectious virus doses as low as 10 p.f.u., a quantification of the infiltrate at the site of infection and use of different virus and mouse strains. The model was then used to compare the pathogenesis of six mutants of VV strain Western Reserve (WR) lacking genes A36R, A40R, A44L, B12R, B13R or B15R with that of appropriate control viruses. All of these genes except B12R and B15R influence the outcome of dermal infection with WR and for A40R and B13R this is the first role that has been reported after infection of mammals. A comparison of new and published results from intradermal and intranasal models is presented, showing that out of 16 gene deletion or insertion mutants of VV, half have phenotypes distinct from controls in only one of these models. Thus, the intranasal and intradermal models are complementary tools for dissecting the genetic basis of VV virulence.

Age Factors↗

PubMed2002

Major histocompatibility complex controls susceptibility and dominant inheritance, but not the severity of the disease in mouse models of rheumatoid arthritis.

Collagen-induced arthritis (CIA) in DBA/1 and proteoglycan-induced arthritis (PGIA) in BALB/c mice are the most frequently used mouse models for studying clinical, immunological and genetic factors contributing to rheumatoid arthritis. DBA/1 ( H2(q)) mice are susceptible to CIA but resistant to PGIA, whereas BALB/c mice ( H2 (d)) are susceptible to PGIA and resistant to CIA. To gain insight into the mechanisms of how the major clinical (disease susceptibility, severity and onset of arthritis) and immunological traits (antigen-specific T- and B-cell responses) are influenced by the major histocompatibility complex (MHC), we have generated a unique intercross of BALB/c and DBA/1 parent strains, and the F1 and F2 hybrids were immunized for either CIA or PGIA. The major clinical and immunological traits were identified as either binary (qualitative) or quantitative traits on Chromosome 17 with a peak at MHC when the entire population was analyzed. In contrast, when only arthritic (susceptible) mice were selected and analyzed, the major clinical traits (severity and onset) 'lost' the linkage to MHC. Thus, MHC dictates disease susceptibility, but not the severity of arthritis. This was even more evident in the case of the H2(q) allele, which was clearly responsible for the dominant inheritance of arthritis in F2 hybrids (either CIA or PGIA). In conclusion, while certain MHC alleles strongly affect disease susceptibility and determine the mode of inheritance of a polygenic autoimmune disease, neither the type of inheritance (dominant vs recessive) nor other MHC components have evident effects upon the clinical symptoms of arthritis.

Animals↗

PubMed1984

Effects of cefotaxime, clindamycin, mezlocillin, and piperacillin on mouse sarcoma L-1 tumor.

For the study described in the paper, the effects of 10 days' chemotherapy with cefotaxime, clindamycin, mezlocillin, and piperacillin on local tumor growth and on spontaneous or artificial metastatic spread into the lungs were studied. For the animal tumor model Balb/c mice and the mouse sarcoma L-1 tumor were used. Chemotherapy was administered before, immediately after, or some time after the injection of tumor cells. The antibiotic dosage given to mice was calculated on a body weight basis from the doses recommended for humans. Cefotaxime and clindamycin did not influence the animal tumor model, whereas mezlocillin and piperacillin showed positive or negative effects depending on the chemotherapy schedule. In vitro none of the four antibiotics caused cytotoxic activity in cell cultures of mouse sarcoma L-1, human lung cancer E-14, or human malignant melanoma MEW.

Animals↗

PubMed1994

Human immunodeficiency virus-1 reverse transcriptase immunodominant CD4+ T cell epitopes: a peptide-based multiparametric assessment in the mouse.

We previously identified an immunodominant CD4+ T cell determinant in the carboxy-terminal region of HIV-1 reverse transcriptase (RT528-543). The present study aimed at enumerating all the potential sites of HIV-1 RT recognized by Th cells in the BALB/c (H-2d) mouse model. To achieve this we used a panel of 62 overlapping 15-mer synthetic peptides covering the whole RT sequence to assay the following parameters: (i) immunogenicity in naive BALB/c mice injected either with peptides pools or individual peptides; (ii) antigenicity, as detected by their ability to restimulate in vitro T cells from BALB/c mice primed with native RT; (iii) MHC class II (Ad)-binding capacity as measured by the inhibition of the antigen-specific, Ad-restricted presentation of unfolded apamin (4-Acm) by fixed antigen-presenting cells to Ad/4-Acm-specific, interleukin-2-producing T hybridoma cells; and (iv) the presence of typical or degenerate consensus Ad-binding motifs. The results in this study permitted identification of three novel immunodominant RT mouse CD4+ T cell sites (RT276-290, RT375-389 and RT411-425) located in regions of limited polymorphism among RT from several HIV isolates. Some of these RT segments were found to be in the vicinity of B cell or H-2Kk- or HLA-A2-restricted cytotoxic T lymphocyte epitopes. Finally, the approach used in this study was found to be very efficient for enumerating most T cell recognition sites in a complex protein, a result that would have not been achieved by a single parameter-based analysis.

Amino Acid Sequence↗

PubMed2005

Effects of orally administered bovine lactoferrin and lactoperoxidase on influenza virus infection in mice.

Milk contains a wide variety of host protective factors against infectious microbes. Among these protective factors, lactoferrin (LF) and lactoperoxidase (LPO) have been reported to exhibit antiviral activities as well as immuno-modulatory effects. In the present study, the effects of orally administered LF and LPO were assessed in a mouse influenza virus infection model. BALB/c mice were intranasally infected with 6.6x10(2) p.f.u. of influenza virus A/PR/8/34(H1N1). Bovine LF or LPO was administered once daily at a dose of 62.5 mg per mouse by gavage, starting 1 day before infection. Mice given LF or LPO showed a significantly lower lung consolidation score on day 6 after infection compared with the control mice that were given water instead. Concurrently, the number of infiltrated leukocytes recovered from bronchoalveolar lavage fluid (BALF) on day 6 was significantly lower in mice given LF or LPO. However, the virus yield in the BALF was not affected by these treatments. The serum level of IL-6, a pro-inflammatory cytokine, positively correlated with the lung consolidation score in each group and was significantly lower on day 6 in the mice given LPO. These results suggest the potential of oral administration of LF or LPO to attenuate pneumonia in influenza-virus-infected mice through the suppression of infiltration of inflammatory cells in the lung.

Administration, Oral↗