RESUMO
Bothrops jararaca venom (BjV) can induce mast cell degranulation. In order to investigate the role of mast cells and the interference of the host genetic background in the inflammation induced by BjV, we have used mouse strains selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory response (AIR). Mice were pretreated with an inhibitor of mast cell degranulation, cromolyn (CROM), and injected in footpads or intraperitoneally (i.p.) with BjV. Pain was measured with von Frey hairs, cell migration in the peritoneum by flow cytometry, and reactive oxygen species (ROS) production by chemiluminescence assays. The nociceptive response to BjV was higher in AIRmax than AIRmin mice; however, this difference was abolished by pretreatment with CROM. BjV induced peritoneal neutrophil (CD11b+ GR-1+) infiltration and ROS secretion in AIRmax mice only, which were partially inhibited by CROM. Our findings evidence a role for mast cells in pain, neutrophil migration, and ROS production triggered by BjV in AIRmax mice that are more susceptible to the action of BjV.
Assuntos
Bothrops , Venenos de Crotalídeos , Animais , Movimento Celular , Venenos de Crotalídeos/efeitos adversos , Inflamação/induzido quimicamente , Mastócitos , Camundongos , Dor , Espécies Reativas de OxigênioRESUMO
Mouse lines selected for maximal (AIRmax) or minimal acute inflammatory reaction (AIRmin) were used to characterize the immune response and the influence of genetic background during pristane-induced arthritis (PIA). Susceptible AIRmax mice demonstrated exacerbated cellular profiles during PIA, with intense infiltration of lymphocytes, as well as monocytes/macrophages and neutrophils, producing higher levels of IL-1ß, IFN-γ, TNF-α, IL-10, total IgG3, and chemokines. Resistant AIRmin mice controlled cell activation more efficiently than the AIRmax during arthritis progression. The weight alterations of the spleen and thymus in the course of PIA were observed. Our data suggest that selected AIRmax cellular and genetic immune mechanisms contribute to cartilage damage and arthritis severity, evidencing many targets for therapeutic actions.
Assuntos
Artrite Experimental/imunologia , Citocinas/imunologia , Imunoglobulina G/imunologia , Terpenos/efeitos adversos , Doença Aguda , Animais , Artrite Experimental/induzido quimicamente , Artrite Experimental/genética , Artrite Experimental/patologia , Citocinas/genética , Imunoglobulina G/genética , Inflamação , Camundongos , Baço/imunologia , Baço/patologia , Terpenos/farmacologia , Timo/imunologia , Timo/patologiaRESUMO
OBJECTIVE AND DESIGN: Pristane-induced arthritis (PIA) in AIRmax mice homozygous for Slc11a1 R and S alleles was used to characterize the influence of Slc11a1 gene polymorphism on immune responses during disease manifestation. Previous reports demonstrated that the presence of the Slc11a1 S allele increased the incidence and severity of PIA in AIRmax SS , suggesting that this gene could interact with inflammatory loci to modulate PIA. We investigated the effects of Slc11a1 alleles on the activation of phagocytes during PIA. TREATMENT: Mice were injected intraperitoneally with two doses of 0.5 mL of mineral oil pristane at 60-day intervals. Arthritis development was accompanied for 180 days. RESULTS: AIRmax SS mice showed differential peritoneal macrophage gene expression profiles during PIA, with higher expression and production of H2O2, NO, IL-1ß, IL-6, TNF-α, and several chemokines. The presence of the Slc11a1 R allele, on the other hand, diminished the intensity of macrophage activation, restricting arthritis development. CONCLUSION: Our data demonstrated the fine-tuning roles of Slc11a1 alleles modulating macrophage activation, and consequent PIA susceptibility, in those mouse lines. (AU)
Assuntos
Animais , Artrite Reumatoide/genética , Inflamação/genética , Polimorfismo Genético , Artrite Experimental , Expressão Gênica , Citocinas , Macrófagos , CamundongosRESUMO
OBJECTIVE AND DESIGN: Pristane-induced arthritis (PIA) in AIRmax mice homozygous for Slc11a1 R and S alleles was used to characterize the influence of Slc11a1 gene polymorphism on immune responses during disease manifestation. Previous reports demonstrated that the presence of the Slc11a1 S allele increased the incidence and severity of PIA in AIRmax SS , suggesting that this gene could interact with inflammatory loci to modulate PIA. We investigated the effects of Slc11a1 alleles on the activation of phagocytes during PIA. TREATMENT: Mice were injected intraperitoneally with two doses of 0.5 mL of mineral oil pristane at 60-day intervals. Arthritis development was accompanied for 180 days. RESULTS: AIRmax SS mice showed differential peritoneal macrophage gene expression profiles during PIA, with higher expression and production of H2O2, NO, IL-1ß, IL-6, TNF-α, and several chemokines. The presence of the Slc11a1 R allele, on the other hand, diminished the intensity of macrophage activation, restricting arthritis development. CONCLUSION: Our data demonstrated the fine-tuning roles of Slc11a1 alleles modulating macrophage activation, and consequent PIA susceptibility, in those mouse lines.
Assuntos
Artrite Experimental/genética , Artrite Experimental/imunologia , Artrite Reumatoide/genética , Artrite Reumatoide/imunologia , Proteínas de Transporte de Cátions/genética , Proteínas de Transporte de Cátions/imunologia , Macrófagos Peritoneais/imunologia , Animais , Artrite Experimental/patologia , Artrite Reumatoide/patologia , Citocinas/sangue , Citocinas/imunologia , Feminino , Peróxido de Hidrogênio/imunologia , Articulações/patologia , Masculino , Camundongos , Óxido Nítrico/imunologia , Terpenos , TranscriptomaRESUMO
Trypanosoma cruzi infection was studied in mouse lines selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory reaction and for high (HIII) or low (LIII) antibody (Ab) responses to complex antigens. Resistance was associated with gender (females) and strain-the high responder lines AIRmax and HIII were resistant. The higher resistance of HIII as compared to LIII mice extended to higher infective doses and was correlated with enhanced production of IFN-γ and nitric oxide production by peritoneal and lymph node cells, in HIII males and females. We also analyzed the involvement of previously mapped Ab and T. cruzi response QTL with the survival of Selection III mice to T. cruzi infections in a segregating backcross [F1(HIII×LIII) ×LIII] population. An Ab production QTL marker mapping to mouse chromosome 1 (34.8 cM) significantly cosegregated with survival after acute T. cruzi infections, indicating that this region also harbors genes whose alleles modulate resistance to acute T. cruzi infection.
Assuntos
Doença de Chagas/genética , Doença de Chagas/imunologia , Ligação Genética/genética , Locos de Características Quantitativas/genética , Trypanosoma cruzi/patogenicidade , Animais , Formação de Anticorpos/genética , Formação de Anticorpos/fisiologia , Feminino , Masculino , Camundongos , Trypanosoma cruzi/imunologiaRESUMO
AIRmax (maximal inflammation) and AIRmin (minimal inflammation) mice show distinct susceptibilities to pristane-induced arthritis (PIA). The Slc11a1 gene, which regulates macrophage and neutrophil activity, is involved in this infirmity. AIRmax (SS) mice homozygous for the non-functional Slc11a1 S (gly169asp) allele obtained by genotype-assisted crosses from AIRmax and AIRmin mice are more susceptible than mice homozygous for the Slc11a1 resistant (R) allele. The present work sought to identify the quantitative trait loci (QTL) regulating PIA and to examine the interactions of these QTL with Slc11a1 alleles in modulating PIA. Mice were given two ip injections of 0.5 mL pristane at 60 day intervals, and the incidence and severity of PIA was scored up to 160 days. Genome-wide linkage studies were performed to search for arthritis QTL in an F2 (AIRmax × AIRmin, nâ=â290) population. Significant arthritis QTL (LODscore>4) were detected on chromosomes 5 and 8, and suggestive QTL on chromosomes 7, 17 and 19. Global gene expression analyses performed on Affymetrix mouse 1.0 ST bioarrays (27k genes) using RNA from arthritic or control mice paws showed 419 differentially expressed genes between AIRmax and AIRmin mice and demonstrated significantly (P<0.001) over-represented genes related to inflammatory responses and chemotaxis. Up-regulation of the chemokine genes Cxcl1, Cxcl9, Cxcl5, Cxcl13 on chromosome 5 was higher in AIRmax(SS) than in the other lines. Macrophage scavenger receptor 1 and hemeoxigenase (decycling) 1 genes on chromosome 8 were also expressed at higher levels in AIRmax(SS) mice. Our results show that the gene expression profiles of the two arthritis QTL (on chromosomes 5 and 8) correlate with Slc11a1 alleles, resulting in enhanced AIRmax(SS) mice susceptibility to PIA.
Assuntos
Artrite/genética , Proteínas de Transporte de Cátions/genética , Locos de Características Quantitativas , Alelos , Animais , Artrite/induzido quimicamente , Suscetibilidade a Doenças , Feminino , Inflamação/induzido quimicamente , Inflamação/genética , Masculino , Camundongos , Terpenos , TranscriptomaRESUMO
High inflammatory AIRmax mice homozygous for Slc11a1 R and S alleles were produced. AIRmaxSS mice showed faster ear tissue regeneration than AIRmaxRR mice, suggesting that the Sallele favored tissue restoration. Here, we investigated the gene expression profiles and the inflammatory reactions of AIRmaxRR and AIRmaxSS mice during the initial phase of ear tissue regeneration. We observed superior levels of analysis of wound myeloperoxidase and edema inAIRmaxSS mice, although similar cell influx was verified in both lines. Of the genes, 794 were up- and 674 down-regulated in AIRmaxRR, while 735 genes were found to be up- and 1616 down-regulated in AIRmaxSS mice 48 h after punch. Both mouse lines showed significant over-represented genes related to cell proliferation; however AIRmaxSS displayed up-regulation of inflammatory response genes. Quantitative PCR experiments showed higher expressions of Tgfb1, Dap12 and Trem1 genes in AIRmaxSS mice. These results indicate that Slc11a1 gene modulated the early inflammatory events of ear tissue regeneration.
Assuntos
Camundongos , Inflamação/genética , Inflamação/imunologia , Regeneração/genética , Regeneração/imunologia , Alelos , Modulação Antigênica/genética , Modulação Antigênica/imunologiaRESUMO
High inflammatory AIRmax mice homozygous for Slc11a1 R and S alleles were produced. AIRmax(SS) mice showed faster ear tissue regeneration than AIRmax(RR) mice, suggesting that the S allele favored tissue restoration. Here, we investigated the gene expression profiles and the inflammatory reactions of AIRmax(RR) and AIRmax(SS) mice during the initial phase of ear tissue regeneration. We observed superior levels of analysis of wound myeloperoxidase and edema in AIRmax(SS) mice, although similar cell influx was verified in both lines. Of the genes, 794 were up- and 674 down-regulated in AIRmax(RR), while 735 genes were found to be up- and 1616 down-regulated in AIRmax(SS) mice 48 h after punch. Both mouse lines showed significant over-represented genes related to cell proliferation; however AIRmax(SS) displayed up-regulation of inflammatory response genes. Quantitative PCR experiments showed higher expressions of Tgfb1, Dap12 and Trem1 genes in AIRmax(SS) mice. These results indicate that Slc11a1 gene modulated the early inflammatory events of ear tissue regeneration.
Assuntos
Proteínas de Transporte de Cátions/genética , Proteínas de Transporte de Cátions/fisiologia , Inflamação/genética , Inflamação/fisiopatologia , Regeneração/genética , Regeneração/fisiologia , Alelos , Animais , Sequência de Bases , Primers do DNA/genética , Orelha Externa/lesões , Orelha Externa/fisiologia , Feminino , Expressão Gênica , Masculino , Camundongos , Camundongos Endogâmicos , Peroxidase/metabolismo , Locos de Características Quantitativas , Reação em Cadeia da Polimerase em Tempo Real , Cicatrização/genética , Cicatrização/fisiologiaRESUMO
AIRmax and AIRmin mouse lines show a differential lung inflammatory response and differential lung tumor susceptibility after urethane treatment. The transcript profile of approximately 24,000 known genes was analyzed in normal lung tissue of untreated and urethane-treated AIRmax and AIRmin mice. In lungs of untreated mice, inflammation-associated genes involved in pathways such as "leukocyte transendothelial migration", "cell adhesion" and "tight junctions" were differentially expressed. Moreover, gene expression levels differed significantly in urethane-treated mice; in AIRmin mice, modulation of expression of genes involved in pathways associated with inflammatory response paralleled the previously observed persistent infiltration of inflammatory cells in the lung of these mice.
Assuntos
Transformação Celular Neoplásica/genética , Neoplasias Pulmonares/genética , Pulmão/fisiologia , Pneumonia/genética , Animais , Transformação Celular Neoplásica/induzido quimicamente , Transformação Celular Neoplásica/patologia , Modelos Animais de Doenças , Feminino , Expressão Gênica/efeitos dos fármacos , Perfilação da Expressão Gênica , Predisposição Genética para Doença , Humanos , Pulmão/efeitos dos fármacos , Pulmão/patologia , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/patologia , Masculino , Camundongos , Pneumonia/induzido quimicamente , Pneumonia/patologia , UretanaRESUMO
Non-inbred AIR (AIRmax, AIRmin) and Car (Car-S, Car-R) mouse lines were generated from the same eight inbred mice through bidirectional selective breeding for acute inflammatory response and for susceptibility to two-stage skin tumorigenesis, respectively. Because AIR lines also showed a differential predisposition to skin tumorigenesis and Car lines differed in the extent of inflammatory response, we carried out genome-wide association studies using SNP arrays to identify the genetic elements affecting skin tumor susceptibility and inflammatory response in AIR and Car lines. We found that the phenotypic outcome reflects a specific genetic profile in each mouse line, suggesting that distinct genetic elements, selected by differential genetic drifts, and exerting pleiotropic effects in each mouse population, control the skin tumor susceptibility and inflammatory response phenotypes. These findings point to the complex link between skin tumor susceptibility and inflammatory response in mice.
Assuntos
Heterogeneidade Genética , Predisposição Genética para Doença , Inflamação/genética , Papiloma/genética , Neoplasias Cutâneas/genética , 9,10-Dimetil-1,2-benzantraceno , Animais , Carcinógenos , Deriva Genética , Estudo de Associação Genômica Ampla , Inflamação/patologia , Camundongos , Infiltração de Neutrófilos , Papiloma/induzido quimicamente , Papiloma/patologia , Fenótipo , Polimorfismo de Nucleotídeo Único , Neoplasias Cutâneas/induzido quimicamente , Neoplasias Cutâneas/patologia , Acetato de TetradecanoilforbolRESUMO
AIRmax and AIRmin mouse lines show a differential lung inflammatory response and differential lung tumor susceptibility after urethane treatment. The transcript profile of 24,000 known genes was analyzed in normal lung tissue of untreated and urethane-treatedAIRmax and AIRmin mice. In lungs of untreated mice, inflammation-associated genes involved in pathways such as leukocyte transendothelial migration, cell adhesion and tight junctions were differentially expressed. Moreover, gene expression levels differed significantly in urethane-treated mice; in AIRmin mice, modulation of expression of genes involved in pathways associated with inflammatory response paralleled the previously observed persistent infiltration of inflammatory cells in the lung of these mice.
Assuntos
Animais , Ratos , Neoplasias Pulmonares , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/imunologia , Análise de Sequência com Séries de Oligonucleotídeos/métodos , Relação Dose-Resposta ImunológicaRESUMO
Non-inbred AIR (AIRmax, AIRmin) and Car (Car-S, Car-R) mouse lines were generated from the same eight inbred mice through bidirectional selective breeding for acute inflammatory response and for susceptibility to two-stage skin tumorigenesis, respectively. Because AIR lines also showed a differential predisposition to skin tumorigenesis and Car lines differed in the extent of inflammatory response, we carried out genome-wide association studies using SNP arrays to identify the genetic elements affecting skin tumor susceptibility and inflammatory response in AIR and Car lines. We found that the phenotypic outcome reflects a specific genetic profile in each mouse line, suggesting that distinct genetic elements, selected by differential genetic drifts, and exerting pleiotropic effects in each mouse population, control the skin tumor susceptibility and inflammatory response phenotypes. These findings point to the complex link between skin tumor susceptibility and inflammatory response in mice
Assuntos
Masculino , Feminino , Animais , Ratos , NeoplasiasRESUMO
Two mouse lines were phenotype-selected for maximum (AIRmax) or minimum (AIRmin) acute inflammation responses to polyacrylamide bead (Biogel) injection. These lines differ in terms of bone marrow granulopoiesis, neutrophil resistance to apoptosis, and inflammatory cytokine production during acute inflammation responses. We compared gene expression profiles in bone marrow cells (BMC) of AIRmax and AIRmin mice during acute inflammatory reactions. The BMC from femurs were recovered 24 hr after subcutaneous injections of Biogel. Global gene expression analysis was performed on CodeLink Bioarrays (36K genes) using RNA pools of BMC from both control and treated AIRmax and AIRmin mice. Differentially expressed genes were statistically established and the over-represented gene ontology biological process categories were identified. Upregulations of about 136 and 198 genes were observed in the BMC of Biogel-treated AIRmax and AIRmin mice, respectively, but 740 genes were found to be downregulated in AIRmin mice compared with 94 genes in AIRmax mice. The over-represented biological themes of the differently expressed genes among AIRmax and AIRmin mice represent inflammatory response, signal transduction, cell proliferation and immune cell chemotaxis. We were able to demonstrate a broad downmodulation of gene transcripts in BMC from AIRmin mice during acute inflammation, and significant differentially expressed genes colocalized with previously mapped regions for inflammation-related phenotypes in chromosomes 1, 3, 6 and 11.
Assuntos
Células da Medula Óssea/imunologia , Inflamação/genética , Resinas Acrílicas/farmacologia , Doença Aguda , Animais , Regulação para Baixo , Feminino , Perfilação da Expressão Gênica , Inflamação/induzido quimicamente , Inflamação/imunologia , Masculino , Camundongos , Análise de Sequência com Séries de Oligonucleotídeos , Regulação para CimaRESUMO
We tested the role of aryl hydrocarbon receptor (Ahr) gene polymorphism in the inflammatory response and in skin and lung tumorigenesis in 2 lines of mice phenotypically selected for maximum or minimum acute inflammatory reaction (AIRmax and AIRmin, respectively). Following 7,12-dimethylbenz[a]anthracene (DMBA) treatment, AIRmin but not AIRmax mice showed early skin reactions and eventually developed malignant skin tumors and lung adenocarcinomas. In skin tissue, transcript levels of IL1beta, Tnf, Il6, Tgfbeta1 and Cyp1b1 genes were upregulated in AIRmin but not AIRmax mice, consistent with the inflammatory responses to the carcinogen. These findings appeared to be related to the homozygosity status of the Ahr functional A375V polymorphism, which influences the binding capability of the receptor for DMBA: the 375A allele, encoding the high-affinity ligand-binding receptor (Ahr(b1)), segregated in AIRmin mice, whereas AIRmax mice carried the 375V, corresponding to the low-affinity binding receptor (Ahr(d)), to DMBA. The differential segregation of Ahr functional Ahr(d)versus Ahr(b1) alleles in AIRmax and AIRmin suggests a role for the Ahr gene in the control of inflammatory responsiveness and tumor development of these mouse lines.
Assuntos
9,10-Dimetil-1,2-benzantraceno/toxicidade , Inflamação/genética , Neoplasias Experimentais/prevenção & controle , Polimorfismo Genético , Receptores de Hidrocarboneto Arílico/genética , Neoplasias Cutâneas/induzido quimicamente , Animais , Carcinógenos/toxicidade , Citocromo P-450 CYP1A1/genética , Primers do DNA , Inflamação/induzido quimicamente , Interferon gama/genética , Interleucina-18/genética , Interleucinas/genética , Camundongos , Neoplasias Experimentais/induzido quimicamente , Neoplasias Experimentais/genética , Fenótipo , Neoplasias Cutâneas/genética , Regulação para CimaRESUMO
The dynamics of the local inflammatory events induced by Bothrops jararaca venom (BjV) inoculation in footpad of mice genetically selected for maximal (AIRmax) and minimal (AIRmin) acute inflammatory reactivity (AIR) was investigated. The BjV injection induced a marked inflammatory cell infiltrate with predominance of neutrophils, with increased blood cell numbers before its accumulation, suggesting a stimulatory action of BjV on mechanisms of cell mobilization from bone marrow. The process of cell migration is regulated by different cell-adhesion molecules (CAM). Our results showed that neutrophil cells from both lines had the same pattern of response concerning CAMs expression, presenting the involvement of l-selectin, Mac-1 and PECAM-1 adhesion molecules in BjV-induced neutrophil accumulation. The effect of BjV on the release of pro-inflammatory cytokines and chemokines related with cellular migration was also studied and IL-1beta, IL-6, TNF-alpha and MIP-2 levels could be detected after venom injection. The AIRmax mice were shown to be more responsive than AIRmin with respect to leukocyte influx, expression of MIP-2 and release of IL-1beta and IL-6. These results demonstrate the importance of host genetic background in the local response and the involvement of alleles accumulated in AIRmax mice in the inflammatory events induced by BjV.
Assuntos
Bothrops , Moléculas de Adesão Celular/biossíntese , Venenos de Crotalídeos/toxicidade , Mediadores da Inflamação/metabolismo , Inflamação/induzido quimicamente , Leucócitos/efeitos dos fármacos , Animais , Células da Medula Óssea/efeitos dos fármacos , Moléculas de Adesão Celular/genética , Movimento Celular/efeitos dos fármacos , Quimiocinas/imunologia , Citocinas/imunologia , Imunidade Celular/efeitos dos fármacos , Inflamação/genética , Inflamação/imunologia , Leucócitos/imunologia , Camundongos , Camundongos Endogâmicos , Neutrófilos/efeitos dos fármacos , Neutrófilos/imunologiaRESUMO
The dynamics of the local inflammatory events induced by Bothrops jararaca venom (BjV) inoculation in footpad of mice genetically selected for maximal (AIRmax) and minimal (AIRmin) acute inflammatory reactivity (AIR) was investigated. The BjV injection induced a marked inflammatory cell infiltrate with predominance of neutrophils, with increased blood cell numbers before its accumulation, suggesting a stimulatory action of BjV on mechanisms of cell mobilization from bone marrow. The process of cell migration is regulated by different cell-adhesion molecules (CAM). Our results showed that neutrophil cells from both lines had the same pattern of response concerning CAMs expression, presenting the involvement of l-selectin, Mac-1 and PECAM-1 adhesion molecules in BjV-induced neutrophil accumulation. The effect of BjV on the release of pro-inflammatory cytokines and chemokines related with cellular migration was also studied and IL-1â, IL-6, TNF-á and MIP-2 levels could be detected after venom injection. The AIRmax mice were shown to be more responsive than AIRmin with respect to leukocyte influx, expression of MIP-2 and release of IL-1â and IL-6. These results demonstrate the importance of host genetic background in the local response and the involvement of alleles accumulated in AIRmax mice in the inflammatory events induced by BjV.
Assuntos
Animais , Bothrops , Mordeduras de Serpentes , Serpentes , Venenos de Serpentes , Citocinas , InflamaçãoRESUMO
We described a prophylactic and therapeutic effect of a DNA vaccine encoding the Mycobacterium leprae 65-kDa heat shock protein (DNA-hsp65) in experimental murine tuberculosis. However, high homology of the vaccine to the corresponding mammalian hsp60, together with the CpG motifs in the plasmidial vector, could trigger or exacerbate an autoimmune disease. In the present study, we evaluate the potential of DNA-hsp65 vaccination to induce or modulate arthritis in mice genetically selected for acute inflammatory reaction (AIR), either maximal (AIRmax) or minimal (AIRmin). Mice immunized with DNA-hsp65 or injected with the corresponding DNA vector (DNAv) developed no arthritis, whereas pristane injection resulted in arthritis in 62% of AIRmax mice and 7.3% of AIRmin mice. Administered after pristane, DNA-hsp65 downregulated arthritis induction in AIRmax animals. Levels of interleukin (IL)-12 were significantly lower in mice receiving pristane plus DNA-hsp65 or DNAv than in mice receiving pristane alone. However, when mice previously injected with pristane were inoculated with DNA-hsp65 or DNAv, the protective effect was significantly correlated with lower IL-6 and IL-12 levels and higher IL-10 levels. Our results strongly suggest that DNA-hsp65 has no arthritogenic potential and is actually protective against experimentally induced arthritis in mice.
Assuntos
Artrite/prevenção & controle , Proteínas de Bactérias/administração & dosagem , Chaperoninas/administração & dosagem , DNA/administração & dosagem , Modelos Animais de Doenças , Animais , Chaperonina 60 , Ensaio de Imunoadsorção Enzimática , Interleucina-12/metabolismo , CamundongosRESUMO
The effect of Bacillus Calmette-Guérin (BCG) treatment in allergic pulmonary reaction was studied in mice genetically selected accordingly to a High (H-IVA) or Low (L-IVA) antibody responsiveness. Mice were immunized with ovalbumin (OVA) or OVA plus BCG. Two days after nasal antigenic challenge, seric IgE and IgG1 anti-OVA, eosinophils in pulmonary tissue, inflammatory cells in bronchoalveolar lavage and the compliance and conductance of respiratory system were evaluated. H-IVA mice were found more susceptible than L-IVA, and BCG was able to inhibit simultaneously the production of IgE, the bronchopulmonary inflammation and bronchial hyperresponsiveness in these genetically selected mice.
Assuntos
Vacina BCG/imunologia , Hiper-Reatividade Brônquica/prevenção & controle , Hipersensibilidade/prevenção & controle , Inflamação/prevenção & controle , Pulmão/imunologia , Anafilaxia Cutânea Passiva/imunologia , Animais , Ensaio de Imunoadsorção Enzimática , Imunoglobulina E/sangue , Imunoglobulina G/sangue , Interferon gama/biossíntese , Leucócitos/fisiologia , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina/imunologia , Ratos , Ratos Endogâmicos WFRESUMO
The effect of Bacillus CalmetteGue´rin (BCG) treatment in allergic pulmonary reaction was studied in micegenetically selected accordingly to a High (H-IVA) or Low (L-IVA) antibody responsiveness. Mice wereimmunized with ovalbumin (OVA) or OVA plus BCG. Two days after nasal antigenic challenge, seric IgE andIgG1 anti-OVA, eosinophils in pulmonary tissue, inflammatory cells in bronchoalveolar lavage and the complianceand conductance of respiratory system were evaluated. H-IVA mice were found more susceptible than L-IVA, andBCG was able to inhibit simultaneously the production of IgE, the bronchopulmonary inflammation and bronchialhyperresponsiveness in these genetically selected mice.