The doctoral dissertacion is focused on the role of inflammation in the pathogenesis of preterm labor. In the first part, we describe the current view on pathophysiology of preterm labor. In the second part, we evaluated the relationship of specific markers of inflammation and endothelial dysfunction to preterm birth and fetal inflammatory response. The most important findings of our study was that we found decreased levels of MMP-2 and decreased levels of sRAGE in women with preterm labor in comparison with the control group of pregnant women. Similarly, we found decreased levels of MMP-2 in women with subsequent diagnosed fetal inflammatory response. sRAGE is currently ranked among patttern recognition receptors. In the case of sRAGE we followed the results of our pilot project, it can be assumed that the its low level are connected with tissue damage. We confirmed that it can play an important role in the pathogenesis of preterm labor. We assume abnormal regulatory mechanisms of the production of MMP-2. In both cases, however, further studies are required to elucidate the functional significance of our results.

Introduction: Hip fracture surgery is the particular problem of very old patinets (>75 years), with high risk of VTE (up to 80%). It is essential to provide VTE prophylaxis. Patients advanced age and their polymorbidity contribute to the thrombophilic status. Objectives and methods: The aim of the study was to determine the changes of coagulation within the 28 post-operative days in 41 patients over 75 years who underwent hip fracture surgery. Another object was to determine acute phase response and an endothelial activation. The third task was to determine how affected is a key component of hemostasis, FXa activity by its specific inhibitor fondaparinux and enoxaparin, which inhibits FXa and thrombin in a 4:1 ratio and if there is bleeding complication in such a risk group patiens after antithrombotics long-term administration. Patients were randomly divided into two anticoagulant groups: fondaparinux (n = 23) and enoxaparin (n = 18). Results: Thrombophilia is demonstrated by a reactive increase of the most of these parameters preoperatively and reveals the effect of the initial trauma. A surgery further aggravates this reaction. This inflammatory and secondary prothrombogenic condition persisted until postoperative day 28. Both antithrombotics effectively inhibit thrombin generation without...

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Pattern recognition receptors (e.g., S100A12 or S100A8/A9) hold promise as inflammatory biomarkers. We prospectively determined and compared serum S100A12 and S100A8/A9 concentrations in dogs with sepsis (n = 11) or systemic inflammatory response syndrome (SIRS; n = 8) over a 3-d period with each other, healthy controls (n = 50), and other clinical and clinicopathologic variables. Serum S100A12 and S100A8/A9 concentrations were significantly higher in dogs with sepsis or SIRS (all p < 0.05) at the time of hospital admission (day 1) compared to healthy controls, with no differences between patient groups. However, septic dogs had significantly lower serum S100A12 concentrations on day 2 and day 3 (both p < 0.05) compared to dogs with SIRS. Likewise, dogs with sepsis had significantly lower S100A8/A9 concentrations on day 2 (p < 0.05). Neither serum S100A12 nor S100A8/A9 concentrations were associated with survival to discharge. Our results suggest a differential expression of the S100/calgranulins between dogs with sepsis and those with SIRS. Serum S100A12 or S100A8/A9 concentration at the time of hospital admission did not differentiate dogs with sepsis from those with SIRS, but the trend of S100/calgranulin concentrations during the following 24–48 h may be a useful surrogate marker for differentiating sepsis from SIRS.

No description available.

No description available.

Co-evolution between parasites and their hosts result in extremely well-orchestrated and intimate relationships that are characterized by remarkable adaptations in the attack response of the parasite and the defense response of the host. To fully understand host-parasite interactions, these adaptations must be considered in the context of the ecological constraints in which they evolved. As a serious pest to salmon mariculture, Lepeophtheirus salmonis has been extensively studied; however, there are still several areas that require further research. Of utmost importance, and the topic of this thesis, is molecular basis for resistance to sea lice. The following chapters investigate this phenomena under the umbrella of ecological immunology using combined modern technologies of transcriptomics, proteomics and functional immunology with a focus on the primary interaction site. In the first chapter, I describe the key players involved in this host-parasite relationship with a focus on the primary interaction site, the louse-salmon interface, where there are responses by the louse (attack) and the salmon host (defense). Previous research indicated that an early aggressive inflammatory response at the louse-skin interface contributes to resistance in coho salmon; however, there are no data characterizing a site-specific response in resistant (pink and coho) and susceptible (Atlantic, chum) species. Accordingly in Chapter 2, I define site-specific cutaneous responses in Atlantic, pink and chum salmon to establish genetic biomarkers of resistance. Chapter 3 focuses on identification of cellular effectors using histochemical localization of biomarkers to characterize cellular populations activated at the louse-attachment site, while broadening the gene targets. Our notion of pink salmon as a resistant species is challenged by the common observation of migrating pink salmon supporting large populations of L. salmonis in the field. Thus the purpose of chapter 4 was to investigate potential mechanisms to explain variations in susceptibility as a function of life history. Host-parasite relationships are a product of both host and parasite responses; therefore, in chapters 5 and 6, I shift focus to the level of the parasite. In chapter 5 I present the first documented large-scale transcriptomic profiling of L. salmonis during feeding on both resistant (coho) and susceptible (Atlantic, sockeye) salmon. This was followed (chapter 6) by describing the proteomic profile of L. salmonis secretions after feeding on Atlantic salmon. In the seventh and final chapter, I present my conclusions on the molecular mechanisms for resistance to sea lice and discuss potential applications of this information for future louse control strategies. / Graduate

O herpesvirus equino tipo 1 (EHV-1) é um importante patógeno que causa doença respiratória, abortamento e desordens neurológicas em equinos. O presente estudo foi realizado visando avaliar a resposta inflamatória causada pelo EHV-1 por meio da análise das manifestações clínicas, alterações histopatológicas e resposta imune do hospedeiro no sistema nervoso central (SNC). Camundongos das linhagens BALB/c (H2d), C57BL/6 (H2b) e C3H/HeJ (H2k) foram inoculados por via intranasal com as estirpes brasileiras A4/72 e A9/92 do EHV-1. Nesse estudo, associou-se a histopatologia, a resposta de citocinas pró-inflamatórias no SNC de camundongos das diferentes linhagens e o método de transcrição reversa seguida pela reação em cadeia da polimerase quantitativa em tempo real (RT-qPCR) para investigar a relação entre a infecção pelo EHV-1 e a resposta inflamatória com o desenvolvimento de lesões. As estirpes brasileiras A4/72 e A9/92 do EHV-1 causaram infecção aguda e letal nas diferentes linhagens de camundongos isogênicos. Os sinais clínicos e neurológicos, tais como perda de peso, pelos arrepiados, postura arqueada, apatia, dispneia, desidratação e sialorreia apareceram entre o 2º e 3º dia pós-infecção (dpi). Essas manifestações foram acompanhadas pelo aumento da sensibilidade a estímulos externos, convulsões, recumbência e morte. As alterações histopatológicas consistiram em necrose neuronal, edema, necrose de liquefação, leptomeningite neutrofílica, manguito perivascular, hemorragia focal, inflamação não supurativa, gliose multifocal e infiltração perivascular de células polimorfonucleares e mononucleares. As características e a extensão das lesões variaram entre as linhagens de camundongos. Animais inoculados com a estirpe A4/72 apresentaram lesões histopatológicas de maior grau de severidade quando comparados com aqueles inoculados com a estirpe A9/92. Observou-se aumento da concentração plasmática de TNF-&#945;, IL-6, CCL2 e IFN-&gamma; nos camundongos infectados pelo EHV-1 no 2º dpi. Detectou-se aumento da concentração plasmática e da expressão de mRNA para TNF-&#945;, IL-6 e CCL2 no SNC dos camundongos infectados pelo EHV-1 no 3º dpi; entretanto, não houve aumento da concentração plasmática nem da expressão de mRNA para IFN-&gamma; no 3º dpi. Evidenciou-se que a estirpe A4/72 do EHV-1 induz uma resposta imune sistêmica mais efetiva, enquanto que o vírus A9/92 culmina em uma resposta imunológica mais efetiva no SNC. Os camundongos com o fundo genético C57BL/6 e BALB/c mostraram níveis mais altos de expressão de mRNA para TNF-&#945;, IL-6 e CCL2, quando comparados com os C3H/HeJ. A gravidade dos sinais clínicos observados em camundongos infectados pode ser correlacionada com o pico dessas citocinas pró-inflamatórias (TNF-&#945; e IL-6) e da quimiocina CCL2, que são produzidas logo após a infecção viral por células residentes da glia e/ou infiltrativas no SNC. Esses achados indicam que as diferentes linhagens de camundongos isogênicos são susceptíveis à infecção por estirpes neuropatogênicas do EHV-1; as diferenças no padrão de alterações histopatológicas mostram que elas dependem do hospedeiro infectado, da estirpe viral e da resposta imunológica; e a supressão do interferon (IFN) tipo 1 sugere ser um mecanismo de escape do EHV-1 frente ao sistema imune. A baixa expressão de IL-6, TNF-&#945; e da quimiocina CCL2 em camundongos C3H/HeJ se explica pela mutação no gene toll-like receptor 4 (TLR-4) existente nessa linhagem de camundongo. Adicionalmente, os camundongos C3H/HeJ apresentaram lesões histopatológicas mais severas no SNC quando comparados com BALB/c e C57BL/6. Sugere-se que o IFN tipo I e o gene TLR-4 apresentam importante papel na patogênese do EHV-1 bem como proteínas do agente viral responsáveis pela supressão do IFN e partículas virais que sejam reconhecidas pelo TLR-4 podem ser alvos para o desenvolvimento de novas abordagens para o tratamento da doença viral e para a eficiência de imunógenos / The equine herpesvirus type 1 (EHV-1) is an important pathogen that causes respiratory disease, abortion and neurological disorders in horses. This study was conducted to evaluate the inflammatory response caused by EHV-1 by the analysis of clinical manifestations, histopathological changes and the host immune response in the central nervous system (CNS). BALB/c (H2d), C57BL/6 (H2b) and C3H/HeJ (H2k) mice were inoculated intranasally with Brazilian EHV-1 strains A4/72 and A9/92. In this study, joined histopathology, the response of proinflammatory cytokines in the CNS of mice of different strains and reverse transcription method followed by quantitative polymerase chain reaction in real time (RT-qPCR) to investigate the relationship between infection by EHV-1 and inflammatory response in the development of lesions. Brazilian strains A4/72 and A9/92 EHV-1 caused acute lethal infection in different strains of inbred mice. Clinical and neurological signs such as weight loss, the bristly hair, hunched posture, apathy, dyspnoea, dehydration and salivary hypersecretion appeared between 2nd and 3rd day after infection (dpi). These events were accompanied by increase in the sensitivity to external stimuli, convulsions, recumbency and death. Histopathological changes were neuronal necrosis, edema, liquefaction necrosis, neutrophilic leptomeningitis, perivascular cuff, focal hemorrhage, non-suppurative inflammation, multifocal gliosis and perivascular infiltration of polymorphonuclear and mononuclear cells. The characteristics and the extent of the injuries varied between strains of mice. Animals inoculated with the A4/72 strain showed histopathological lesions of greater severity when compared with those inoculated with the A9/92 strain. There was an increase in plasma concentrations of TNF-&#945;, IL-6, CCL2 and IFN-&gamma; in mice infected by EHV-1 in 2nd dpi. Plasma concentrations and the expression of mRNA for TNF-&#945;, IL-6 and CCL2 in the CNS of mice infected with EHV-1 at 3rd dpi were increased; however, there was no increase in plasma concentration or expression for the mRNA of IFN-&gamma; at 3rd dpi. It was evident that the EHV-1 strain A4/72 induces a more effective systemic immune response, whereas the A9/92 virus culminates in a more effective immune response in the CNS. The C57BL/6 and BALB/c mice showed higher levels of mRNA expression for TNF-&#945;, IL-6 and CCL2, compared to C3H/HeJ mice. The severity of clinical signs observed in infected mice can be correlated with the peak of these proinflammatory cytokines (TNF-&#945; and IL-6) and CCL2 chemokine, which are then produced after viral infection by resident glial cells and/or infiltrative cells in the CNS. These findings indicate that different strains of inbred mice are susceptible to infection neuropathogenic EHV-1 strains; the differences in the pattern of pathological changes show that they depend on the infected host, the EHV-1 strain and the immune response; and the suppression of interferon (IFN) type I suggested to be an escape mechanism for the EHV-1 against the immune system. The low expression of IL-6, TNF-&#945; and chemokine CCL2 in C3H/HeJ mice can be explained by a mutation in toll-like receptor 4 (TLR-4) gene existing in this mouse strain. Additionally, C3H/HeJ mice exhibited more severe histopathological lesions in the CNS as compared to BALB/c and C57BL/6. It is suggested that type I IFN and TLR-4 gene have important role in the pathogenesis of EHV-1 and viral agent proteins responsible for the suppression of IFN and the viral particles that are recognized by TLR-4 can be targets for the development of new approaches for the treatment of viral disease and the efficiency of immunogens

Lectinas consistem de um vasto grupo de proteínas de origem não-imunológica e de caráter não enzimático, que reconhecem carboidratos de modo específico e não-covalente. Além disso, essas proteínas participam de vários eventos fisiológicos e patológicos, com embriogenese, resposta imunológica, apoptose, diferenciação celular e câncer. Recentemente, foi purificada da peçonha da serpente Bothrops atrox uma lectina do tipo-C, ligante de lactose, com propriedades bioquímicas e funcionais semelhantes à de outras lectinas de serpentes do gênero, denominada Galatrox. O presente projeto teve como objetivos a investigação do envolvimento da Galatrox no processo inflamatório agudo através de experimentos in vivo e in vitro e a produção de anticorpos policlonais anti-Galatrox. A lectina isolada foi obtida através de dois processos cromatográficos, apresentando um valor final de recuperação protéica de 0,3% (mg) em relação ao conteúdo protéico da peçonha bruta. De modo interessante, a Galatrox conjugada ao fluorocromo FITC (8µg/mL) foi capaz de ligar-se a superfície de neutrófilos (91,47%±0,5650). Além disso, está proteína reconheceu a laminina imobilizada, e não a fibronectina, uma glicoproteína da matriz extracelular que contém sequencias de poli-N-acetillactosamina. Avaliando seu potencial inflamatório, Galatrox mostrou-se capaz de induzir a migração de neutrófilos humanos in vitro de forma dose-dependente, tendo máxima atividade quimiotática na concentração de 32µg/mL (41,57±3,42 neutrófilos por campo). Apesar da Galatrox induzir um discreto nível de burst oxidativo em neutrófilos humanos não primados, ela apresentou um efeito três vezes maior quando essas células foram primadas com fMLP. Esta lectina quando injetada na cavidade peritoneal de camundongos Balb/C provocou migração leucocitária, sendo que na dose (50g/cavidade) e no tempo (4 horas) ótimos ocorreu um influxo celular de 2,05x106±0,101 leucócitos/mL. Ainda, esse infiltrado celular mostrou-se, basicamentre, composto por neutrófilos. Avaliando o perfil de mediadores da resposta inflamatória nesse ensaio in vivo, nos lavados peritoneais foi indicada a liberação máxima de IL-1 e IL-6 após 4 horas de tratamento, mas não foram detectadas a presença de TNF- e óxido nitrico em qualquer tempo de resposta. Células de baços murinos tratados com Galatrox produziram as citocinas pró-inflamatórias TNF- e IFN- e não produziram IL-10 ou NO. A produção de anticorpos policlonais foi realizada por imunização de camundongos e purificação cromatografia de afinidade em colunas com Galatrox imobilizada. A monitoração por ELISA e Western blot comprovaram a produção de anticorpos da classe IgG anti-Galatrox reconhecedores da lectina em sua forma nativa e desnaturada além de suas formas monoméricas e diméricas. Em todos os ensaios biológicos que a Galatrox foi testada na presença da lactose (carboidrato ligante da Galatrox, 20 mM) ocorreram inibições significativas das atividades dessa lectina, indicando que o seu domínio de reconhecimento de carboidrato participa das funções dessa molécula. Com base nos resultados obtidos é possível sugerir que a Galatrox participe da resposta imune inata por mediar eventos biológicos da resposta inflamatória aguda. No entanto, a lectina mostrou-se como um moderado agente pró-inflamatória, quando relacionada à peçonha bruta tendo em vista a fisiopatologia inflamatória do envenenamento. O anticorpo anti-Galatrox poderá ser usado como uma importante ferramenta estudos moleculares e funcionais dessa lectina de serpente. / Lectins are proteins with no enzymatic activity and are able to bind specifically and non-covalently (reversible manner) to carbohydrates. In addition, these proteins are involved in several physiological and pathological events, as embryogenesis, immune response, cancer, and others. Galatrox, a lactose-binding protein, was purified from Bothrops atrox snake venom and partially characterized concerning its biochemical and functional properties. The present work aimed to investigate the involvement of Galatrox in the inflammatory process. In addition, was carry out the production of a polyclonal antibody against Galatrox. This lectin was purified by one chromatographic step with yield around 0.3% (w/w) of total protein from Bothrops atrox crude venom. Interestingly, Galatrox-FITC (8g/mL) binds on human neutrophil surface (91.47% ± 0.5650). Also, this lectin recognized laminin, but not fibronectin, a glycoprotein of the extracellular matrix that contains poly-N-acetyllactosamine sequences. Galatrox was able to induce human neutrophils migration in vitro in a dose-dependent manner, with maximum chemotactic activity at 32g/mL (41.57 ± 3.42 neutrophils per well). Galatrox is more efficient to induce oxidative burst on fMLP primed neutrophils rather than non-primed neutrophils. When injected into mouse peritoneal cavity, Galatrox induced dose and time-dependent leukocyte migration, with optimal effect at 50g/animal after 4 hours of the injection (2.05x106±0.101 leukocytes/mL). Galatrox also induced release of IL-1 and IL-6 up to 12 hours after injection in the peritoneal cavity. However, TNF- and NO were not detected. The treatment of splenocytes with Galatrox in vitro promotes the production of INF- and TNF-. The biological activities of Galatrox were inhibited by lactose (specific sugar, 20 mM), indicating that its recognition carbohydrate domain participates of its functions. The production of polyclonal antibody anti-Galatrox was performed by immunization of mice and purified by affinity chromatography using immobilized Galatrox resin. Gamma-globulins against Galatrox were able to recognize this lectin under native and reduced conditions, using ELISA and Western-blot, respectively. The antibody anti-Galatrox can be use as important tool to further molecular and functional characterization of this snake venom lectin. These results suggest that Galatrox is immunogenic and may participate in the acute inflammatory process, acting as a pro-inflammatory agent through its lectin property.

Idealizou-se o presente ensaio com o objetivo de padronizar o perfil hematológico, bioquímico, eletroforético (proteinograma sérico) e quantificação das células linfocitárias CD4, CD5, CD8 por citometria de fluxo de cães da raça Golden Retrivier normais (grupos GR) e de cães distróficos (grupos GRMD). Para tanto, considerou-se a divisão dos grupos de acordo com a idade dos animais, desde o nascimento até a idade adulta, compondo assim seis grupos, sendo eles GR I, II, III e GRMD I, II, III. No presente projeto realizamos os estudos eletroforéticos de cães pertencentes a todos os grupos, estudos hematológicos e bioquímicos dos cães pertencentes aos grupos GR II, III, GRMD II e III, imunofenotipagem linfocitária dos grupos GR III e GRMD III. Os resultados eritroleucométricos e trombométricos obtidos para os cães pertencentes aos grupos GR II e GR III apresentaram valores médios dentro normalidade. Com relação aos cães pertencentes aos grupos GRMD III, observamos que o eritrograma se encontra dentro dos valores de referência. Contudo, considerando o leucograma, os valores médios (3,79/ mm3) referentes à mensuração de basófilos apresentaram-se acima dos valores de normalidade, variando de 0 a 159/mm3. Ademais, considerando os valores máximos, alguns animais pertencentes ao grupo em questão, apresentaram leucocitose com neutrofilia sem desvio à esquerda, além de trombocitose, monocitose e linfopenia, no momento das coletas. As dosagens bioquímicas séricas de todos os cães afetados apresentaram valores médios acima dos valores de normalidade para a dosagem de AST, ALT e CK. Para o estudo das proteínas séricas, a técnica SDS-PAGE permitiu o fracionamento de vinte e três proteínas, cujos pesos moleculares variaram de 16.000 a 260.000 daltons em todos os grupos estudados. Destas, foi possível identificar nominalmente doze frações protéicas: IgA (PM 142.000 Da), proteína C-reativa (PM122.000 Da), ceruloplasmina (PM 110.000 Da), fosforilase (PM 95.000 Da), transferrina (PM 82.000 Da), hemopexina (PM 78.000 Da), albumina (PM 66.000 Da), alfa1 antitripsina (PM 62.000 Da), IgG de cadeia pesada (PM 55.000 Da), haptoglobina (PM 45.000 Da), glicoproteína ácida (PM 40.000 Da) e IgG de cadeia leve (PM 23.000 Da). As demais proteínas foram identificadas pelos respectivos pesos moleculares. Não foi possível identificar nominalmente as frações protéicas de pesos moleculares 260.000 Da, 230.000 Da, 180.000 Da, 165.000 Da, 158.000 Da, 91.000 Da, 35.000 Da, 30.000 Da, 28.000 Da e 16.000 Da. Dentre essas proteínas foi possível observar que a proteína de peso molecular 91.000 Da foi encontrada apenas nos grupos GR I e GRMD I não sendo identificada nos outros grupos estudados. Considerando as alterações encontradas com relação às proteínas de fase aguda, evidenciamos as respostas de fase aguda frente às lesões musculares que ocorrem progressivamente em cães distróficos, principalmente em animais distróficos jovens, podendo inferir que os mesmos apresentaram alterações protéicas perante a injúria tecidual como é relatado em vários processos inflamatórios relacionados com outras patologias. Da mesma forma, os animais afetados pela distrofia, possuem alterações imunoglobulínicas quando comparados a animais normais. Com relação a imunofenotipagem linfocitária foi confeccionado um histograma das populações de linfócitos CD4+, CD5+ e CD8+ a partir da região do gate de linfócitos. Todos os animais afetados pela distrofia apresentaram porcentagem significativamente maior com relação à população linfocitária CD4+ e CD5+ quando comparados aos cães normais. Desta forma, podemos inferir que o processo progressivo da distrofia, esta relacionado com alterações nas populações celulares que compõe o sistema imune dos pacientes, pois devido a ausência de distrofina o músculo fica mais susceptível á lesões, sendo que na sua ocorrência, há liberação de citocinas que estimulam as células hepáticas a secretarem as proteínas de fase aguda e a promoverem uma co-estimulação de linfócitos T. Assim, podemos sugerir que os resultados encontrados em nosso trabalho são conseqüências da resposta inflamatória gerada pela lesão muscular. Esperamos com esse estudo, fornecer mais informações sobre a fisiopatogenia da doença, bem como promover um maior entendimento sobre a avaliação imunológica e resposta inflamatória neste modelo de estudo. Ademais, que os valores de base encontrados possam auxiliar na avaliação de possíveis reações nos testes pré-clínicos, facilitando assim, o entendimento das reações benéficas ou adversas para validar e explicar o mecanismo de ação de uma terapia celular, gênica ou mesmo medicamentosa / Devised to test this in order to standardize the hematological, biochemical, electrophoretic (Serum protein) and quantification of CD4 lymphocyte cells, CD5, CD8 by flow cytometry of Golden Retriever dogs normal (group GR) and dogs dystrophic (GRMD groups). To this end, we considered the division of groups according to age of animals, from birth to adulthood, thus composing six groups, as Gr I, II, III and GRMD I, II, III. In this project we performed electrophoretic studies of dogs belonging to all groups, haematological and biochemical studies of dogs belonging to the groups GR II, III, II and III GRMD, lymphocyte immunophenotyping in groups III and GR GRMD III. The results obtained for trombometric, erythometric and dogs belonging to the groups and GR II GR III showed mean values within normal limits. With respect to dogs belonging to groups III GRMD, we observed that the erythrocyte is within the reference values. However, considering the WBC, the mean (3.79 / mm3) relating to the measurement of basophils were above normal values, ranging from 0 to 159/mm3. Moreover, considering the maximum, some animals belonging to the group in question had leukocytosis with neutrophilia without left shift, and thrombocytosis, monocytosis and lymphopenia at the time of collection. The biochemical serum of all affected dogs had mean values above the normal range for the determination of AST, ALT and CK. For the study of proteins, SDS-PAGE technique allowed the fractionation of twenty-three proteins whose molecular weights ranged from 16,000 to 260,000 daltons in all groups. These could be identified by name twelve fractions: IgA (PM 142,000 Da), C-reactive protein (PM122.000 Da), ceruloplasmin (PM 110,000 Da), phosphorylase (95,000 Da PM), transferrin (82,000 Da PM), hemopexin (PM 78 000 Da), albumin (66,000 Da PM), alpha1 antitrypsin (PM 62,000 Da), IgG heavy chain (55,000 Da PM), haptoglobin (PM 45,000 Da), glycoprotein (PM 40,000 Da) and IgG light chain (PM 23 000 Da). The other proteins were identified by their molecular weights. We could not identify by name the protein fractions of molecular weight 260,000 Da, 230,000 Da, 180,000 Da, 165,000 Da, 158,000 Da, 91,000 Da, 35,000 Da, 30,000 Da, 28,000 Da and 16,000 Da. Among these proteins was observed that the protein molecular weight of 91,000 Da was found only in groups GR I and GRMD I was not identified in other groups. Considering the changes found with relation to acute phase proteins, we noted the acute phase response in the face of muscle injuries that occur gradually in dystrophic dogs, especially in young dystrophic animals, which may infer that they had abnormal protein before tissue injury as reported in many inflammatory-related pathologies. Likewise, animals affected by muscular dystrophy, alterations immunoglobulin when compared to normal animals. With respect to lymphocyte immunophenotyping was made a histogram of the populations of CD4, CD5 and CD8 from the region of the gate of lymphocytes. All animals affected by muscular dystrophy showed significantly higher percentage with respect to CD4 and CD5 lymphocyte population compared to normal dogs. Thus, we can infer that the process of progressive muscular dystrophy, is associated with changes in cell populations that make up the immune system of patients, because due to the absence of dystrophin, the muscle is more susceptible to damage, and its occurrence , a release of cytokines that stimulate liver cells to secrete acute phase proteins and promote a co-stimulation of T lymphocytes Thus, we suggest that the findings in our study are consequences of the inflammatory response generated by muscle injury.We hope that this study, provide more information about the pathophysiolgy of the disease, and promote a greater understanding of the immune and inflammatory responde assessment in this study model. Moreover, the base values found could help in assessing possible responses in preclinical testing, aiding the understanding of the beneficial or adverse reactions to validate and explain the mechanism of action of a cell therapy, gene or drug treatments