Resumo O objetivo deste estudo foi avaliar a expressão de MMP2 e MMP9 durante a progressão da periodontite apical (AP) em camundongos knockout para TLR2 (TLR2 KO) e MyD88 (MyD88 KO) comparados aos camundongos wild type (WT). A AP foi induzida nos primeiros molares inferiores dos camundongos TLR2 KO (n = 18), MyD88 KO (n = 18) e WT (n = 18). Após 7, 21 e 42 dias, os animais foram eutanaziados e as mandíbulas foram dissecadas e submetidas a processamento histotécnico. As lâminas foram coradas por imuno-histoquímica e analisadas para a detecção de MMP2 e MMP9. A análise estatística semi-quantitativa da imuno-histoquímica foi realizada pelo teste qui-quadrado (α = 0,05). Nos períodos iniciais de progressão AP, foi observada uma expressão aumentada de MMP9 nos camundongos TLR2 KO e MyD88 KO. Nos períodos finais de progressão AP, observou-se uma redução da expressão de MMP2 e um aumento da expressão de MMP9 nos camundongos TLR2 KO. A produção de MMP2 e MMP9 foi modulada por TLR2 e MyD88 durante a progressão da periodontite apical.

Abstract The aim of this study was to evaluate the expression of MMP2 and MMP9 during apical periodontitis (AP) progression in TLR2 (TLR2 KO) and in MyD88 (MyD88 KO) knockout mice compared to wild type (WT) mice. AP was induced in mandibular first molars of TLR2 KO (n= 18), MyD88 KO (n= 18), and WT mice (n= 18). After 7, 21, and 42 days, the animals were euthanized and the jaws were dissected and subjected to histotechnical processing. Subsequent sections were stained by immunohistochemistry and evaluated for detection of MMP2 and MMP9. Statistical analysis of the semi-quantitative analysis of immunohistochemistry was performed using chi-square test (α = 0.05). In the initial periods of AP progression, an increased expression of MMP9 in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 expression and an increase of MMP9 expression in the TLR2 KO mice were observed. MMP2 and MMP9 production was modulated for TLR2 and MyD88 during apical periodontitis progression.

The aim of the present study was to comparatively evaluate hemogram, blood serum components and anatomopathologic alterations in commercial layers experimentally challenged with an attenuated vaccine candidate strain (SG∆cobS∆cbiA) and other two pathogenic strains (SGDcobS and SGNalr) of Gallinarum (SG). In total, 280 commercial layers were randomly divided into 4 groups (G1, G2, G3 and G4). At five days of age, birds from groups G1 received approximately 107 colony forming units (CFU) of SGDcobS; meanwhile birds from group G2 and G3 received the same dose of SGNalr and SG∆cobS∆cbiA, respectively. Birds from G4 were not infected. At 24 hours before (DBI) and 24 hours after (1 DAI), and three (3 DAI), five (5 DAI), seven (7 DAI) ten (10 DAI), and fifteen (15 DAI) days after the infection, 10 birds of each group were humanely killed and blood samples collected to hematological and serum tests. Samples of liver, spleen, thymus, bursa of Fabricius, kidney and heart were also collected for the histological examination. Birds inoculated with SGDcobS and SGNalr showed similar alterations in hemogram, blood serum components and anatomopathologic exams. On the other hand, the exams of birds inoculated with SG∆cobS∆cbiA strain were similar to those of the uninfected birds. However, changes could be noticed in levels of uric acid and cholesterol during the course of the infection of birds from G3. Decrease in levels of light IgG 3 DAI was also observed in birds from this group. Pyknosis in kidney cells was a microscopic alteration found in birds from G3. Further studies must be done to verify if these alterations will not interfere in the performance of the vaccinate birds with SG∆cobS∆cbiA strain.

The aim of the present study was to evaluate white blood cell counts and serum protein profiles of commercial layers experimentally infected with Salmonella Gallinarum (SG) in order to better understand the pathophysiology of the disease caused by this bacterium. 180 five-day-old commercial layers were divided into 3 groups (G); G1 and G2 received 0.2 mL of inoculate containing 3.3x10(8) CFU or 3.3x10(5) CFU SG resistant to nalidix acid (Nal r)/mL, respectively, directly into their crops. G3 group did not receive the inoculum. Birds were sacrificed 24 hours before (T1) and 24 hours after the infection (T2), and three (T3), five (T4), seven (T5), and ten (T6) days after the administration of the inoculum. White blood cell counts were carried out in a Neubauer hemocytometer and in blood smears. Serum protein concentrations, including acute-phase proteins, were determined using sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). Data were submitted to analysis of variance, and means were compared by Tukey's test (P <0.05). G1 and G2 groups presented higher leukocyte counts on T4 and T5, respectively, due to the increase of circulating lymphocytes and heterophils, with a significant difference relative to G3. In electrophoresis, an increase in the serum levels of ceruloplasmin, haptoglobin, and hemopexin and a decrease in transferrin, which are acute-phase proteins, was verified. IgA serum levels did not change; however, IgG concentration increased during the infection. In conclusion, the results provide information for the better understanding of the pathophysiology of fowl typhoid.