Dr Association of bone morphogenetic protein 15 and growth differentiation factor 9 with litter size in livestock: a review study

Litter size is one of the crucial factors in livestock production and is of high economic value, which is affected by ovulation rate, hormones, and growth factors.Growth factors play a multifaceted role in reproductive physiology. This review aims to investigate the association of bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9)with litter size in livestock.The transforming growth factor ß(TGF-ß) superfamily includes more than 34 members; GDF9 and BMP15 are among the most significantfactors for regulating fertility and litter size in most livestock species. Ovarian follicles release BMP15 and GDF9 that are involved in the maturation of primary follicles into the basal form, proliferation of granulosa and theca cells, steroidogenesis, ovulation, and formation of the corpus luteum. Besides, these factors are highly expressed in oocytes and are necessary for female fertility and multiple ovulation in several livestock species. Animals with two inactive copies of these factors are sterile, while those with one inactive copy are fertile. Thus, the present reviewprovides valuable information on the association of BMP15 and GDF9with litter size in livestock that can be used as biological markers of multiple ovulation or for improving fertility in livestock.(AU)

Expression of TGF-ß/Smads in Cecum and Spleen of Chicken Infected with E. Tenella

Chicken coccidiosis is a common and severe parasitic disease caused by infection from Eimeria spp., which affects the integrity of the intestinal mucosa. TGF-ß has been shown to play an important role in the healing of intestinal mucosas, immunity, and the maintenance of bowel mucosa integrity. Very little is known about the presence of the components of TGF-ß/Smads signaling pathway of chicken at different times following coccidian infection. In the present study, we measured the levels of TGF-ß2, 3, 4, receptor TßRI, II, down-stream Smad 2, 3, 7 in cecum and spleen of chicken at different times after inoculation with Eimeria tenella using quantitative real-time PCR. The results showed that the TGF-ß/Smads signaling pathway was not activated in cecum in the early stage of infection. However, on the 8th day, the expression of TGF-ß2, 4, down-stream protein Smad 2, 7 were significant up-regulated in the spleen, which indicated that the TGF-ß/Smads signaling was changed in the E. tenella infection and was differentially expressed in various tissues in the early stages of infection.(AU)

Impact of history of periodontitis on gene expression of bone-related factors in young patients.

Although dental implants and bone regenerative procedures are important approaches for the reestablishment of esthetics and function in young patients with a history of generalized aggressive periodontitis (GAP), no predictable outcomes have been reported, and the host osteo-immunoinflammatory response may play a relevant role in this context. In view of the lack of molecular investigations into the bone tissue condition of young patients with periodontitis, the aim of this study was to evaluate the gene expression of bone-related factors in this population. Bone biopsies were obtained from the posterior mandible in 16 individuals previously diagnosed with GAP and on periodontal support therapy and from 17 periodontally healthy (PH) patients. The gene expression of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-ß, receptor activator of the NF-κB ligand (RANKL), osteoprotegerin (OPG), osteocalcin (OC), bone sialoprotein (BSP), and type I collagen (COL-I), important biomarkers of bone turnover, was evaluated by qRT-PCR. Lower TGF-ß and OPG mRNA levels were observed in GAP patients compared to PH individuals (p ≤ 0.05). There were no between-group differences in levels of TNF-α, BSP, RANKL, OC, or COL-I mRNA (p>0.05). In young adults, a history of periodontal disease can negatively modulate the gene expression of important bone-related factors in alveolar bone tissue. These molecular outcomes may contribute to the future development of therapeutic approaches to benefit bone healing in young patients with history of periodontitis via modulation of osteo-immuno-inflammatory biomarkers.

Effects of E. Coli Infection on the Expressions of TGF-/Smads Signaling Pathway in Broiler Intestine

This experiment aimed to investigate whether Escherichia coli (E. coli) infection could affect the TGF-/smads signaling pathway in the jejunal tissue of chickens. One-day-old Cobb 500 broilers were randomly divided into 2 groups and treated with intraperitoneal E. coli or broth injection. Clinical signs of the birds were assessed every day. Spleen and bursa of Fabricius of the birds, post-infection (pi), were collected to evaluate immune organ index. Jejunal tissues were collected to ascertain the expression of TGF-s, TRs, and Smads. The results showed that the infected birds had significantly higher index of the spleen (24hrs and 48hrs pi) compared with birds in the control group (p 0.05). The relative gene expression of TGF-4 increased (p 0.05), while the expression of Smad7 down-regulated in the E. coli group (p 0.01). There was no significant difference in TGF-2, TGF-3, TR I, TR II, Smad2, Smad3 expression (p>0.05). In conclusion, TGF-/Smad signaling pathway was associated with the immune response of broilers in E. coli infection and TGF-4 was the main subtype interacting with E. coli infection.

The Expression of NF-kB Signaling Pathway Was Inhibited by Silencing TGF-b4 in Chicken IECs Infected with E. tenella

Chicken coccidiosis is a parasitic disease caused by one or more species of Eimeria infection with severe consequences. The NF-B signaling pathway and TGF-4 play an important role in the inflammation and immune response caused by coccidiosis infection. This study was designed to investigate the changes of NF-B signaling pathway and the effects of TGF-4 silencing on the expression of NF-B signaling pathway in chickens intestinal epithelial cells (IECs) after infecting with E. tenella sporozoites. TGF-4 small interfering RNA (TGF-4 siRNA) sequences were transfected into chicken IECs for reducing TGF-4 expression. The results showed that compared with uninfected control group (Con.), the proinflammatory factors of NF-B, IL-6, IL-2, IL-1 increased significantly in the E. tenella infected group (ET) (p 0.05). In comparison with the IECs in the ET, the expression level of NF-B, IL-6, IL-2, IL-1 dropped significantly in the group infected both by E. tenella and TGF-4 siRNA vector (ET+siRNA) (p 0.05). The results of this experiment indicate that NF-B signaling pathway is closely correlated with TGF-4 in IECs infected with coccidia sporozoites. TGF-4 plays an important role in regulating the immune function of coccidia-infected chicken epithelial cells through NF-B signaling pathway and preventing immune-mediated pathological changes.

Effects of E. Coli Infection on the Expressions of TGF-/Smads Signaling Pathway in Broiler Intestine

This experiment aimed to investigate whether Escherichia coli (E. coli) infection could affect the TGF-/smads signaling pathway in the jejunal tissue of chickens. One-day-old Cobb 500 broilers were randomly divided into 2 groups and treated with intraperitoneal E. coli or broth injection. Clinical signs of the birds were assessed every day. Spleen and bursa of Fabricius of the birds, post-infection (pi), were collected to evaluate immune organ index. Jejunal tissues were collected to ascertain the expression of TGF-s, TRs, and Smads. The results showed that the infected birds had significantly higher index of the spleen (24hrs and 48hrs pi) compared with birds in the control group (p 0.05). The relative gene expression of TGF-4 increased (p 0.05), while the expression of Smad7 down-regulated in the E. coli group (p 0.01). There was no significant difference in TGF-2, TGF-3, TR I, TR II, Smad2, Smad3 expression (p>0.05). In conclusion, TGF-/Smad signaling pathway was associated with the immune response of broilers in E. coli infection and TGF-4 was the main subtype interacting with E. coli infection.(AU)

The Expression of NF-kB Signaling Pathway Was Inhibited by Silencing TGF-b4 in Chicken IECs Infected with E. tenella

Chicken coccidiosis is a parasitic disease caused by one or more species of Eimeria infection with severe consequences. The NF-B signaling pathway and TGF-4 play an important role in the inflammation and immune response caused by coccidiosis infection. This study was designed to investigate the changes of NF-B signaling pathway and the effects of TGF-4 silencing on the expression of NF-B signaling pathway in chickens intestinal epithelial cells (IECs) after infecting with E. tenella sporozoites. TGF-4 small interfering RNA (TGF-4 siRNA) sequences were transfected into chicken IECs for reducing TGF-4 expression. The results showed that compared with uninfected control group (Con.), the proinflammatory factors of NF-B, IL-6, IL-2, IL-1 increased significantly in the E. tenella infected group (ET) (p 0.05). In comparison with the IECs in the ET, the expression level of NF-B, IL-6, IL-2, IL-1 dropped significantly in the group infected both by E. tenella and TGF-4 siRNA vector (ET+siRNA) (p 0.05). The results of this experiment indicate that NF-B signaling pathway is closely correlated with TGF-4 in IECs infected with coccidia sporozoites. TGF-4 plays an important role in regulating the immune function of coccidia-infected chicken epithelial cells through NF-B signaling pathway and preventing immune-mediated pathological changes.(AU)

Impact of history of periodontitis on gene expression of bone-related factors in young patients

Abstract Although dental implants and bone regenerative procedures are important approaches for the reestablishment of esthetics and function in young patients with a history of generalized aggressive periodontitis (GAP), no predictable outcomes have been reported, and the host osteo-immunoinflammatory response may play a relevant role in this context. In view of the lack of molecular investigations into the bone tissue condition of young patients with periodontitis, the aim of this study was to evaluate the gene expression of bone-related factors in this population. Bone biopsies were obtained from the posterior mandible in 16 individuals previously diagnosed with GAP and on periodontal support therapy and from 17 periodontally healthy (PH) patients. The gene expression of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, receptor activator of the NF-κB ligand (RANKL), osteoprotegerin (OPG), osteocalcin (OC), bone sialoprotein (BSP), and type I collagen (COL-I), important biomarkers of bone turnover, was evaluated by qRT-PCR. Lower TGF-β and OPG mRNA levels were observed in GAP patients compared to PH individuals (p ≤ 0.05). There were no between-group differences in levels of TNF-α, BSP, RANKL, OC, or COL-I mRNA (p>0.05). In young adults, a history of periodontal disease can negatively modulate the gene expression of important bone-related factors in alveolar bone tissue. These molecular outcomes may contribute to the future development of therapeutic approaches to benefit bone healing in young patients with history of periodontitis via modulation of osteo-immuno-inflammatory biomarkers.

Cytokines and chemokines associated with Treg/Th17 response in chronic inflammatory periapical disease.

Cytokines and chemokines have a fundamental role in the maintenance of inflammation and bone response, which culminate in the development of chronic periapical lesions. Regulatory (Treg) and Th17 cytokines play a key role in regulating the immune response involved in this process. The aim of this study was to investigate the role of Treg and Th17 cells in chronic inflammatory periapical disease, by comparing the expression of the immunoregulatory mediators TGF-ß, IL-10, CCL4, and the proinflammatory IL-17 and CCL20 in the periapical tissue of teeth with pulp necrosis, with and without associated chronic lesions. Eighty-six periapical tissue samples were obtained from human teeth. The samples were divided into three groups: pulp necrosis with a periapical lesion (n=26); pulp necrosis without a periapical lesion (n=30), and control (n=30). All samples were submitted to histopathological analysis and cytokine and chemokine measurement through ELISA. Statistical analyses were done with Kruskal-Wallis and Mann-Whitney tests and Spearman correlation. The group with pulp necrosis and a periapical lesion showed a higher expression of CCL4 and TGF-ß in comparison with pulp necrosis without a lesion. CCL20 was higher in the group with a periapical lesion when compared to the control. In all groups there was a weak positive correlation between IL-17/CCL20, IL-10/CCL4, and IL-17/TGF-ß. Both types of cytokines, pro-inflammatory and immunoregulatory, occur simultaneously in periapical tissue. However, a rise in immunosuppressive cytokines and chemokines (CCL4 and TGF-ß) in periapical lesions suggests a role of these cytokines in stable periapical disease.

Imunomarcação de TGF-β em próstatas caninas normais e com lesões proliferativas / Immunoexpression of TGF-β in normal canine prostates and with proliferative lesions

O fator de crescimento transformador-β (TGF-β), um mediador do crescimento prostático, induz a angiogênese e inibe a proliferação celular. Neste estudo, esse marcador foi utilizado com o objetivo de avaliar sua imunomarcação no tecido normal e com lesões proliferativas benignas, pré-neoplásicas e neoplásicas da próstata canina. Para isso, foram selecionadas 54 glândulas com histomorfologia normal, hiperplasia prostática benigna (HPB) epitelial, HPB estromal, atrofia inflamatória proliferativa (PIA), neoplasia intraepitelial prostática (PIN) e carcinoma, utilizadas para a confecção de um bloco de microarranjo tecidual (Tissue Microarray - TMA). As lâminas de TMA foram submetidas à técnica de imunoistoquímica com o anticorpo anti-TGF-β, sendo avaliada a intensidade de imunomarcação nas células epiteliais e estromais. Houve imunomarcação de TGF-β no tecido normal e naqueles com lesões proliferativas. Maior imunomarcação de TGF-β foi constatada nas células do tecido prostático normal e com HPB, enquanto as células prostáticas com PIA, PIN e carcinoma exibiram menor imunomarcação dessa citocina, o que sugere a ação do TGF-β na manutenção da homeostase do tecido normal e com lesão proliferativa benigna e na progressão das lesões proliferativas pré-malignas e malignas da próstata canina.(AU)

The transforming growth factor-β (TGF-β), a mediator of prostatic growth induces angiogenesis and inhibits cell proliferation. It was used in this study in order to evaluate its expression in normal prostatic tissue and those with benign proliferative lesions, pre-malignant and malignant prostatic diseases. A total of 54 glands with normal histomorphology, epithelial benign prostatic hyperplasia (BPH), stromal BPH, prostatic inflammatory atrophy (PIA), prostatic intraepithelial neoplasia (PIN), and adenocarcinoma were selected and used in the tissue microarray block (TMA). The TMA slides were subjected to the immunohistochemistry with anti-TGF-β and its staining intensity in epithelial and stromal cells was evaluated. There was TGF-β immunostaining by both normal tissues and those with proliferative lesions. Higher TGF-β immunostaining was observed in cells from normal prostatic tissues and with HPB, whereas prostatic cells with PIA, PIN and carcinoma exhibited lower immunostaining of this cytokine, suggesting the action of TGF-β in the maintenance of normal tissue homeostasis and with benign proliferative lesion and in the progression of pre-malignant and malignant proliferative lesions of the canine prostate.(AU)

LAP+ Cells Modulate Protection Induced by Oral Vaccination with Rhesus Rotavirus in a Neonatal Mouse Model.

Transforming growth factor ß (TGF-ß) has been shown to play a role in immunity against different pathogens in vitro and against parasites in vivo However, its role in viral infections in vivo is incompletely understood. Using a neonatal mouse model of heterologous rhesus rotavirus (RV) vaccination, we show that the vaccine induced rotavirus-specific CD4 T cells, the majority of which lacked expression of KLRG1 or CD127, and a few regulatory rotavirus-specific CD4 T cells that expressed surface latency-associated peptide (LAP)-TGF-ß. In these mice, inhibiting TGF-ß, with both a neutralizing antibody and an inhibitor of TGF-ß receptor signaling (activin receptor-like kinase 5 inhibitor [ALK5i]), did not change the development or intensity of the mild diarrhea induced by the vaccine, the rotavirus-specific T cell response, or protection against a subsequent challenge with a murine EC-rotavirus. However, mice treated with anti-LAP antibodies had improved protection after a homologous EC-rotavirus challenge, compared with control rhesus rotavirus-immunized mice. Thus, oral vaccination with a heterologous rotavirus stimulates regulatory RV-specific CD4 LAP-positive (LAP+) T cells, and depletion of LAP+ cells increases vaccine-induced protection.IMPORTANCE Despite the introduction of several live attenuated animal and human rotaviruses as efficient oral vaccines, rotaviruses continue to be the leading etiological agent for diarrhea mortality among children under 5 years of age worldwide. Improvement of these vaccines has been partially delayed because immunity to rotaviruses is incompletely understood. In the intestine (where rotavirus replicates), regulatory T cells that express latency-associated peptide (LAP) play a prominent role, which has been explored for many diseases but not specifically for infectious agents. In this paper, we show that neonatal mice given a live oral rotavirus vaccine develop rotavirus-specific LAP+ T cells and that depletion of these cells improves the efficiency of the vaccine. These findings may prove useful for the design of strategies to improve rotavirus vaccines.

Positive outcomes of phosphodiesterase type 5 inhibitor on histopathologic and biochemical changes induced by ureteral obstruction.

OBJECTIVES: We examined the effects of tadalafil, one of the phosphodiesterase type 5 (PDE5) inhibitors, in a rat model of with partial and complete unilateral ureteral obstruction (UUO). METHODS: The rats were divided into 5 groups: sham (n=6), partial unilateral ureteral obstruction (PUUO, n=6), PUUO with tadalafil treatment (PUUO+T; Cialis, 10 mg/72 h, intragastric; Lilly, Indianapolis, Indiana, USA), complete unilateral ureteral obstruction (CUUO, n=6), and CUUO with tadalafil treatment (CUUO+T). RESULTS: Fifteen days after the UUO, the ureter presented changes in the layers of urothelium and significant infiltration of inflammatory cells in the PUUO and CUUO groups. Compared with the sham, PUUO and CUUO groups had severe increased inflammatory cell infiltration. The urothelial epithelium exhibited cell degeneration and loss because of the swollen, atrophic, and denuded epithelial cells in the PUUO and CUUO groups. In the PUUO+T and CUUO+T groups, the urothelium revealed less epithelial cell degeneration and loss.The expressions of α-smooth muscle actin (α-SMA) and transforming growth factor-ß (TGF-ß) exhibited up-regulation in the PUUO and CUUO groups. The expression of TGF-ß decreased positively correlated with that of α-SMA in the tadalafil therapy groups, PUUO+T and CUUO+T. CONCLUSION: The phosphodiesterase type 5 inhibitor's tadalafil reduced expressions of α-SMA and TGF-ß in the obstructed ureters, measured by biochemical examinations. In addition, tadalafil decreased urothelium degeneration due to the decreased epithelial cell loss and inflammatory cell infiltration. Our results show that tadalafil prevents or slows down the onset of ureter inflammation and urothelial degeneration in rats with UUO.

Positive outcomes of phosphodiesterase type 5 inhibitor on histopathologic and biochemical changes induced by ureteral obstruction

SUMMARY OBJECTIVES: We examined the effects of tadalafil, one of the phosphodiesterase type 5 (PDE5) inhibitors, in a rat model of with partial and complete unilateral ureteral obstruction (UUO). METHODS: The rats were divided into 5 groups: sham (n=6), partial unilateral ureteral obstruction (PUUO, n=6), PUUO with tadalafil treatment (PUUO+T; Cialis, 10 mg/72 h, intragastric; Lilly, Indianapolis, Indiana, USA), complete unilateral ureteral obstruction (CUUO, n=6), and CUUO with tadalafil treatment (CUUO+T). RESULTS: Fifteen days after the UUO, the ureter presented changes in the layers of urothelium and significant infiltration of inflammatory cells in the PUUO and CUUO groups. Compared with the sham, PUUO and CUUO groups had severe increased inflammatory cell infiltration. The urothelial epithelium exhibited cell degeneration and loss because of the swollen, atrophic, and denuded epithelial cells in the PUUO and CUUO groups. In the PUUO+T and CUUO+T groups, the urothelium revealed less epithelial cell degeneration and loss. The expressions of α-smooth muscle actin (α-SMA) and transforming growth factor-β (TGF-β) exhibited up-regulation in the PUUO and CUUO groups. The expression of TGF-β decreased positively correlated with that of α-SMA in the tadalafil therapy groups, PUUO+T and CUUO+T. CONCLUSION: The phosphodiesterase type 5 inhibitor's tadalafil reduced expressions of α-SMA and TGF-β in the obstructed ureters, measured by biochemical examinations. In addition, tadalafil decreased urothelium degeneration due to the decreased epithelial cell loss and inflammatory cell infiltration. Our results show that tadalafil prevents or slows down the onset of ureter inflammation and urothelial degeneration in rats with UUO.

RESUMO OBJETIVOS: Examinamos os efeitos do tadalafil em um dos inibidores da fosfodiesterase tipo 5 (PDE5) em um modelo de rato com obstrução ureteral unilateral parcial e completa (UUO). MÉTODOS: Os ratos foram divididos em cinco grupos: sham (n = 6), obstrução ureteral unilateral parcial (PUUO, n = 6), PUUO com tadalafil (PUUO T; Cialis, 10 mg/72 h, intragástrica; Lilly, Indianapolis, Indiana, EUA), completa obstrução ureteral unilateral (CUUO, n = 6) e CUUO com tratamento com tadalafil (CUUO T). RESULTADOS: Quinze dias após a UUO, o ureter apresentou alterações nas camadas de urotélio e infiltração significativa de células inflamatórias nos grupos PUUO e CUUO. Em comparação com os grupos sham, PUUO e CUUO, houve um aumento grave da infiltração de células inflamatórias. O epitélio urotelial exibiu degeneração e perda celular devido às células epiteliais inchadas, atróficas e desnudas nos grupos PUUO e CUUO. Nos grupos PUUO T e CUUO T, o urotélio revelou menor degeneração e perda de células epiteliais. Nós mostramos que a expressão da actina do músculo liso-α (α-SMA) e do fator de crescimento transformador-β (TGF-β) foram exibidas como sub-regulação nos grupos PUUO e CUUO. A expressão do TGF-β foi diminuída positivamente correlacionada com a da α-SMA nos grupos de terapia com tadalafil, PUUO T e CUUO T. CONCLUSÃO: O tadalafil do inibidor da fosfodiesterase tipo 5 reduziu as expressões α-SMA e TGF-β nos ureteres obstruídos, medidos por exames bioquímicos. Além disso, o tadalafil diminuiu a degeneração do urotélio devido à diminuição da perda de células epiteliais e da infiltração de células inflamatórias. Nossos resultados mostram que o tadalafil previne ou retarda o início da inflamação do ureter e degeneração urotelial em ratos com UUO.

Evaluating clinical and laboratory effects of ozone in non-surgical periodontal treatment: a randomized controlled trial.

OBJECTIVE: This study aims to evaluate the clinical and biochemical (oxidative stress and pro-inflammatory mediators) effects of the gaseous ozone use accompanied by scaling and root planning (SRP) in periodontal treatment. MATERIAL AND METHODS: The study population consisted of 40 patients with chronic periodontitis (CP) randomly sorted into two groups of 20. The experimental group received SRP plus 3 watts gaseous ozone in two separate applications five days apart, whereas the control group received SRP plus placebo. Clinical periodontal parameters were assayed and saliva samples were taken before the initial and one month after the second treatment. Periodontal examination assessed plaque index (PI), gingival index (GI), probing depth, and clinical attachment level (CAL). Total antioxidant status (TAS), total oxidant status (TOS), nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG), myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA), and transforming growth factor-beta (TGF-ß) levels were evaluated from saliva samples. RESULTS: Changes following treatment in PI, GI, probing depth, and CAL scores were similar for both groups (p>0.05). Of note, TGF-ß levels were observed to be higher in the treatment group than in controls (p<0.05). Changes in 8-OHdG, TAS, TOS, NO, MPO, GSH and MDA levels, however, were not significantly different between groups (p>0.05). CONCLUSION: The findings of this study indicate that SRP plus gaseous ozone versus SRP alone does not correlate to a significant improvement in periodontal recovery.

Cytokines and chemokines associated with Treg/Th17 response in chronic inflammatory periapical disease

Abstract Cytokines and chemokines have a fundamental role in the maintenance of inflammation and bone response, which culminate in the development of chronic periapical lesions. Regulatory (Treg) and Th17 cytokines play a key role in regulating the immune response involved in this process. The aim of this study was to investigate the role of Treg and Th17 cells in chronic inflammatory periapical disease, by comparing the expression of the immunoregulatory mediators TGF-β, IL-10, CCL4, and the proinflammatory IL-17 and CCL20 in the periapical tissue of teeth with pulp necrosis, with and without associated chronic lesions. Eighty-six periapical tissue samples were obtained from human teeth. The samples were divided into three groups: pulp necrosis with a periapical lesion (n=26); pulp necrosis without a periapical lesion (n=30), and control (n=30). All samples were submitted to histopathological analysis and cytokine and chemokine measurement through ELISA. Statistical analyses were done with Kruskal-Wallis and Mann-Whitney tests and Spearman correlation. The group with pulp necrosis and a periapical lesion showed a higher expression of CCL4 and TGF-β in comparison with pulp necrosis without a lesion. CCL20 was higher in the group with a periapical lesion when compared to the control. In all groups there was a weak positive correlation between IL-17/CCL20, IL-10/CCL4, and IL-17/TGF-β. Both types of cytokines, pro-inflammatory and immunoregulatory, occur simultaneously in periapical tissue. However, a rise in immunosuppressive cytokines and chemokines (CCL4 and TGF-β) in periapical lesions suggests a role of these cytokines in stable periapical disease.

Imunomarcação de TGF-β em próstatas caninas normais e com lesões proliferativas / Immunoexpression of TGF-β in normal canine prostates and with proliferative lesions

O fator de crescimento transformador-β (TGF-β), um mediador do crescimento prostático, induz a angiogênese e inibe a proliferação celular. Neste estudo, esse marcador foi utilizado com o objetivo de avaliar sua imunomarcação no tecido normal e com lesões proliferativas benignas, pré-neoplásicas e neoplásicas da próstata canina. Para isso, foram selecionadas 54 glândulas com histomorfologia normal, hiperplasia prostática benigna (HPB) epitelial, HPB estromal, atrofia inflamatória proliferativa (PIA), neoplasia intraepitelial prostática (PIN) e carcinoma, utilizadas para a confecção de um bloco de microarranjo tecidual (Tissue Microarray - TMA). As lâminas de TMA foram submetidas à técnica de imunoistoquímica com o anticorpo anti-TGF-β, sendo avaliada a intensidade de imunomarcação nas células epiteliais e estromais. Houve imunomarcação de TGF-β no tecido normal e naqueles com lesões proliferativas. Maior imunomarcação de TGF-β foi constatada nas células do tecido prostático normal e com HPB, enquanto as células prostáticas com PIA, PIN e carcinoma exibiram menor imunomarcação dessa citocina, o que sugere a ação do TGF-β na manutenção da homeostase do tecido normal e com lesão proliferativa benigna e na progressão das lesões proliferativas pré-malignas e malignas da próstata canina.

The transforming growth factor-β (TGF-β), a mediator of prostatic growth induces angiogenesis and inhibits cell proliferation. It was used in this study in order to evaluate its expression in normal prostatic tissue and those with benign proliferative lesions, pre-malignant and malignant prostatic diseases. A total of 54 glands with normal histomorphology, epithelial benign prostatic hyperplasia (BPH), stromal BPH, prostatic inflammatory atrophy (PIA), prostatic intraepithelial neoplasia (PIN), and adenocarcinoma were selected and used in the tissue microarray block (TMA). The TMA slides were subjected to the immunohistochemistry with anti-TGF-β and its staining intensity in epithelial and stromal cells was evaluated. There was TGF-β immunostaining by both normal tissues and those with proliferative lesions. Higher TGF-β immunostaining was observed in cells from normal prostatic tissues and with HPB, whereas prostatic cells with PIA, PIN and carcinoma exhibited lower immunostaining of this cytokine, suggesting the action of TGF-β in the maintenance of normal tissue homeostasis and with benign proliferative lesion and in the progression of pre-malignant and malignant proliferative lesions of the canine prostate.

Transforming growth factor-beta family members are regulated during induced luteolysis in cattle

The transforming growth factors beta (TGFβ) are local factors produced by ovarian cells which, after binding to their receptors, regulate follicular deviation and ovulation. However, their regulation and function during corpus luteum (CL) regression has been poorly investigated. The present study evaluated the mRNA regulation of some TGFβ family ligands and their receptors in the bovine CL during induced luteolysis in vivo. On day 10 of the estrous cycle, cows received an injection of prostaglandin F2α (PGF) and luteal samples were obtained from separate groups of cows (n= 4-5 cows per time-point) at 0, 2, 12, 24 or 48 h after treatment. Since TGF beta family comprises more than 30 ligands, we focused in some candidates genes such as activin receptors (ACVR-1A, -1B, -2A, -2B) AMH, AMHR2, BMPs (BMP-1, -2, -3, -4, -6 and -7), BMP receptors (BMPR-1A, -1B and -2), inhibin subunits (INH-A, -BA, -BB) and betaglycan (TGFBR3). The mRNA levels of BMP4, BMP6 and INHBA were higher at 2 h after PGF administration (P<0.05) in comparison to 0 h. The relative mRNA abundance of BMP1, BMP2, BMP3, BMP4, BMP6, ACVR1B, INHBA and INHBB was upregulated up to 12 h post PGF (P<0.05). On the other hand, TGFBR3 mRNA that codes for a reservoir of ligands that bind to TGF-beta receptors, was lower at 48 h. In conclusion, findings from this study demonstrated that genes encoding several TGFβ family members are expressed in a time-specific manner after PGF administration.

Transforming growth factor-beta family members are regulated during induced luteolysis in cattle

The transforming growth factors beta (TGFβ) are local factors produced by ovarian cells which, after binding to their receptors, regulate follicular deviation and ovulation. However, their regulation and function during corpus luteum (CL) regression has been poorly investigated. The present study evaluated the mRNA regulation of some TGFβ family ligands and their receptors in the bovine CL during induced luteolysis in vivo. On day 10 of the estrous cycle, cows received an injection of prostaglandin F2α (PGF) and luteal samples were obtained from separate groups of cows (n= 4-5 cows per time-point) at 0, 2, 12, 24 or 48 h after treatment. Since TGF beta family comprises more than 30 ligands, we focused in some candidates genes such as activin receptors (ACVR-1A, -1B, -2A, -2B) AMH, AMHR2, BMPs (BMP-1, -2, -3, -4, -6 and -7), BMP receptors (BMPR-1A, -1B and -2), inhibin subunits (INH-A, -BA, -BB) and betaglycan (TGFBR3). The mRNA levels of BMP4, BMP6 and INHBA were higher at 2 h after PGF administration (P<0.05) in comparison to 0 h. The relative mRNA abundance of BMP1, BMP2, BMP3, BMP4, BMP6, ACVR1B, INHBA and INHBB was upregulated up to 12 h post PGF (P<0.05). On the other hand, TGFBR3 mRNA that codes for a reservoir of ligands that bind to TGF-beta receptors, was lower at 48 h. In conclusion, findings from this study demonstrated that genes encoding several TGFβ family members are expressed in a time-specific manner after PGF administration.(AU)

Effect of topical ozonetherapy on gingival wound healing in pigs: histological and immuno-histochemical analysis

Abstract In this study, the effects of ozonetherapy on secondary wound healing were evaluated histologically and immuno-histochemically. Material and Methods: 8 healthy pigs were used in this study. Six wounds with 10 mm in diameter were created through the punch technique on the palatinal gingiva of each pig. Ozone gas was applied on only 3 wounds (test group) and the remaining 3 were left to natural healing (control group). Biopsy samples were taken from one of the wounds in each group on the third day, from another wound of each group on the seventh day, and from another one on the tenth day. Routine histological analysis and immuno-histochemical staining were performed to investigate transforming growth factor-beta (TGF-β) and (VEGF) expressions. Results: No statistical difference was found between the test and control groups in terms of collagen fibers, epithelial formation and inflammation scores. A VEGF expression found in the test group was statistically higher than control group samples taken on the 3rd and 7th day. There was no statistical difference between the test and control groups in terms of TGF-β expression on any of the sampling days. Conclusion: The topical application of ozone gas could be effective in the early stages of wound healing by increasing the amount of VEGF expression. Clinical Relevance: Topical application of ozone gas may be effective in the early stages of oral wound healing.

Evaluating clinical and laboratory effects of ozone in non-surgical periodontal treatment: a randomized controlled trial

Abstract Objective: This study aims to evaluate the clinical and biochemical (oxidative stress and pro-inflammatory mediators) effects of the gaseous ozone use accompanied by scaling and root planning (SRP) in periodontal treatment. Material and Methods: The study population consisted of 40 patients with chronic periodontitis (CP) randomly sorted into two groups of 20. The experimental group received SRP plus 3 watts gaseous ozone in two separate applications five days apart, whereas the control group received SRP plus placebo. Clinical periodontal parameters were assayed and saliva samples were taken before the initial and one month after the second treatment. Periodontal examination assessed plaque index (PI), gingival index (GI), probing depth, and clinical attachment level (CAL). Total antioxidant status (TAS), total oxidant status (TOS), nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG), myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA), and transforming growth factor-beta (TGF-β) levels were evaluated from saliva samples. Results: Changes following treatment in PI, GI, probing depth, and CAL scores were similar for both groups (p>0.05). Of note, TGF-β levels were observed to be higher in the treatment group than in controls (p<0.05). Changes in 8-OHdG, TAS, TOS, NO, MPO, GSH and MDA levels, however, were not significantly different between groups (p>0.05). Conclusion: The findings of this study indicate that SRP plus gaseous ozone versus SRP alone does not correlate to a significant improvement in periodontal recovery.