Estimation of Conformation Score in Relation to Body Measurements Using 3D Scanner in Swamp Buffaloes

The objective of this study was to develop the appropriate equations to estimate the conformation score both in male and female swamp buffaloes using body part measurements from 3D scanner. The buffaloes' conformation was evaluated using 3D scanning technique in 72 males and 78 females at Surin, Uthaithanee, Bangkok, Nakornpanom and Sakaew provinces of Thailand. Height (A), heart girth (B), shoulder width (C), iliac width (D), ischial tuberosity width (E), the length between shoulder and ileal wing (F, G), the length between ileal wing to ischial tuberosity (H, I), the length between shoulder to ischial tuberosity (J1, J2), tail length (K), knee circumference (L), the width measuring between the tip (M), the middle (N) and the base of horns (O), the horn length (P) and the length measured from the base to the tip of the horn on the same site (Q) were measured. The results found that A B, D, E, FG, J1J2, L and P were significantly higher along with age in both males and females. The scores obtained currently between academics and the philosophers were closely correlated in every categories in both male and females buffaloes over four and three years of age, respectively, except for the reproductive organ in females. The coefficient of determination (R2) for score prediction in male buffaloes under 4 years old was highest when body length and knee circumference were included in the equation: Score = [(0.568 J1J2) + (1.584 L) - 77.89] (R2 = 0.57, n = 19). The prime factor affecting score in male over 4 years of age was heart girth (R2 = 0.70). However, R2 was rise up to 0.85 when girdle width was included into the equation: Score = [(0.485 B) + (1.892 D) - 156.54] (n = 53). In females under 3 years old, the R2 were low in all type of equation (one traits to four traits equation; 0.25-0.42, n = 21). However, in females over 3 years of age the R2 is high (0.66) when girdle width was included in the equation : Score = [2.655 D - 91.52] (n = 57). Therefore, different traits should be used to evaluate the conformation in immature and mature males and females

Estimation of body weight and body surface area in swamp buffaloes using visual image analysis

The three dimensional computerized visual image analysis was performed to evaluate the body weight (BW) and body surface area (BSA) in swamp buffaloes. Nineteen swamp buffaloes were measured the conformation by linear measurement compared to 3D body scanner at different points : body height (A), heart girth (B), shoulder width (C), iliac width (D), ischial tuberosity width (E), the length between shoulder and ileal wing (F, G), the length between ileal wing to ischial tuberosity (H, I) and the length between shoulder to ischial tuberosity (J1, J2).  The significant correlation was found between these two methods.  The 3D body scanner was then performed in 28 males and 39 females for BW and 68 males and 74 non-pregnant and 31 pregnant females for BSA estimation. The appropriate models to estimate BW in buffaloes were BW = - 1174.07 + 4.31 (B) + 7.75 (FG) (R2 = 0.76, P<0.001), BW (male) = -1265.99 + 4.94(B) + 14.41(D)  (R2 = 0.81; P<0.001) and BW (female) = -563.66 + 7.94 (C ) + 14.77 (E)  (R2 = 0.86; P<0.001).  For BSA, the appropriate equations were BSA = -4.31 + 0.034(A) + 0.036(J1J2) (R2 = 0.82, P<0.001), BSA (male) = -4.01 + 0.032(A) + 0.037(J1J2) (R2 = 0.816, P<0.001) and BSA (female) = -3.50 + 0.013(A) + 0.012(B) + 0.040(E) + 0.015(J1J2) (R2 = 0.916, P<0.001). In conclusion, the 3D body scanner can be used to estimate BW and BSA in buffaloes with different models among males and females

Toxoplasma gondii effectors are master regulators of the inflammatory response

Toxoplasma is a highly successful parasite that establishes a life-long chronic infection. To do this, it must carefully regulate immune activation and host cell effector mechanisms. Here we review the latest developments in our understanding of how Toxoplasma counteracts the immune response of the host, and in some cases provokes it, through the use of specific parasite effector proteins. An emerging theme from these discoveries is that Toxoplasma effectors are master regulators of the pro-inflammatory response, which elicits many of the toxoplasmacidal mechanisms of the host. We speculate that combinations of these effectors present in certain Toxoplasma strains work to maintain an optimal parasite burden in different hosts to ensure parasite transmission.Knights Templar Eye Foundation, Inc.American Heart Association (0835099N)Massachusetts Life Sciences Center (New Investigator Award)Singapore-MIT Alliance for Research and Technology (SMART)National Institutes of Health (U.S.) (NIH RO1-AI080621)New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases (NERCE Developmental Grant)National Cancer Institute (U.S.) (Irvington Postdoctoral Fellowship Program

Impaired Innate Immunity in Tlr4−/− Mice but Preserved CD8+ T Cell Responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-Deficient Mice

The murine model of T. cruzi infection has provided compelling evidence that development of host resistance against intracellular protozoans critically depends on the activation of members of the Toll-like receptor (TLR) family via the MyD88 adaptor molecule. However, the possibility that TLR/MyD88 signaling pathways also control the induction of immunoprotective CD8+ T cell-mediated effector functions has not been investigated to date. We addressed this question by measuring the frequencies of IFN-γ secreting CD8+ T cells specific for H-2Kb-restricted immunodominant peptides as well as the in vivo Ag-specific cytotoxic response in infected animals that are deficient either in TLR2, TLR4, TLR9 or MyD88 signaling pathways. Strikingly, we found that T. cruzi-infected Tlr2−/−, Tlr4−/−, Tlr9−/− or Myd88−/− mice generated both specific cytotoxic responses and IFN-γ secreting CD8+ T cells at levels comparable to WT mice, although the frequency of IFN-γ+CD4+ cells was diminished in infected Myd88−/− mice. We also analyzed the efficiency of TLR4-driven immune responses against T. cruzi using TLR4-deficient mice on the C57BL genetic background (B6 and B10). Our studies demonstrated that TLR4 signaling is required for optimal production of IFN-γ, TNF-α and nitric oxide (NO) in the spleen of infected animals and, as a consequence, Tlr4−/− mice display higher parasitemia levels. Collectively, our results indicate that TLR4, as well as previously shown for TLR2, TLR9 and MyD88, contributes to the innate immune response and, consequently, resistance in the acute phase of infection, although each of these pathways is not individually essential for the generation of class I-restricted responses against T. cruzi

The role of DNA microarrays in Toxoplasma gondii research, the causative agent of ocular toxoplasmosis

Ocular toxoplasmosis, which is caused by the protozoan parasite Toxoplasma gondii, is the leading cause of retinochoroiditis. Toxoplasma is an obligate intracellular pathogen that replicates within a parasitophorous vacuole. Infections are initiated by digestion of parasites deposited in cat feces or in undercooked meat. Parasites then disseminate to target tissues that include the retina where they then develop into long-lived asymptomatic tissue cysts. Occasionally, cysts reactivate and growth of newly emerged parasites must be controlled by the host’s immune system or disease will occur. The mechanisms by which Toxoplasma grows within its host cell, encysts, and interacts with the host’s immune system are important questions. Here, we will discuss how the use of DNA microarrays in transcriptional profiling, genotyping, and epigenetic experiments has impacted our understanding of these processes. Finally, we will discuss how these advances relate to ocular toxoplasmosis and how future research on ocular toxoplasmosis can benefit from DNA microarrays

FUNCTION OF JNK2 AND MYD88 DURING TOXOPLASMA GONDII INFECTION

The intracellular protozoan parasite Toxoplasma gondii infects humans and other warm-blooded animals. Understanding the pathogenesis of infection and immunity to the parasite is important since this pathogen is capable of causing fatal disease in immunocompromised hosts. T. gondii infection elicits IL-12 release from innate immune cells, resulting in high level IFN-g production. This confers resistance to infection through T cell dependent Type I immunity. Signal transduction pathways involved in IL-12 production, a little understood area, are the major focus of this dissertation. Neutrophils are innate immune cells capable of IL-12 production during T. gondii infection. I found that JNK2 MAPK is the major isoform expressed in mouse neutrophils. My results show that JNK2 plays a major role in PMN IL-12 and CCL/MCP-1 production during in vitro parasite stimulation. Neutrophil chemotaxis was also partially dependent upon JNK2, whereas oxidative burst and phagocytic activities were not affected by absence of this MAPK protein. I examined the role of JNK2 in response to T. gondii infection in vivo. I found that JNK2 plays a role in T. gondii-induced immunopathology since absence of JNK2 contributed to enhanced disease resistance associated with alleviated pathology in the small intestine and decreased neutrophil recruitment at this site. Surprisingly, and in contrast to my in vitro data, JNK2 negatively regulated IL-12 production during in vivo infection. Toll-like receptor adaptor protein MyD88 is important for IL-12 induction during Toxoplasma infection. During oral T. gondii infection, I found that MyD88 was essential for controlling parasite burden leading to disease resistance. In addition, I found that neutrophil recruitment and expression of IGTP, a molecule required for control of infection, was also dependent upon MyD88 signaling. Interestingly, while IL-12 was greatly diminished in the absence of this molecule, T cell dependent IFN-g responses were nevertheless generated. Importantly, I found that MyD88 was not required for development of protective immunity to T. gondii. Thus, while MyD88 signaling was required for microbicidal control of infection, it was not necessary for initiation of adaptive immunity to this parasite. In summary, this dissertation elucidates the complex roles of JNK2 and MyD88 signaling pathways in IL-12 production and resistance to Toxoplasma infection. Investigating the functions of these molecules in response to T. gondii contributes to a clearer understanding of the immunopathogenesis of infection with Toxoplasma and other microbial pathogens.Anandamahidol Foundation, National Institute of Healt

Toxoplasma gondii Inhibits Toll-Like Receptor 4 Ligand-Induced Mobilization of Intracellular Tumor Necrosis Factor Alpha to the Surface of Mouse Peritoneal Neutrophils

Neutrophils are well-known to rapidly respond to infection through chemotactic infiltration at sites of inflammation, followed by rapid release of microbicidal molecules, chemokines, and proinflammatory cytokines. For tumor necrosis factor alpha (TNF-α), we recently found that neutrophils contain intracellular pools of the cytokine and display the capacity to upregulate transcriptional activity of the gene during lipopolysaccharide (LPS) stimulation. We now show that triggering of mouse peritoneal neutrophils with Toll-like receptor 2 (TLR2), TLR4, and TLR9 ligands, but not ligands of TLR3, induces upregulation of surface membrane TNF-α. However, neutrophils infected with the protozoan Toxoplasma gondii displayed an inability to respond fully in terms of TLR ligand-induced increases in membrane TNF-α expression. Infected neutrophils failed to display decreased levels of intracellular TNF-α upon LPS exposure. In contrast to intermediate inhibitory effects in nontreated neutrophils, T. gondii induced a complete blockade in LPS-induced surface TNF-α expression in the presence of the protein synthesis inhibitor cycloheximide. Despite these inhibitory effects, the parasite did not affect LPS-induced upregulation of TNF-α gene transcription. Collectively, the results show that Toxoplasma prevents TLR ligand-triggered mobilization of TNF-α to the neutrophil surface, revealing a novel immunosuppressive activity of the parasite

Phosphoinositide-3-Kinase-Dependent, MyD88-Independent Induction of CC-Type Chemokines Characterizes the Macrophage Response to Toxoplasma gondii Strains with High Virulence▿

Chemokines play an important role in inflammation and infection due to their ability to recruit cells of innate and adaptive immunity. Here we examined mouse macrophage chemokine responses during intracellular infections with high- and low-virulence Toxoplasma gondii strains. The high-virulence type I strain RH induced a large panel of CC-type chemokines, whereas responses elicited by strains PTG (type II) and M7741 (type III) were much weaker. Strikingly, the T. gondii-induced chemokine response occurred independently of signaling through the Toll-like receptor adaptor MyD88. Instead, production of chemokines during infection was heavily dependent upon phosphoinositide-3-kinase signaling pathways. Because infection with type I strains such as RH results in an uncontrolled proinflammatory cytokine response, we hypothesize that this virulence phenotype is a consequence of early strong induction of chemokines by type I, but not type II or III, Toxoplasma strains