Student Monthly Progress を開催しました　2025年10月

10月31日 (金)にStudent Monthly Progressが開催されました。３名の大学院生が研究内容について発表されました。

 

【発表者】

1. OE Sao：Laboratory of Anatomy

<Studies on feline ureteral obstruction in pathological changes>

 

2. CHIKUFENJI Boniface Onesmo：Division of Collaboration and Education

<From apparent absence to detection: The emergence of canine leishmaniasis in Malawi>

 

3. MOTAI Yoshinosuke：Laboratory of Infectious Diseases

<Effect of polymorphisms in the meq oncogene of Marek’s disease virus distributed in Japan on virulence>

 

【座長】

NUNEZ Hexelsa Joy Cuesta  : Laboratory of Theriogenology

TSUBO Tomoya : Division of International Research Promotion

 

 

 

   

❖座長レポート❖

 

 

《Studies on feline ureteral obstruction in pathological changes》

　OE Sao

 

　 

 

Ureteral obstruction (UO) is a frequent disease in cats and is often associated with chronic kidney disease. The ureter carries urine from the kidney to the bladder, relying on smooth muscle peristalsis and the barrier function of the urothelium. However, the mechanisms linking nerve activity and urothelial changes during UO remain unclear.
This study examined (1) sympathetic nerve activity in feline ureters and (2) epithelial injury using a mouse model. In cats, obstructed segments showed significantly lower expression of tyrosine hydroxylase (TH) and adrenergic receptor ADRA1A compared with non-obstructed segments. In mice, loss of the urothelium led to the appearance of regenerating KRT14+, COL17A1+, and KI67+ cells, along with neutrophil infiltration and increased expression of inflammatory cytokines Il1b and Cxcl2.
These results suggest that reduced sympathetic function may impair ureteral peristalsis in feline UO, while epithelial disruption triggers inflammation and tissue injury. The findings provide new insight into the mechanisms underlying feline ureteral obstruction.

 

 

《From apparent absence to detection: The emergence of canine leishmaniasis in Malawi》

　CHIKUFENJI Boniface Onesmo

 

　 

 

Canine leishmaniasis caused by Leishmania infantum had long been considered absent from Malawi, with only fragmentary historical evidence. Because the visceral form often mimics malaria, the disease may be under-diagnosed in low-resource settings. Given that dogs act as the principal reservoirs for zoonotic transmission, updated epidemiological data were urgently needed.

In 2024, a cross-sectional survey examined 557 dogs from Mchinji, Nkhotakota, and Zomba districts during mass rabies-vaccination campaigns. Blood and plasma samples were tested using PCR assays (targeting SSU rRNA, ITS2, and kinetoplast DNA) and ELISA with crude (LdSLA) and recombinant (rK39r4) antigens. Overall, 8.1 % of dogs were PCR-positive and 4.1 % were seropositive. A parasite culture from a lymph-node aspirate yielded L. infantum, confirmed by sequence analysis. Zomba showed the highest molecular and serological positivity.

These findings provide the first clear evidence that L. infantum is circulating in dogs in Malawi, suggesting an emerging or re-emerging zoonotic focus. Continuous surveillance, diagnostic capacity building, and public-health interventions are now essential to mitigate this potential One Health threat.

   

 

《Effect of polymorphisms in the meq oncogene of Marek’s disease virus distributed in Japan on virulence》

　MOTAI Yoshinosuke

 

　

 

Marek’s disease virus (MDV) causes T-cell lymphomas and neurological disorders in chickens, such as paralysis and torticollis. Although vaccination has effectively reduced outbreaks, highly virulent MDV strains continue to emerge. The viral oncoprotein Meq functions as a transcription factor that drives tumor formation, and amino-acid polymorphisms in Meq are known to influence pathogenicity. In Japan, sporadic Marek’s disease (MD) cases still occur despite routine vaccination, and Japanese Meq variants display unique mutations of unclear significance.
To investigate these differences, researchers constructed recombinant MDVs encoding Meq from the Japanese isolate Nr-c1 (vNr-c1-Meq) or the parental virulent strain RB-1B (vRB-1B). Experimental infection in chickens showed that vNr-c1-Meq produced lower mortality and tumor incidence but caused distinct respiratory signs such as depression and open-mouth breathing. Viral loads and CD4⁺ T-cell proportions were reduced, while γδ T cells and IFN-γ expression increased in the lungs.
These findings suggest that Meq polymorphisms modulate MDV virulence and clinical manifestations. Further surveillance of field cases and viral genomes in Japan is needed to prevent potential economic losses.