The Investigation of Cell Adhesion Molecules in the Lung Tissues of Cattle with Cystic Echinococcosis

Yıl 2019, Cilt: 30 Sayı: 1, 14 - 19, 30.06.2019

Orhan Yavuz Güngör Çağdaş Dinçel Sami Gökpınar Ali Evren Haydardedeoğlu

https://doi.org/10.35864/evmd.586538

Öz

Cystic echinococcosis is a zoonotic disease with worldwide distribution caused by Echinococcus granulosus, 

represents a substantial global health problem. Hydatid cyst (Echinococcus) has a remarkable negative effect on the 

health of people and the economic development of the country. The objective of this study was to investigate the CD68, 

nicotinamide nucleotide adenylyltransferase 3 (NMNAT 3), Neuregulin 1 (NRG1) and Neuregulin 2 (NRG2) expres-

sions in bovine lungs infected with E. granulosus and to identify whether they have any correlation with pulmonary 

pathology. For this purpose, 30 bovine lung tissues were used between January 2016 and December 2016 collected in 

Kırıkkale  slaughterhouse.  In  histopathologic  examinations,  proliferation  of  fibrous  connective  tissue  and  infiltration 

of mononuclear cells were detected in the lung tissues of the bovine. Most of the cysts were seen to be quite thick 

capsule. There was also a cellular line rich in abundant fibroblasts and mononuclear cells. The cyst wall was found to 

be an eosinophilic laminar structure. There was infiltration with lymphocytes and macrophages, especially eosinophils 

and giant cells. Immunohistochemically, CD68 positivity was seen around the bronchi, bronchioles and cystic matter. 

However; NMNAT 3, NRG1 and NRG2 showed no positive reactions in macrophages, bronchi, bronchioles and alveo-

lar epithelium. These results indicate that NMNAT 3, NRG1 and NRG2 pathways were not used in pulmonary pathol-

ogy. Therefore, it is the most important result of the study that the adhesion molecules in pulmonary pathology are not 

originating from NMNAT 3, NRG1 and NRG2.

Anahtar Kelimeler

CD68, NMNAT 3, Neuregulin 1, Neuregulin 2, Pathology

Destekleyen Kurum

Aksaray University Scientific Research Committee

Proje Numarası

2018-002.

Teşekkür

This study was funded by Aksaray University Scientific Research Committee (ASÜBAP) with project number: 2018-002.

Kistik Ekinokokkozisli Sığır Akciğerlerinde Hücre Adezyon Moleküllerinin Araştırılması

Öz

Kistik ekinokokkozis, dünya çapında Echinococcus granulosus’un neden olduğu geniş dağılımı olan zoonotik 

bir hastalıktır ve önemli bir küresel sağlık sorunudur. Kist hidatid (Echinococcus), insan sağlığı ve ülkenin ekonomik 

gelişimi üzerinde dikkate değer bir olumsuz etkiye sahiptir. Bu çalışmanın amacı E. granulosus ile enfekte olmuş sığır 

akciğerlerinde  CD68,  nikotinamid  nükleotid  adenililtransferaz  3  (NMNAT  3),  Neuregulin  1  (NRG1)  ve  Neuregulin 

2 (NRG2) ekspresyonlarını araştırmak ve pulmoner patoloji ile herhangi bir korelasyon olup olmadığını saptamaktır. 

Bu amaçla Kırıkkale kesimhanesinde Ocak 2016 ile Aralık 2016 arasında toplanan 30 adet büyükbaş akciğer dokusu 

kullanıldı. Histopatolojik incelemede, sığırların akciğer dokularında fibröz bağ dokusu proliferasyonu ve mononükleer 

hücrelerin infiltrasyonu saptandı. Kistlerin çoğunun oldukça kalın bir kapsülü olduğu görüldü. Ayrıca fibroblastlar ve 

mononüklear hücreler bakımından zengin bir hücresel hat vardı. Kist duvarının eozinofilik bir laminar yapı gösterdiği 

tespit edildi. Lenfosit, makrofaj, özellikle eozinofil infiltrasyonları ve dev hücrelerinin de görüldüğü yangısal alanlar 

dikkati çekti. İmmünhistokimyasal olarak, CD68 ekspresyonları bronş, bronşiyol ve kistik yapının etrafında gözlendi. 

NMNAT 3, NRG1 ve NRG2 makrofajlarda, bronş, bronşiyol ve alveolar epitellerinde hiçbir pozitif reaksiyon göster-

memiştir. Bu sonuçlar, pulmoner patolojide NMNAT 3, NRG1 ve NRG2 yollarının kullanılmadığını göstermektedir. 

Bu nedenle, çalışmanın en önemli sonucu, pulmoner patolojide adezyon moleküllerinin NMNAT 3, Neuregulin 1 ve 

Neuregulin 2’den kaynaklanmadığıdır.

Anahtar Kelimeler

CD68, NMNAT 3, Neuregulin 1, Neuregulin 2, Patoloji

Proje Numarası

2018-002.

Kaynakça

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