구.농수식품
Abstract
Salik Nazki1,†, Amina Khatun1,2,†, Chang‑Gi Jeong1,†, Sameer ul Salam Mattoo3, Suna Gu3, Sim‑In Lee1, Seung‑Chai Kim1, Ji‑Hyo Park1, Myoun‑Sik Yang1, Bumseok Kim1, Choi‑Kyu Park4, Sang‑Myeong Lee3,* and Won‑Il Kim1,*
1 College of Veterinary Medicine, Jeonbuk National University, Iksan, South Korea. 2 Department of Pathology, Faculty of Animal Science and Veterinary Medicine, Sher‑e‑Bangla Agricultural University, Dhaka 1207, Bangladesh. 3 Division of Biotechnology, Advanced Institute of Environment and Bioscience, College of Environmental & Biosource Science, Jeonbuk National University, Iksan, South Korea. 4 College of Veterinary Medicine, Kyungpook National University, Daegu, South Korea.
*Correspondence
†Salik Nazki, Amina Khatun and Chang‑Gi Jeong contributed equally to this study
Abstract
The host-associated defence system responsible for the clearance of porcine reproductive and respiratory syndrome virus (PRRSV) from infected pigs is currently poorly understood. To better understand the dynamics of host–pathogen interactions, seventy-five of 100 pigs infected with PRRSV-JA142 and 25 control pigs were euthanized at 3, 10, 21, 28 and 35 days post-challenge (dpc). Blood, lung, bronchoalveolar lavage (BAL) and bronchial lymph node (BLN) samples were collected to evaluate the cellular immune responses. The humoral responses were evaluated by measuring the levels of anti-PRRSV IgG and serum virus-neutralizing (SVN) antibodies. Consequently, the highest viral loads in the sera and lungs of the infected pigs were detected between 3 and 10 dpc, and these resulted in moderate to mild interstitial pneumonia, which resolved accompanied by the clearance of most of the virus by 28 dpc. At peak viremia, the frequencies of alveolar macrophages in infected pigs were significantly decreased, whereas the monocyte-derived DC/macrophage and conventional DC frequencies were increased, and these effects coincided with the early induction of local T-cell responses and the presence of proinflammatory cytokines/chemokines in the lungs, BAL, and BLN as early as 10 dpc. Conversely, the systemic T-cell responses measured in the peripheral blood mononuclear cells were delayed and significantly induced only after the peak viremic stage between 3 and 10 dpc. Taken together, our results suggest that activation of immune responses in the lung could be the key elements for restraining PRRSV through the early induction of T-cell responses at the sites of virus replication.
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