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Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens

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A Special Issue of Animals (ISSN 2076-2615) belonging to the section "Veterinary Clinical Studies".

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 4663

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Prof. Dr. Quanxi Wang

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Guest Editor

College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China
Interests: host–pathogen interaction mechanism; adjuvant function of traditional Chinese veterinary medicine
Special Issues, Collections and Topics in MDPI journals

Dr. Jian Li

E-Mail Website
Guest Editor

College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China
Interests: traditional Chinese medicine; pharmacology; gut; oxidative stress; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Animals (economic animals, pets, wild animals) are frequently exposed to various pathogens (bacteria, viruses, parasites) during their lives. Pathogen infections can cause various types of damage to the bodies of animals, and can even lead to death. However, animals can activate various defense mechanisms such as innate immunity, adaptive immunity, anti-inflammatory and antioxidant effects, and apoptosis to combat pathogens. Of course, effective drug treatments can significantly enhance the ability of animals to resist infections. Traditional Chinese Medicine (TCM), natural herbs and plant extracts play an important role in the prevention and treatment of animal diseases. However, the mechanisms underlying their therapeutic effects remain largely unexplored. Therefore, this Special Issue focuses on elucidating pathogenic infection mechanisms and presenting natural product/phytochemical interventions. These insights will facilitate the discovery of novel therapeutics and strategies for the prevention and treatment of pathogen infections in animals.

Prof. Dr. Quanxi Wang
Dr. Jian Li
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Animals is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

animals
pathogen infections
veterinary drugs
natural products
plant extracts

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Related Special Issue

Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens: 2nd Edition in Animals

Published Papers (5 papers)

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Research

17 pages, 15209 KB

Open AccessArticle

Magnolol Modulates the RIG-I/NF-κB Signaling Pathway to Alleviate JEV Infection-Induced ST Cell Damage

by Bohan Zheng, Mengzhao Jiang, Hongjie Cui, Qinjin Li, Zhaoyan Lin and Xiaohong Huang

Animals 2026, 16(15), 2389; https://doi.org/10.3390/ani16152389 - 3 Aug 2026

Viewed by 436

Abstract

Japanese encephalitis virus (JEV) is a zoonotic pathogen. Infection in breeding boars triggers severe testicular inflammatory storms, resulting in testicular swelling, asthenospermia, oligozoospermia and even irreversible loss of reproductive capacity. Magnolol, a natural extract, exhibits remarkable anti-inflammatory and antioxidant activities. This study utilized swine testicular (ST) cells as an in vitro model to explore magnolol’s protective effects against JEV-mediated inflammation and its underlying mechanism. ST cells were infected with JEV at an MOI of 1 and treated with magnolol at 8, 12 and 16 μg/mL. We detected pro-inflammatory cytokine expression, performed 4D-FastDIA quantitative proteomics to screen differentially expressed proteins, verified key RIG-I and NF-κB cascade molecules at mRNA and protein levels, and tracked p65 nuclear translocation through immunofluorescence. The data showed that JEV significantly elevated TNF-α, IL-1β, IL-6, IL-8 and CCL5, while magnolol reduced these cytokines in a dose-dependent manner. JEV reshaped the proteome of innate immunity and inflammation, and excessively activated the RIG-I/NF-κB axis to increase IKKβ, TRAF2, TRAF6 transcription and p65 phosphorylation and nuclear import; 24 h treatment with 16 μg/mL magnolol greatly restrained this overactivation. In summary, magnolol alleviates JEV-triggered inflammatory injury by inhibiting the RIG-I/NF-κB pathway, offering experimental evidence for its use as a natural agent to mitigate JEV-induced cellular inflammatory response in boars. Full article

(This article belongs to the Special Issue Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens)

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17 pages, 14895 KB

Open AccessArticle

An ORFV F1L mRNA Vaccine Candidate: Preparation, Immunogenicity, and Comparison with a Commercial Live Vaccine

by Yusheng Lin, Jinxiu Jiang, Weiwei Liu, Kul Raj Rai and Yongliang Che

Animals 2026, 16(14), 2274; https://doi.org/10.3390/ani16142274 - 22 Jul 2026

Viewed by 1322

Abstract

Orf virus (ORFV) is a major pathogen in goats and sheep, and control currently depends mainly on commercial live vaccines. Although mRNA vaccines have revolutionized human medicine, their use in veterinary settings is largely unexplored. In this study, an mRNA vaccine candidate encoding the ORFV F1L protein (F1L-mRNA-LNP) was developed via in vitro transcription and encapsulated in lipid nanoparticles. BALB/c mice were divided into five groups (n = 14 each): three receiving different doses of F1L-mRNA-LNP (5, 10, or 15 μg), one receiving a commercial live vaccine (CV), and a PBS control group. Mice were immunized intramuscularly and boosted after 14 days; immune responses were assessed 14 days later following ARRIVE 2.0 guidelines. Both the F1L-mRNA-LNP and CV vaccines induced specific antibodies versus PBS (p < 0.01). The 10 μg mRNA group showed Th1 cytokine and CD8⁺ T cell responses comparable to CV (p > 0.05), whereas IL-4 (Th2) was significantly higher in the CV group (p < 0.05). Neutralizing antibody titers did not differ between groups, indicating that the mRNA vaccine induces comparable Th1 cellular immunity but weaker Th2 humoral immunity. Upon ORFV challenge, the 10 μg F1L-mRNA-LNP vaccine protected BALB/c mice, as evidenced by stable body weight, no clinical symptoms, and reduced viral load, with efficacy comparable to CV (p > 0.05). This study provides strong evidence supporting the optimization of ORFV mRNA vaccines and highlights the translational potential of the F1L-mRNA-LNP candidate vaccine for veterinary applications. Full article

(This article belongs to the Special Issue Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens)

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19 pages, 11776 KB

Open AccessArticle

Radix pseudostellariae Saponins Promote Immunocyte Migration and Chemotaxis via the CCL5/CCR4 Signaling Axis

by Jiaqi Chen, Xiangduan Wei, Yuting Cao, Beilei Chen, Qixian Feng, Zhengrun Xiao, Lihui Xu, Yufang Ma and Quanxi Wang

Animals 2026, 16(12), 1929; https://doi.org/10.3390/ani16121929 - 22 Jun 2026

Viewed by 451

Abstract

Radix pseudostellariae saponins (RPS) enhance immune responses in animals; however, the regulatory mechanisms of these effects remain unclear. This study observed that 14 days post-intranasal immunization with RPS and a Mycoplasma gallisepticum-attenuated vaccine (MGAV), MGAV-specific antibody titers were significantly increased in the blood, and chemokine (C-C motif) ligand 5 (CCL5) messenger RNA expression was significantly increased in the trachea and blood of chickens. Transcriptomic analysis demonstrated that RPS treatment significantly upregulated specific Kyoto Encyclopedia of Genes and Genomes pathways, notably the cytokine–cytokine receptor interaction pathway, which is linked to immune cell migration and involves chemokine receptor chemokine (C-C motif) receptor 4 (CCR4). This finding was corroborated at the protein level by immunohistochemical evidence showing increased CCL5 expression in tracheal tissue. In vitro studies showed that RPS enhanced the phagocytic capacity of RAW264.7 macrophages against ovalbumin, with immunofluorescence revealing time-dependent and dose-dependent CCL5 in these cells. Transwell and scratch-healing assays confirmed that RPS promoted this migration of both RAW264.7 cells and CCR4-positive lymphocytes. Collectively, the findings revealed that RPS modulated the activation, chemotaxis, and migration of macrophages and lymphocytes and is associated with the promotion of the CCL5/CCR4 signaling axis, providing novel evidence for the immune-enhancing effects of RPS by enhancing immunogenicity. Full article

(This article belongs to the Special Issue Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens)

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15 pages, 7070 KB

Open AccessArticle

Synergistic Roles of InlA, InlB and LLO in the Infection of Trigeminal Ganglion Neurons by Ovine-Derived Listeria monocytogenes LM90SB2

by Yue Lv, Qiuyan Deng, Ye Li, Yuxuan Lu, Jiahui Xie, Jingjing Ren and Jianjun Jiang

Animals 2026, 16(9), 1383; https://doi.org/10.3390/ani16091383 - 30 Apr 2026

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Abstract

Listeria monocytogenes (Lm) is an important zoonotic foodborne pathogen that causes severe rhombencephalitis in ruminants. The trigeminal ganglion is a critical node for Lm invasion of the central nervous system via neural pathways. However, the roles of key virulence factors InlA, InlB, and LLO from ovine-derived Lm in trigeminal ganglion neuron infection remain unclear. In this study, LM90SB2, an ovine-derived Lm strain isolated from a sheep with encephalitis in Xinjiang, China, was used as the wild type, and its ΔInlAB double-gene deletion and ΔInlABO triple-gene deletion mutants were constructed. Primary mouse trigeminal ganglion cells (TGCs) were infected with these strains, and cell-association and invasion assays, bacterial colonization analysis, cell scratch tests, Western blotting, and qRT-PCR were performed to explore the effects of InlA, InlB, and LLO on Lm infection of TGCs and their regulatory roles in host adhesion molecules N-cadherin and NCAM1. The results showed that the wild-type LM90SB2 had significantly stronger cell-association, invasion, and colonization abilities in TGCs than the ΔInlAB and ΔInlABO mutants (p < 0.01 or p < 0.0001). LM90SB2 infection significantly upregulated the mRNA and protein expression levels of N-cadherin and NCAM1 in TGCs and enhanced TGC migration, while these effects were gradually attenuated with the sequential deletion of InlA, InlB and LLO. This study clarifies the synergistic roles of InlA, InlB, and LLO in mediating the infection of trigeminal ganglion neurons by ovine-derived Lm and reveals the molecular mechanism by which Lm promotes neural invasion by regulating the expression of host cell adhesion molecules. Our findings provide important experimental data for elucidating the neural invasion pathway of Lm in ruminants and lay a theoretical foundation for the development of targeted prevention and control strategies for ruminant listeriosis in veterinary clinical practices. Full article

(This article belongs to the Special Issue Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens)

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17 pages, 7232 KB

Open AccessArticle

Crotoxin Upregulating NLRP-3 Inflammasome and IL-18 and Activating CD4⁺ and CD8⁺ Lymphocytes in Experimental Encephalitozoon cuniculi Infection

by João Lourival de Souza, Júnior, Eluane de Luca da Silva Martins, Anuska Marcelino Alvares Saraiva, Elizabeth Christina Perez, Ronalda Silva de Araújo, Sandra Coccuzzo Sampaio, Rodrigo Augusto Faganholi da Silva and Maria Anete Lallo

Animals 2026, 16(6), 955; https://doi.org/10.3390/ani16060955 - 18 Mar 2026

Viewed by 628

Abstract

Encephalitozoon cuniculi is an atypical, opportunistic, obligate intracellular fungal pathogen that infects vertebrates. It survives within the host by modulating the host immune response. Crotoxin (CTX), a bioactive compound isolated from the venom of Crotalus durissus terrificus, has been reported to modulate immune responses. This study evaluated the effects of CTX on the immune response of mice infected with E. cuniculi. Mice were immunosuppressed with cyclophosphamide (Cy), infected with E. cuniculi spores, and treated with a single dose of CTX on the day of experimental. The animals were euthanized on day 14 post-infection. Levels of T helper (Th1, Th2, and Th17) cytokines were measured in plasma, and macrophage and lymphocyte populations were analyzed in peritoneal lavage fluid and spleen. In addition, histopathological alterations, hepatic fungal burden, and mRNA expression levels of NLRP3 inflammasome–related genes were assessed. CTX upregulated NLRP3 inflammasome expression and increased IL-18 production, while reducing fungal burden in E. cuniculi-infected mice. Moreover, CTX increased the proportions of macrophages and B cells and enhanced IFN-γ expression in CD4⁺ and CD8⁺ T lymphocytes. Collectively, these findings indicate that CTX reduces fungal load in Cy-immunosuppressed mice infected with E. cuniculi by priming the NLRP3 inflammasome complex and upregulating IL-18 production. Full article

(This article belongs to the Special Issue Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens)

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