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Animals
Special Issues
Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens
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Advances in Pathogenic Mechanisms and Drug Strategies of Veterinary Pathogens

A special issue of Animals (ISSN 2076-2615). This special issue belongs to the section "Veterinary Clinical Studies".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1148

Special Issue Editors

Prof. Dr. Quanxi Wang

E-Mail Website
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
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 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-blind 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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • animals
  • pathogen infections
  • veterinary drugs
  • natural products
  • plant extracts

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

15 pages, 7070 KB  
Article
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
Viewed by 275
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 [...] Read more.
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  
Article
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 408
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 [...] Read more.
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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