Microbial Infections and Host Immunity

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Molecular Microbiology and Immunology".

Deadline for manuscript submissions: closed (31 January 2026) | Viewed by 8646

Special Issue Editor


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Guest Editor
School of Biomedical Sciences, University of Plymouth, Drake Circus, Plymouth PL4 8AA, UK
Interests: immunology; inflammation; probiotics; antimicrobial responses; infection; oral and gastrointestinal mucosae

Special Issue Information

Dear Colleagues,

The Special Issue on “Microbial Infections and Host Immunity” aims to shed light on the intricate interactions between microbial pathogens and the host immune system. This Special Issue seeks to explore the latest advancements in the understanding the mechanisms behind microbial infections and the corresponding host immune responses. We welcome original research articles, reviews, and perspectives that investigate the pathogenesis of various microbial infections, the development of novel treatment strategies, and the host immune system’s role in combating these infections. We encourage submissions that tackle fundamental questions in microbiology and immunology, as well as those that offer clinical insights relevant to human health. By fostering interdisciplinary dialogue, this Special Issue endeavours to contribute to the growing body of knowledge in microbial infections and host immunity. Submissions are expected to provide valuable contributions to the academic community, advancing our understanding of these interrelated fields.

Dr. Andrew Foey
Guest Editor

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Keywords

  • microbial pathogens
  • host immunity
  • infections
  • mechanisms
  • treatment strategies

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Published Papers (7 papers)

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Research

Jump to: Review

26 pages, 2229 KB  
Article
Prolactin and 17β-Estradiol Are Epigenetic Regulators That Modify the Effector Response of Bovine Macrophages During Staphylococcus aureus Challenge
by Marco Antonio Barajas-Mendiola, Josmarth Remigio-Hernández, Marisol Pérez-Galicia, Joel Edmundo López-Meza and Alejandra Ochoa-Zarzosa
Microorganisms 2026, 14(3), 576; https://doi.org/10.3390/microorganisms14030576 - 3 Mar 2026
Viewed by 410
Abstract
Staphylococcus aureus (S. aureus) is the most prevalent pathogen associated with subclinical mastitis, which significantly impacts dairy farming worldwide. Fluctuations in reproductive hormones, such as bovine prolactin (bPRL) and 17β-estradiol (E2), are known to compromise the innate immune response (IIR) of [...] Read more.
Staphylococcus aureus (S. aureus) is the most prevalent pathogen associated with subclinical mastitis, which significantly impacts dairy farming worldwide. Fluctuations in reproductive hormones, such as bovine prolactin (bPRL) and 17β-estradiol (E2), are known to compromise the innate immune response (IIR) of the mammary gland (MG). In this study, we evaluated the effects of bPRL and E2 on the effector response of primary bovine macrophages, isolated from lactating Holstein cows, challenged with S. aureus. We demonstrated that physiological concentrations of bPRL (5 ng/mL) and E2 (50 pg/mL) induced differential changes in the expression of pro-inflammatory (TNF-α, IL-6, and IL-1β) and anti-inflammatory (IL-10) cytokines, chemokines (IL-8), antimicrobial peptides (BNBD10 and S100A7), and miRNAs (miR-451, miR-155, miR-7863, miR-146a, miR-21a, Let-7a-5p, miR-30b, and miR-23a) in S. aureus-challenged macrophages. Moreover, these hormones promoted global histone H3 acetylation and the epigenetic H3K9ac mark without affecting H3K9me2 levels. Hormonal treatment also modulated histone deacetylase (HDAC) activity. Furthermore, hormonal treatment altered macrophage chemotaxis and phagocytosis. In conclusion, bPRL and E2 modulate the effector functions of bovine macrophages during S. aureus infection. This process could be associated with the regulation of histone H3 modifications, such as H3K9ac, in IIR-related genes. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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15 pages, 2649 KB  
Article
Antiviral Immune Responses Against Murine Cytomegalovirus Induced by an Oral Salmonella-Based Vaccine Expressing Viral M33 Protein
by Hao Gong, Yujun Liu, Bin Yan and Fenyong Liu
Microorganisms 2025, 13(7), 1510; https://doi.org/10.3390/microorganisms13071510 - 28 Jun 2025
Viewed by 837
Abstract
Human cytomegalovirus (CMV) is the leading cause of congenital infections, often leading to mental retardation and neurological disorders. It is a major public health priority to develop a vaccine for preventing and controlling human CMV infection. In this report, we generated an oral [...] Read more.
Human cytomegalovirus (CMV) is the leading cause of congenital infections, often leading to mental retardation and neurological disorders. It is a major public health priority to develop a vaccine for preventing and controlling human CMV infection. In this report, we generated an oral Salmonella-based vaccine to express the M33 protein of murine cytomegalovirus (MCMV) and investigated the anti-MCMV immune responses induced in mice immunized with this vaccine. Compared to those administered with phosphate-buffered saline (PBS) or a control vaccine without M33 expression, mice immunized with the vaccine expressing the M33 protein exhibited a remarkable induction of antiviral serum IgG and mucosal IgA humoral responses and a significant elicitation of antiviral T cell responses. Successful inhibition of viral growth in lungs, spleens, livers, and salivary glands was also found in the vaccinated animals compared to the PBS-treated animals or those immunized with the control vaccine without M33 expression. Furthermore, substantial protection against MCMV challenge was observed in mice immunized with the vaccine. Thus, Salmonella-based vaccine expressing MCMV M33 can induce anti-MCMV effective immune responses and protection. Our study implies that attenuated Salmonella expressing human CMV antigens, including its homologue to M33, may represent promising oral anti-CMV vaccine candidates. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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16 pages, 2668 KB  
Article
Revisiting Host-Binding Properties of LigA and LigB Recombinant Domains
by Henrique M. Pires, Igor R. M. Silva, Aline F. Teixeira and Ana L. T. O. Nascimento
Microorganisms 2025, 13(6), 1293; https://doi.org/10.3390/microorganisms13061293 - 31 May 2025
Cited by 1 | Viewed by 1087
Abstract
Pathogenic bacteria of the genus Leptospira are the etiological agents of leptospirosis, a disease that affects humans and animals worldwide. Despite the increasing number of studies, the mechanisms of leptospiral pathogenesis remain poorly comprehended. In this study, we report various interactions of the [...] Read more.
Pathogenic bacteria of the genus Leptospira are the etiological agents of leptospirosis, a disease that affects humans and animals worldwide. Despite the increasing number of studies, the mechanisms of leptospiral pathogenesis remain poorly comprehended. In this study, we report various interactions of the LigA7’-13’ and LigB1’-7’ domains with host components. The LigA7’-13’ and LigB1’-7’ were cloned into the pET28a vector, and the recombinant proteins were expressed in E. coli C43 (DE3) and E. coli BL21 (DE3), respectively. Both recombinant protein domains were expressed in soluble form and purified using nickel-chelating chromatography. The rLigA7’-13’ and rLigB1’-7’ domains exhibited binding to several types of integrins, with most interactions occurring in a dose-dependent and saturable manner, consistent with the characteristics of typical receptor-ligand interactions. The recombinant domain LigA7’-13’ demonstrated affinity for the glycosaminoglycans (GAGs) chondroitin-4-sulfate, chondroitin sulfate, heparin, chondroitin sulfate B, and heparan sulfate, while no binding was detected for LigB1’-7’ with these molecules. Both rLigA7’-13’ and rLigB1’-7’ interacted with components of the terminal complement pathway and were capable of recruiting C9 from normal human serum (NHS). These interactions may inhibit the formation of polyC9, ultimately preventing the assembly of the membrane attack complex (MAC). Collectively, our data expand the repertoire of host components that interact with rLigA7’-13’ and rLigB1’-7’, opening new avenues for understanding leptospiral immune evasion and broadening the roles of these domains in bacterial virulence. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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19 pages, 2148 KB  
Article
Evaluation of Probiotic Bacillus velezensis for the Control of Pathogens That Cause Post-Weaning Diarrhea in Piglets—Results from In Vitro Testing and an In Vivo Model Using Caenorhabditis elegans
by Pia Bilde Rasmussen, Josh Walker, Stacey Robida Stubbs, Andreea Cornelia Udrea and Chong Shen
Microorganisms 2025, 13(6), 1247; https://doi.org/10.3390/microorganisms13061247 - 28 May 2025
Cited by 1 | Viewed by 1546
Abstract
We investigated the effect of probiotic Bacillus velezensis strains (LSSA01, 15AP4 and 2084) on pathogens causing post-weaning diarrhea in piglets (Enterotoxigenic Escherichia coli, Clostridium perfringens, Salmonella spp.). We studied the effect of B. velezensis and its cell-free supernatant on (1) pathogen [...] Read more.
We investigated the effect of probiotic Bacillus velezensis strains (LSSA01, 15AP4 and 2084) on pathogens causing post-weaning diarrhea in piglets (Enterotoxigenic Escherichia coli, Clostridium perfringens, Salmonella spp.). We studied the effect of B. velezensis and its cell-free supernatant on (1) pathogen growth; (2) IPEC-J2 cell cytokine and tight junction protein expression; (3) IPEC-J2 cell ‘wound’ recovery; (4) adhesion to IPEC-J2 cells and pathogen exclusion; and (5) Caenorhabditis elegans survival following pathogen exposure. Cell-free supernatant (CFS) from all strains inhibited the growth of ETEC F4 and F18 (by 36.9–53.2%; p < 0.05). One or more strains inhibited C. perfringens and Salmonella spp. (p < 0.05). Strain 2084 CFS increased IL-8 expression (+12.0% vs. control; p < 0.05; 6 h incubation), whereas LSSA01 CFS increased the expression of tight junction proteins (p < 0.05 vs. control; 6 h incubation) and accelerated 96 h ‘wound’ healing. Colony-forming units (CFUs) of all strains displayed a higher binding affinity to IPEC-J2 cells than 12 ETEC isolates, reduced adhesion of ETEC F4 and F18 and extended C. elegans survival over 30 d. The results indicate that probiotic B. velezensis strains have potential for use in the control of PWD pathogens. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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22 pages, 2642 KB  
Article
Molecular Insights into Cell-Mediated Immunity in Atypical Non-Ulcerated Cutaneous Leishmaniasis
by Luís Fábio S. Batista, Carmen M. Sandoval Pacheco, Gabriela V. Araujo Flores, Frederico M. Ferreira, André N. A. Gonçalves, Wilfredo H. Sosa-Ochoa, Vânia L. R. da Matta, Claudia M. C. Gomes, Concepción Zúniga, Carlos E. P. Corbett, Daniel C. Jeffares, Helder I. Nakaya, Fernando T. Silveira and Márcia D. Laurenti
Microorganisms 2025, 13(2), 413; https://doi.org/10.3390/microorganisms13020413 - 13 Feb 2025
Cited by 1 | Viewed by 1967
Abstract
Leishmania (Leishmania) infantum chagasi infections range from asymptomatic (AS) to severe visceral leishmaniasis (VL). One of the manifestations is an atypical non-ulcerated cutaneous leishmaniasis (NUCL), which occurs in some locations of Central America with few cases of VL. We conducted a [...] Read more.
Leishmania (Leishmania) infantum chagasi infections range from asymptomatic (AS) to severe visceral leishmaniasis (VL). One of the manifestations is an atypical non-ulcerated cutaneous leishmaniasis (NUCL), which occurs in some locations of Central America with few cases of VL. We conducted a transcriptomic analysis of cell-mediated immunity (CMI) on blood samples from NUCL, AS, VL patients from Amapala, Honduras, and healthy controls. RNA-seq revealed a similar perturbation of gene expression in NUCL and AS. Eight gene signatures of CMI were found in NUCL involved in CD8+ T lymphocyte infiltration, reactive oxygen species generation, PD-1 receptor ligand, inflammasome assembly, chemotaxis, complement receptor and suppressor immune cell infiltration. NUCL was distinguished from VL by its up-regulation of differently expressed genes (DEGs) related to T lymphocyte exhaustion, adhesion and transmigration of leukocytes, and down-regulation of oxidative stress genes. In contrast, VL exhibited up-regulated DEGs involved in antigen cross-presentation, and similar to VL from Brazil, down-regulated DEGs involved in innate immunity. Corroborating the transcriptome findings, both the Leishmanin skin test, and the immunopathology of NUCL skin lesion defined NUCL as a proinflammatory condition, intermediate between the AS and VL clinical outcomes. That condition may be the underlying element for the benign nature of the NUCL. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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19 pages, 9063 KB  
Article
NcSWP8, a New Spore Wall Protein, Interacts with Polar Tube Proteins in the Parasitic Microsporidia Vairimorpha (Nosema) ceranae
by Pengfei Wang, Dufu Li, Qianmin Hai, Siming Liu, Yueyue Zhang, Jun Zhang, Jinshan Xu, Zhengang Ma and Zeyang Zhou
Microorganisms 2025, 13(1), 142; https://doi.org/10.3390/microorganisms13010142 - 12 Jan 2025
Cited by 1 | Viewed by 2086
Abstract
Vairimorpha (Nosema) ceranae is a pathogen that affects Apis mellifera and Apis ceranae Fabricius, capable of spreading within and between honeybee colonies. The spore wall of microsporidia is the initial structure to contact the host cell directly, which may play a crucial role [...] Read more.
Vairimorpha (Nosema) ceranae is a pathogen that affects Apis mellifera and Apis ceranae Fabricius, capable of spreading within and between honeybee colonies. The spore wall of microsporidia is the initial structure to contact the host cell directly, which may play a crucial role in the infection process. Currently, several spore wall proteins have been identified in microsporidia, but only two spore wall proteins from V. ceranae have been characterized. Here, we report the expression and identification of a novel spore wall protein, NcSWP8, with a molecular mass of 21.37 kDa in V. ceranae. Subcellular localization analysis revealed that NcSWP8 was localized on the spore wall of V. ceranae. Co-immunoprecipitation and Far-Western blotting experiments demonstrated that NcSWP8 could stably interact with polar tube proteins, NcPTP2 and NcPTP3. The antibody blocking assay significantly decreased their infection rate, indicating that NcSWP8 played a significant role in the process of V. ceranae infection. These results together suggested that NcSWP8 was a new spore wall protein localized to the spore wall and interacted with the polar tube proteins, playing a crucial role in supporting the formation of the spore wall and potentially affecting the process of infection of V. ceranae. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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Review

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18 pages, 951 KB  
Review
Periodontal Disease and Its Association with Porphyromonas gingivalis: Current Understanding of Microbial Dysbiosis, Immunopathology and Immune Evasion
by Samantha Robins, Alex Strachan, Vehid Salih and Andrew Foey
Microorganisms 2026, 14(3), 641; https://doi.org/10.3390/microorganisms14030641 - 12 Mar 2026
Viewed by 219
Abstract
Porphyromonas gingivalis is described as a keystone pathogen associated with periodontal disease (PD), which exhibits enhanced representation upon microbial dysbiosis in such a chronic inflammatory disease. This oral pathogen drives and contributes to a dysregulated immune response, resulting in stages of aggressive destructive [...] Read more.
Porphyromonas gingivalis is described as a keystone pathogen associated with periodontal disease (PD), which exhibits enhanced representation upon microbial dysbiosis in such a chronic inflammatory disease. This oral pathogen drives and contributes to a dysregulated immune response, resulting in stages of aggressive destructive immune activation and inflammation punctuated by immune suppression, which underlies the relapsing–remitting nature of this disease. The understanding of key mechanisms and balance between protective innate, adaptive immune responses and dysregulated responses, linked to changes in the oral mucosal microbial environment, will afford researchers the potential to manipulate oral mucosal environments for clinical benefit. This review focuses on the dynamic interactions between the oral pathogen P. gingivalis and the immune system with an emphasis on immune evasion and how the potential correction of these mechanisms may benefit future therapeutic interventions, leading to the successful treatment of PD. Full article
(This article belongs to the Special Issue Microbial Infections and Host Immunity)
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