Editorial: Cell migration and tissue remodeling in infectious diseases

Pathogens are responsible for severe diseases that result in significant morbidity and mortality worldwide. During the pathogenesis of infectious diseases, cell migration and tissue remodeling play pivotal roles in shaping disease progression and clinical outcomes (Medzhitov, 2008;Wynn and Vannella, 2016). While these responses are essential for host defense, they may also contribute to tissue damage and environmental changes favoring pathogen persistence and coinfections (Nathan and Ding, 2010;Lei et al., 2025). Therefore, a deeper understanding of the mechanisms underlying host cell adhesion, migration, and tissue remodeling is critical for the development of innovative therapeutic strategies.This Research Topic brings together cutting-edge studies that explore recent advances in our understanding of immune cell adhesion and migration, as well as tissue remodeling, in the context of infectious diseases. Collectively, these contributions provide important insights into the immunopathogenesis of infections and highlight potential avenues for the development of novel therapeutic approaches.Zika virus (ZIKV) infection has been extensively associated with neurological and congenital abnormalities; however, its impact on other tissues, such as skeletal muscle, remains less well understood. In this Research Topic, the study entitled "Zika virus infection disturbs development of human muscle progenitor cells" provides important insights into how viral infection interferes with muscle regeneration processes. Using an in vitro model of human the authors demonstrate 30 that ZIKV efficiently infects proliferating myoblasts, leading to alterations in key cellular functions. 31Infected cells exhibited impaired cell cycle progression, proliferation, and significant defects 32 in adhesion, migration, and membrane dynamics, all of which are essential for proper muscle 33 development and repair. Moreover, ZIKV infection disrupted myoblast fusion, ultimately 34 compromising the formation of mature myotubes. Interestingly, while differentiated myotubes were 35 able to control viral replication, infected myoblasts displayed a markedly altered myogenic program. 36These findings highlight how ZIKV targets early stages of muscle cell differentiation, affecting 37 fundamental processes such as cell migration and tissue remodeling, and suggest that viral interference 38 with myogenesis may contribute to both developmental abnormalities and impaired muscle 39 regeneration (Rocha et al., 2025). 40Expanding from virus-induced alterations in progenitor cell function to chronic infectious 41 contexts, dysregulated cell migration and tissue remodeling are also central to the persistence of 42 bacterial infections. In this context, the review entitled "Wound Repair and Immune Function in the 43 Pseudomonas infected CF Lung: Before and After Highly Effective Modulator Therapy" discusses how 44 impaired wound repair and immune responses shape the pathophysiology of cystic fibrosis (CF) lung 45 disease. The authors highlight that persistent infection with Pseudomonas aeruginosa drives a cycle of 46 chronic inflammation and defective tissue repair, in which epithelial damage, altered immune cell 47 function, and unresolved injury perpetuate lung remodeling. Importantly, although highly effective 48 cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies, such as 49 elexacaftor/tezacaftor/ivacaftor, have significantly improved clinical outcomes and partially restored 50 epithelial function, key processes involved in immune regulation and tissue repair do not fully return 51 to a non-CF state. Moreover, incomplete eradication of P. aeruginosa and the potential for recurrent 52 colonization underscore the continued disruption of host-pathogen interactions. This work emphasizes 53 how persistent microbial presence and dysregulated immune cell dynamics sustain pathological tissue 54 remodeling, reinforcing the need for complementary therapeutic strategies targeting inflammation, 55 infection, and repair mechanisms (Matthews et al., 2025). 56At the molecular level, pathogen-driven modulation of host and parasite cellular machinery 57 further illustrates the complexity of processes governing cell migration and tissue invasion. In this 58 context, the study entitled "EhVps35, a retromer component, is a key factor in secretion, motility, and 59 tissue invasion by Entamoeba histolytica" uncovers key mechanisms underlying parasite virulence.The authors demonstrate that EhVps35, a central component of the complex, functionally 61 interacts with the ESCRT machinery, forming a coordinated network involved in protein trafficking, 62 secretion, and cellular remodeling. Notably, EhVps35 was shown to associate with a wide range of 63 proteins and to be secreted in vesicles alongside ESCRT components, highlighting its role in vesicular 64 transport pathways. Functional analyses revealed that silencing of EhVps35 significantly impairs 65 trophozoite migration and reduces tissue invasion capacity, while also altering the localization of key 66 proteins involved in membrane dynamics. These findings provide compelling evidence that 67 intracellular trafficking and vesicle-mediated processes are critical regulators of parasite motility and 68 host tissue invasion, reinforcing the concept that modulation of cellular architecture is a central strategy 69 employed by pathogens to promote infection and dissemination (Diaz et al., 2024). 70Further highlighting the molecular strategies employed by pathogens to modulate host-pathogen 71 interactions, the study entitled "A Toxoplasma gondii thioredoxin with cell adhesion and antioxidant 72 function" characterizes a multifunctional parasite protein involved in both redox balance and host cell 73 interaction. The authors describe Trx21 as a thioredoxin-like protein containing glycosaminoglycan 74 (GAG)-binding motifs and a transmembrane region, supporting its role in host cell adhesion. 75 Functional analyses revealed that Trx21 exhibits antioxidant activity, protecting DNA from oxidative 76 damage, while also mediating adhesion to host cells. These findings indicate that Trx21 contributes to 77 parasite survival by integrating oxidative stress control with adhesion mechanisms, highlighting how 78Toxoplasma gondii exploits multifunctional proteins to facilitate host cell invasion, persistence, and 79 modulation of the tissue microenvironment (Wang et al., 2024). 80Collectively, the studies included in this Research Topic provide a wide view of how infectious 81 agents modulate cell migration and tissue remodeling across different biological contexts, ranging from 82 alterations in progenitor cell function to chronic inflammation and finely tuned molecular mechanisms 83 of pathogen virulence. These contributions highlight the multifaceted nature of host-pathogen 84 interactions, in which both host responses and pathogen-derived factors converge to shape cellular 85 dynamics and tissue architecture. Importantly, they also underscore that dysregulation of these 86 processes is a central feature of disease pathogenesis, contributing to tissue damage, impaired repair, critical to develop innovative strategies aimed at restoring tissue and improving clinical 91 outcomes in infectious diseases.